Facts But Also Fear: HIV testing


According the UK Department of Health, 35 percent of people living with HIV in the UK are unaware of their status, suggesting the need for a testing awareness day here, as well as in the United States. But what do the experts think?

"National AIDS Day goes by without a whisper nowadays. Funding is down for HIV and AIDS. So any awareness raising agenda is important", says Graham Downes, who has been an expert on the European Union Task Force for AIDS. "In terms of testing, one of the real problems is reaching people and letting them know that getting tested is doing the right thing," he says.

Conscious that part of the problem for people thinking about getting an HIV test is convenience, The UK Charity The Terence Higgins Trust has recently established 22 "fast test" centres around the UK where people can get the results of an HIV test in an hour. "We're trying to make these clinics more accessible by running them out of normal working hours and in the community, for example in youth centres or leisure centres," says a Trust spokesperson.

At the UK National AIDS Trust, Rachel Bruce says that prevention and education remain the priority. "What we really need is more actual investment in prevention measures, such as access to condoms", she says. "Education about HIV and how to avoid it needs to be improved too. Too few people still have too little information about HIV and AIDS prevention."

Doing the right thing. Access. Education. These are all vital components on the agenda. But the one person who was really on message today about HIV testing was—somewhat randomly as I was seeking expert advice on the issue—George Michael, who admitted that he was scared of having an HIV test.

The fear of knowing that you are in a high risk group. The fear that a test is only going to be bad news. The fear that you will be judged for being HIV-positive. The fear that you won't be able to afford treatment. All these fears, and the many individual manifestations of them, must be recognized and addressed as part of any strategy reaching out to encourage people to get an HIV test.

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  • invalid-0

    When it’s like being handed a death sentence? The prospect of living with HIV means looking forward to severe depression, toxic side effects from drugs, an abrupt halt to one’s sexual enjoyment and sexual life, social discrimination, stigma, possible job loss, a possible end to relationships, and other serious repercussions.

    Why not let the supposed HIV-positives who-don’t-know-it-yet just carry on? I don’t understand why people want to persuade others to ruin their lives for insufficient cause. After all, don’t many HIV-positives who don’t take drugs or other HIV treatment essentially become “long-term non progressors”? Apparently, one thing that most of this group has in common is not taking anti-retroviral drugs at all, or quitting them early on (http://gateway.nlm.nih.gov/MeetingAbstracts/102239330.html, other studies listed here: http://www.healtoronto.com/survivors.html#wells).

    Perhaps the cure is worse than the disease, in other words.

  • scott-swenson

    Dear Anonymous: With such "wisdom" why not sign your post? Where to begin:

    1. Knowing one's HIV status prevents a person from unwittingly passing the virus on. The only thing worse than getting the virus is knowing that you might have infected someone else – Knowledge is Power. It also allows a person to determine where they are in the course of the disease and what the best course of action is for them. There are a variety of options that can prolong the time before one has to go on medications, if that is the choice made by the individual.

    2. Becoming HIV positive is NOT a death sentence. Some people alive today have been positive for 20+ years and with proper health care, nutrition, mental and physical health, will continue to live full lives.

    3. It would be hard for people not to be depressed if anything you said above were true, thankfully there are many HIV support groups, peer-to-peer counselors and other organizations working on connecting HIV positive people so they do not suffer the stigma from attitudes like you expressed.

    4. The medications are toxic, there is no doubt about it, and that is why poz people have to monitor their health very closely if they are on medications. People can now go for years without medications at all, and while there is mixed information, some people successfully incorporate drug holidays/breaks to help reduce toxicity — in careful consultation with HIV specialists. That, however, is almost beside the point, because when you look at populations that do not have access to medications, you find much higher death rates. It is clear that the medications have issues that people continue to work through, but there is NO DOUBT they they are extending life for those with access, and thus hope for millions. The fight now is continuing to improve the medications and sharing the access so more people can join in a journey of hope to see more progress in the fight against AIDS.

    5. As for stigma, job loss, sex life …. Others will always stigmatize, but it is up to the individual to have a balanced perspective on life and not allow that to get to them — you could help by joining the fight in a more affirming way. For example, work for laws to protect poz people's rights, to change health care so that insurance and the right to health care are not tied to job status. And as for sex life, if a person enjoyed sex before there is no reason they should not enjoy it after. They just need to be honest, safe, and responsible — knowing your HIV status allows you to be honest because you know.

    6. As for the treatment (there is no cure – yet) being worse than the disease, millions of people are fighting to get the treatment because it works. The most important thing is that every BODY is unique and reacts differently to different treatments. Some long-term non-progressors, fortunate as they are, do not represent the vast majority of experience people have with HIV. There is much to be learned as the disease continues and when you can put studies up that show the numbers of people surviving without drugs as are surviving with them, great.

    Anybody who has any doubts should spend more time at: AIDSTruth.org


    Be the change you seek,

    Scott Swenson, Editor

  • http://.www.MySpace.com/TheHIVIndustryExposed invalid-0

    Where to begin:

    1. Knowing one’s HIV status prevents a person from unwittingly passing the virus on.

    I believe Doctor Luc Montagnier said that somewhere in an interview too…and also he said “We Did not Purify”.. Pubmed is listed with hundreds of abstracts defining the global HIV Testing spree as worthless

    2. Becoming HIV positive is NOT a death sentence.

    of Course not.. Only the HIV Industry gives “HIV” ALL power under heaven and earth. Professor Duesberg describes HIV as a natural ‘Passenger Virus” (see pubmed).

    3. there are many HIV support groups, peer-to-peer counselors and other organizations working on connecting HIV positive people so they do not suffer the stigma from attitudes like you expressed.

    Preaching the same old HIV/AIDS sermons making “side effects” subside in the background while HIV is blamed.. Amen

    4. The medications are toxic, there is no doubt about it, and that is why poz people have to monitor their health very closely if they are on medications.

    The Fact is there is nothing Medicinal about the drugs nor Specific and as more studies evolve the fact remains that so called HIV/AIDS patients have been dying from Liver Failure all along never mind HIV.

    5. As for stigma, job loss, sex life …. Others will always stigmatize, but it is up to the individual to have a balanced perspective on life and not allow that to get to them —

    The HIV/AIDS $camdemic has done well at creating the “sick” sedistic voodoo and once it has been exposed future generations will no longer be stigmatized in the name of corruption and greed.

    6. As for the treatment (there is no cure – yet)

    This is correct all of the Clinical Trials for the Toxic Drugs declare that Everything is Unknown or SEVERE.

    There is much to be learned as the disease continues and when you can put studies up that show the numbers of people surviving without drugs as are surviving with them, great.,

    HIV is supposed to be a Retrovirus NOT a Disease the Government WARNINGS bear this out the studies you have suggested should have been done along time ago it’s too late to change your minds now EVERYONE is Dead or Dying

    Anybody who has any doubts should spend more time at: AIDSTruth.org

    Didn’t a Member of the “Lancet”at the Toronto AIDS Conference Scold Mr John Moore for such DESPERATION?

  • invalid-0

    I always hear this nonesense….35% of Britians are HIV positive, but don’t know their status…this has been said as well in the US for over 20 years. Well, if this were the case and we use the latency period of 10-15 years from HIV to AIDS, then we should naturally have seen an influx of these naive seropositives going to hosipitals with AIDS defining conditions….

    BUT WE DON’T!!!!!!!!!!!!!!!!!!!

    Something is Wrong here!

  • http://myspace.com/nerosopeningact invalid-0

    1. Please cite the study or studies which proved HIV is transmissible at all. I’ve searched for years for such a study, and what I’ve found is that there are two types of studies which deal with HIV transmission: Those that *assume* transmissibility, and those that actually *study* transmissibility. Of those that actually study transmissibility, ALL have proven that HIV isn’t transmissible, but they hide this fact behind a claim of low transmissibility. (Exempli gratia among many: Padian et al 1997). If you cannot provide the proof that HIV is transmissible, then you are assuming that it is, and we both know what happens when we assume, don’t we?

    I myself have been HIV-positive for 9 years, and in that time I’ve had 3 long-term relationships with women with whom I’ve had unprotected vaginal and anal sex literally thousands of times (and yes, they all knew my alleged HIV status.) To date, all have been tested repeatedly, and all are HIV-negative.

    I also met a guy, shortly after my (mis)diagnosis, who’d been a “bug chaser” for 13 years. Guess what? After 13 years of actively TRYING to get HIV, he was still HIV-negative.

    2. You’re right — becoming HIV-positive is NOT a death sentence. It’s what happens to you afterwards that kills you, such as having your doctor utterly ignore real health issues because your numbers are so “good” (as happened to me, nearly resulting in my death in November 2000,) and/or killing you with highly toxic drugs for a virus that has never been proven to exist in your blood (as happened to Ryan White.)

    3. You’ve obviously never lived as an HIV-positive, or you wouldn’t be saying this. You sound like a white person trying to explain to a black person that racism doesn’t exist anymore. If ignorance is bliss, then your planet must be Paradise. Your insensitivity to the issues faced every day by PWAs is appalling, and you should be ashamed.

    4. The medications are toxic, there is no doubt about it. Period. After only one year of triple drug therapy, I was already showing signs of liver damage. Incidentally, the #1 killer of AIDS patients in the US since 1999 is liver failure caused by the medications.

    Now, let’s do the math. According to the CDC, about a 3rd of all HIV-positives don’t even know their status, therefore they could not possibly be taking ARVs. Another 40% or so are aware of their status, but aren’t taking meds, leaving about 25% of HIV-positives who are actually taking meds.

    Now, with only a small minority of HIV-positives actually taking meds, the largest single fraction of those who actually die in any given year die from liver failure brought on by the meds (not to mention those that die of stroke and other complications from the meds).

    Oh yeah, there is NO DOUBT that ARVs are extending lives, is there?

    5. Thanks for the suggestion. It just so happens that “joining the fight in a more affirming way” is exactly what I’m doing, by going out among the public to fight ignorance about this fraud which has spawned a multi-trillion dollar industry. ( http://www.shillfactor.net )

    As an HIV-positive who is joining the fight in an affirming way as you suggest, how much do you want to bet that by this time tomorrow, my post will no longer be here?

    6. Even if what you said (“millions are fighting to get the treatment…”) were true, that wouldn’t prove that it works. Either you can provide the scientific studies to prove it, or you don’t know what you’re talking about.

    An article published in the August 5, 2006 edition of Lancet tells a MUCH different story (HIV treatment response and prognosis in Europe and North America in the first decade of highly active antiretroviral therapy: a collaborative analysis. – May MT, Sterne JA, et al, Antiretroviral Therapy (ART) Cohort Collaboration
    Lancet 2006 Aug 5 368(9534):451-8 http://www.duesberg.com/articles/2006,%20Lancet,%20HIV%20treatment%20resp..pdf)

    In the article, it is demonstrated that while Highly Active Antiretroviral Therapy (HAART) is effective at reducing viral load and increasing CD4 count, this does not translate into better clinical outcomes, and HAART actually appears to increase the risk of developing AIDS.

    …But at least HAART increases CD4 count, right? Yes, it does, but according to a study published only a month later in JAMA (http://jama.ama-assn.org/cgi/content/abstract/296/12/1498) higher CD4 counts have very little correlation (a single-digit percentage of correlation in all cases) to eventual progression to AIDS.

    I myself had a CD4 count of over 1400 before starting ARVs, and was as sick as a dog with what otherwise would certainly have been called “AIDS”. Once I started meds, my CD4 count shot up to over 1700, and I got even sicker. However, when I’d ask my doctor about my illness, she’d say, “What illness? Your numbers are great; you’re healthy as a horse!” She even went so far as to publicly call me her “miracle patient” on several occasions.

    Within two years, I suffered a near-fatal case of pneumonia, with a CD4 count that was substantially higher than normal, and I have (as you put it) NO DOUBT that if I’d died, it would have been called “AIDS”. As it turns out, it was due to a severe mold allergy, and when I got a proper diagnosis and treatment, it cleared right up, after I’d suffered severe illness for two years with an HIV doctor who insisted that there was nothing wrong with me, because my CD4 counts were substantially higher than normal.

    By all means, your readers should visit aidstruth.org, and I say that as someone who strongly disagrees with what that website has to say. However, I’d highly recommend getting all sides of the story, for anyone who doesn’t want to learn the REAL facts about AIDS the hard way like I did:

    http://www.virusmyth.net
    http://www.aliveandwell.org
    http://www.helpforhiv.com
    http://www.rethinkingaids.com
    http://www.shillfactor.net
    http://www.duesberg.com
    http://www.karymullis.com

    Signed (since you seem to think that’s important),
    — Gos
    gos@nerosopeningact.com
    “Nobody here but us heretics…”

  • invalid-0

    Dear Scott,

    Maybe everyone would not be just giddy about having to deal with stigma etc… Maybe they feel that they have the right to ask questions about why they have to be labeled and stigmatized in the first place (maybe they feel that they have the right to investigate information that gives them a second opinion about thier stigmatized state). And also it should not matter wheather a person signs there name or not if they want to share their thoughts or wisdom. Science has always been able to be questioned at least it did before HIV. Also if there are many things that can cause a false positive test result people have a right to know and make and informed decision if they wan to take the risk of having one. And if there are somemany positive peolple who don’t klnow that they are positive yet are not falling ill, then these non-progressors must make up a large number of people.

  • invalid-0

    HIV has never even been shown to exist in the sense of a true virus. Retroviruses are nothing more than random proteins in the blood that do no harm. They do not replicate. Please see Dr Stephan Lanka’s research. HIV is not the real cause of AIDS.

    Troy Heimer, MD
    Stanford University School of Medicine

  • invalid-0

    “Please cite the study or studies which proved HIV is transmissible at all.”

    I’ve appended a few below. Gos is also grossly misrepresenting the Lancet study, because it only followed people for the first year of ART and survival was 98% or greater after one year. The better viral load & CD4 results after one year of ART seen in more recent periods should translate into a longer duration of benefit, which will require longer follow up of people on ART than one year (at least there’s a link to the paper so you can read this yourself). There was a slightly higher incidence of AIDS during the first year of ART in the most recent period (2003) because of the higher numbers of people with TB (this is also in the paper).

    Gos is lying about Benigno Rodriguez’s JAMA paper, which did not show “higher CD4 counts have very little correlation (a single-digit percentage of correlation in all cases) to eventual progression to AIDS.” The paper evaluated the ability of a single viral load measurement to explain the variability in CD4 counts measured six months later. A study evaluating the prognostic value of viral load and CD4 count in terms of AIDS or death in the same cohort was published recently, it reported that: “Median HIV-1 RNA explained 51% and 58% of the variability in AIDS and death, and median CD4 cell count explained 29% and 35% of the variability in AIDS and death, respectively.” (JAMA.2007; 297: 2349-2350).

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=8028613&query_hl=26&itool=pubmed_DocSum

    http://content.nejm.org/cgi/content/abstract/331/6/341 (free full text with registration)

    de Vincenzi I.
    A longitudinal study of human immunodeficiency virus transmission by heterosexual partners. European Study Group on Heterosexual Transmission of HIV.
    N Engl J Med. 1994 Aug 11;331(6):341-6.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=10738050&query_hl=26&itool=pubmed_DocSum

    http://content.nejm.org/cgi/content/abstract/342/13/921 (free full text with registration)

    Quinn TC, Wawer MJ, Sewankambo N, Serwadda D, Li C, Wabwire-Mangen F, Meehan MO, Lutalo T, Gray RH.
    Viral load and heterosexual transmission of human immunodeficiency virus type 1. Rakai Project Study Group.
    N Engl J Med. 2000 Mar 30;342(13):921-9.

    http://www.journals.uchicago.edu/JID/journal/issues/v181n4/991196/991196.html

    Hisada M, O’Brien TR, Rosenberg PS, Goedert JJ.
    Virus load and risk of heterosexual transmission of human immunodeficiency virus and hepatitis C virus by men with hemophilia. The Multicenter Hemophilia Cohort Study.
    J Infect Dis. 2000 Apr;181(4):1475-8. Epub 2000 Apr 7.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=11461676&query_hl=57&itool=pubmed_docsum

    Fideli US, Allen SA, Musonda R, Trask S, Hahn BH, Weiss H, Mulenga J, Kasolo F, Vermund SH, Aldrovandi GM.
    Virologic and immunologic determinants of heterosexual transmission of human immunodeficiency virus type 1 in Africa.
    AIDS Res Hum Retroviruses. 2001 Jul 1;17(10):901-10.

    (1022 discordant couples followed prospectively)

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=11323041&query_hl=57&itool=pubmed_docsum

    Gray RH, Wawer MJ, Brookmeyer R, Sewankambo NK, Serwadda D, Wabwire-Mangen F, Lutalo T, Li X, vanCott T, Quinn TC; Rakai Project Team.
    Probability of HIV-1 transmission per coital act in monogamous, heterosexual, HIV-1-discordant couples in Rakai, Uganda.
    Lancet. 2001 Apr 14;357(9263):1149-53.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=14624374&query_hl=1&itool=pubmed_DocSum

    Serwadda D, Gray RH, Sewankambo NK, Wabwire-Mangen F, Chen MZ, Quinn TC, Lutalo T, Kiwanuka N, Kigozi G, Nalugoda F, Meehan MP, Ashley Morrow R, Wawer MJ.
    Human immunodeficiency virus acquisition associated with genital ulcer disease and herpes simplex virus type 2 infection: a nested case-control study in Rakai, Uganda.
    J Infect Dis. 2003 Nov 15;188(10):1492-7. Epub 2003 Oct 28.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=3126891&query_hl=26&itool=pubmed_DocSum

    France AJ, Skidmore CA, Robertson JR, Brettle RP, Roberts JJ, Burns SM, Foster CA, Inglis JM, Galloway WB, Davidson SJ.
    Heterosexual spread of human immunodeficiency virus in Edinburgh.
    Br Med J (Clin Res Ed). 1988 Feb 20;296(6621):526-9.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=2502150&query_hl=26&itool=pubmed_DocSum

    Johnson AM, Petherick A, Davidson SJ, Brettle R, Hooker M, Howard L, McLean KA, Osborne LE, Robertson R, Sonnex C, et al.
    Transmission of HIV to heterosexual partners of infected men and women.
    AIDS. 1989 Jun;3(6):367-72.

    http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=2495045

    Risk factors for male to female transmission of HIV. European Study Group.
    BMJ. 1989 Feb 18;298(6671):411-5.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=2059362&query_hl=26&itool=pubmed_DocSum

    Kamenga M, Ryder RW, Jingu M, Mbuyi N, Mbu L, Behets F, Brown C, Heyward WL.
    Evidence of marked sexual behavior change associated with low HIV-1 seroconversion in 149 married couples with discordant HIV-1 serostatus: experience at an HIV counselling center in Zaire.
    AIDS. 1991 Jan;5(1):61-7.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=1628088&query_hl=26&itool=pubmed_DocSum

    Allen S, Tice J, Van de Perre P, Serufilira A, Hudes E, Nsengumuremyi F, Bogaerts J, Lindan C, Hulley S.
    Effect of serotesting with counselling on condom use and seroconversion among HIV discordant couples in Africa.
    BMJ. 1992 Jun 20;304(6842):1605-9.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=1392708&query_hl=26&itool=pubmed_DocSum

    Comparison of female to male and male to female transmission of HIV in 563 stable couples. European Study Group on Heterosexual Transmission of HIV.
    BMJ. 1992 Mar 28;304(6830):809-13.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=8097789&query_hl=26&itool=pubmed_DocSum

    Saracco A, Musicco M, Nicolosi A, Angarano G, Arici C, Gavazzeni G, Costigliola P, Gafa S, Gervasoni C, Luzzati R, et al.
    Man-to-woman sexual transmission of HIV: longitudinal study of 343 steady partners of infected men.
    J Acquir Immune Defic Syndr. 1993 May;6(5):497-502.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=7744488&query_hl=26&itool=pubmed_DocSum

    Rockstroh JK, Ewig S, Bauer T, Luchters G, Oldenburg J, Bailly E, Kaiser R, Schneweis KE, Brackmann HH, Dengler HJ, et al.
    Male-to-female transmission of HIV in a cohort of hemophiliacs–frequency, risk factors and effect of sexual counseling.
    Infection. 1995 Jan-Feb;23(1):29-32.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=7841237&query_hl=26&itool=pubmed_DocSum

    Nicolosi A, Correa Leite ML, Musicco M, Arici C, Gavazzeni G, Lazzarin A.
    The efficiency of male-to-female and female-to-male sexual transmission of the human immunodeficiency virus: a study of 730 stable couples. Italian Study Group on HIV Heterosexual Transmission.
    Epidemiology. 1994 Nov;5(6):570-5.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=7677133&query_hl=26&itool=pubmed_DocSum

    Guimaraes MD, Munoz A, Boschi-Pinto C, Castilho EA.
    HIV infection among female partners of seropositive men in Brazil. Rio de Janeiro Heterosexual Study Group.
    Am J Epidemiol. 1995 Sep 1;142(5):538-47.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=7576332&query_hl=26&itool=pubmed_DocSum

    N’Gbichi JM, De Cock KM, Batter V, Yeboue K, Ackah A, Zadi F, Diallo MO, Kadio A, Gayle HD.
    HIV status of female sex partners of men reactive to HIV-1, HIV-2 or both viruses in Abidjan, Cote d’Ivoire.
    AIDS. 1995 Aug;9(8):951-4.

    http://www.annals.org/cgi/content/full/125/4/324

    Deschamps MM, Pape JW, Hafner A, Johnson WD Jr.
    Heterosexual transmission of HIV in Haiti.
    Ann Intern Med. 1996 Aug 15;125(4):324-30.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=9233454&query_hl=26&itool=pubmed_DocSum

    Fiore JR, Zhang YJ, Bjorndal A, Di Stefano M, Angarano G, Pastore G, Fenyo EM.
    Biological correlates of HIV-1 heterosexual transmission.
    AIDS. 1997 Jul 15;11(9):1089-94.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=10397539&query_hl=26&itool=pubmed_DocSum

    Carpenter LM, Kamali A, Ruberantwari A, Malamba SS, Whitworth JA.
    Rates of HIV-1 transmission within marriage in rural Uganda in relation to the HIV sero-status of the partners.
    AIDS. 1999 Jun 18;13(9):1083-9.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=10360803&query_hl=26&itool=pubmed_DocSum

    Pedraza MA, del Romero J, Roldan F, Garcia S, Ayerbe MC, Noriega AR, Alcami J.
    Heterosexual transmission of HIV-1 is associated with high plasma viral load levels and a positive viral isolation in the infected partner.
    J Acquir Immune Defic Syndr. 1999 Jun 1;21(2):120-5.

    http://www.guttmacher.org/pubs/journals/3127299.html

    Family Planning Perspectives
    Volume 31, Number 6, November/December 1999
    The Effectiveness of Condoms in Reducing Heterosexual Transmission of HIV
    By Karen R. Davis and Susan C. Weller

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=11464148&query_hl=26&itool=pubmed_DocSum

    Lockett SF, Robertson JR, Brettle RP, Yap PL, Middleton D, Leigh Brown AJ.
    Mismatched human leukocyte antigen alleles protect against heterosexual HIV transmission.
    J Acquir Immune Defic Syndr. 2001 Jul 1;27(3):277-80.

    http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=11739704

    Trask SA, Derdeyn CA, Fideli U, Chen Y, Meleth S, Kasolo F, Musonda R, Hunter E, Gao F, Allen S, Hahn BH.
    Molecular epidemiology of human immunodeficiency virus type 1 transmission in a heterosexual cohort of discordant couples in Zambia.
    J Virol. 2002 Jan;76(1):397-405.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=12048366&query_hl=26&itool=pubmed_DocSum

    Hugonnet S, Mosha F, Todd J, Mugeye K, Klokke A, Ndeki L, Ross D, Grosskurth H, Hayes R.
    Incidence of HIV infection in stable sexual partnerships: a retrospective cohort study of 1802 couples in Mwanza Region, Tanzania.
    J Acquir Immune Defic Syndr. 2002 May 1;30(1):73-80.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=11873077&query_hl=26&itool=pubmed_DocSum

    Tovanabutra S, Robison V, Wongtrakul J, Sennum S, Suriyanon V, Kingkeow D, Kawichai S, Tanan P, Duerr A, Nelson KE.
    Male viral load and heterosexual transmission of HIV-1 subtype E in northern Thailand.
    J Acquir Immune Defic Syndr. 2002 Mar 1;29(3):275-83.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=9436757&query_hl=57&itool=pubmed_docsum

    Ragni MV, Faruki H, Kingsley LA.
    Heterosexual HIV-1 transmission and viral load in hemophilic patients.
    J Acquir Immune Defic Syndr Hum Retrovirol. 1998 Jan 1;17(1):42-5.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=9345119&query_hl=57&itool=pubmed_DocSum

    http://aje.oxfordjournals.org/cgi/reprint/146/8/655 (free pdf reprint)

    Operskalski EA, Stram DO, Busch MP, Huang W, Harris M, Dietrich SL, Schiff ER, Donegan E, Mosley JW.
    Role of viral load in heterosexual transmission of human immunodeficiency virus type 1 by blood transfusion recipients. Transfusion Safety Study Group.
    Am J Epidemiol. 1997 Oct 15;146(8):655-61.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=7546420&query_hl=41&itool=pubmed_docsum

    Serwadda D, Gray RH, Wawer MJ, Stallings RY, Sewankambo NK, Konde-Lule JK, Lainjo B, Kelly R.
    The social dynamics of HIV transmission as reflected through discordant couples in rural Uganda.
    AIDS. 1995 Jul;9(7):745-50.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=8074601&query_hl=41&itool=pubmed_docsum

    Musicco M, Lazzarin A, Nicolosi A, Gasparini M, Costigliola P, Arici C, Saracco A.
    Antiretroviral treatment of men infected with human immunodeficiency virus type 1 reduces the incidence of heterosexual transmission. Italian Study Group on HIV Heterosexual Transmission.
    Arch Intern Med. 1994 Sep 12;154(17):1971-6.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=1961169&query_hl=41&itool=pubmed_DocSum

    Henry K.
    Documented male-to-female transmission of HIV-1 after minimal vaginal exposure in the absence of other cofactors for infection.
    Minn Med. 1991 Oct;74(10):32-4.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=8601226&query_hl=41&itool=pubmed_DocSum

    Downs AM, De Vincenzi I.
    Probability of heterosexual transmission of HIV: relationship to the number of unprotected sexual contacts. European Study Group in Heterosexual Transmission of HIV.
    J Acquir Immune Defic Syndr Hum Retrovirol. 1996 Apr 1;11(4):388-95.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=16549978&query_hl=9&itool=pubmed_DocSum

    Brooks JT, Robbins KE, Youngpairoj AS, Rotblatt H, Kerndt PR, Taylor MM, Daar ES, Kalish ML.
    Molecular analysis of HIV strains from a cluster of worker infections in the adult film industry, Los Angeles 2004.
    AIDS. 2006 Apr 4;20(6):923-8.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=12564239&query_hl=9&itool=pubmed_DocSum

    Allen KW, Moss TR, Evans BG, Nguyen-Van-Tam JS, Rogstad KE, Radford J, Jewes LA.
    Doncaster: the public health response to a local cluster of heterosexually acquired HIV infection.
    Commun Dis Public Health. 2002 Dec;5(4):271-5.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=12402955&query_hl=9&itool=pubmed_DocSum

    Robbins KE, Weidle PJ, Brown TM, Saekhou AM, Coles B, Holmberg SD, Folks TM, Kalish ML.
    Molecular analysis in support of an investigation of a cluster of HIV-1-infected women.
    AIDS Res Hum Retroviruses. 2002 Oct 10;18(15):1157-61.

    http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=11522190&query_hl=9&itool=pubmed_DocSum

    Kane CT, Montavon C, Toure MA, Faye MA, Ndiaye AG, Diallo AG, Ndoye I, Liegeois F, Delaporte E, Mboup S, Peeters M.
    Full-length genome sequencing of HIV type 1 group O viruses isolated from a heterosexual transmission cluster in Senegal.
    AIDS Res Hum Retroviruses. 2001 Aug 10;17(12):1211-6.

    http://jama.ama-assn.org/cgi/content/full/282/1/20

    JAMA. 1999;282:20-21.
    From the Centers for Disease Control and Prevention: Morbidity and Mortality Weekly Report
    Cluster of HIV-Positive Young Women—New York, 1997-1998
    MMWR. 1999;48:413-416

  • invalid-0

    Richard Jefferys wrote: “The better viral load & CD4 results after one year of ART seen in more recent periods should translate into a longer duration of benefit…” [emphasis mine]

    It should, but it doesn’t. If it did, you’d be able to cite the proof, considering the reams and reams of “citations” you provided (more on that in a sec). I myself am living proof that it’s possible to nearly die from what would otherwise be called “AIDS-related pneumonia” while one’s CD4 count is a multiple of what would otherwise be considered normal. On the flip side of the same coin, there have been HIV-negative athletes who have been documented to have CD4 counts below 200, and be in perfect health.

    Your very use of the word “should” exposes an assumption, (as opposed to a proven fact) and in science, what happens when we assume, boys and girls? That’s right, we make an ass out of you, and nearly made a corpse out of me, when my doctor was looking me right in my yellow-eyed, gaunt, wheezing, emaciated face for two solid years, and telling me that I was as healthy as a horse, and calling me her “miracle patient” who would never get AIDS because my CD4 counts were more than twice what might be expected in an HIV-negative person. Meanwhile, the sicker I got, the higher my CD4 count climbed; which probably should have been a sign of illness and might well have been interpreted that way, if my doctor wasn’t so busy ignoring a real illness on the strength of an assumption that my high CD4 count “should” mean that I was super-healthy and could expect robust health for a long time to come.

    To the accusation that I’ve misrepresented the study, here’s a direct quote: “The results of this collaborative study, which involved 12 prospective cohorts and over 20 000 patients with HIV-1 from Europe and North America, show that the virological response after starting HAART has improved steadily since 1996. However, there was no corresponding decrease in the rates of AIDS, or death, up to 1 year of follow-up. Conversely, there was some evidence for an increase in the rate of AIDS in the most recent period.”

    Or for that matter, readers may obtain the entire article, without having to register, right here.

    As for Rodriguez et al, here’s a quote from the abstract: “only a small proportion of CD4 cell loss variability (4%-6%) could be explained by presenting plasma HIV RNA level. Analyses using multiple HIV RNA measurements or restricting to participants with high HIV RNA levels improved this correlation minimally (R2, 0.09), and measurement error was estimated to attenuate these associations only marginally (deattenuated R2 in the 2 cohorts, 0.05 and 0.08, respectively). CONCLUSIONS: Presenting HIV RNA level predicts the rate of CD4 cell decline only minimally in untreated persons. Other factors, as yet undefined, likely drive CD4 cell losses in HIV infection.” [emphasis mine]

    And again, lest anyone accuse me of misquoting, here’s a link.

    Of all the “citations” you made, the only one I’m going to address here is the Vincenzi article, for two reasons: First, it’s impossible for me to pack a discussion of so many articles into a single reply, and second, you’ve made your argument “irrefutable”, not because it is correct, but merely because it cannot be refuted — mostly because it is nonexistent, since you haven’t attached any claims to your “citations”. (Which is why I keep putting “citations” in quotes, because a true citation in a scientific article would take the form of a footnote to a given assertion, not merely the inclusion of the citation text. This is so that readers can look up the article in question, and make sure that it says what you claim it says.)

    To the layman, this may appear that you have provided “overwhelming” and “irrefutable” proof that HIV is sexually transmissible, but only because you’ve made refutation in this forum impossible by making it as voluminous as possible. For all anyone knows, you could have copied and pasted those citations from other articles, and may or may not yourself have read any of them.

    Thus, I will address only the first of these, not because I couldn’t be here for weeks showing you how each one assumes sexual transmission rather than proving it, but because I won’t.

    http://content.nejm.org/cgi/content/abstract/331/6/341

    Among the 121 couples who used condoms inconsistently, the rate of seroconversion was 4.8 per 100 person-years

    That translates into roughly 1 chance every 21 person-years for HIV to be transmitted from an HIV-positive spouse to an HIV-negative spouse, assuming that one were to have sex with one’s infected spouse on a regular basis for 21 years. If that person doesn’t survive for 21 years or the relationship doesn’t last that long, then the odds are actually against HIV being transmitted at all.

    An elementary concept of mathematical biology, as applied to epidemiology, is known as the “Basic Reproductive Ratio“. From the article linked above, Basic Reproductive Ratio is “defined by epidemiologists as ‘the average number of secondary cases caused by an infectious individual in a totally susceptible population’. As such [the Basic Reproductive Ratio] tells us about the initial rate of increase of the disease over a generation. When [this ratio] is greater than 1, the disease can enter a totally susceptible population and the number of cases will increase, whereas when [the ratio] is less than 1, the disease will always fail to spread. Therefore, in its simplest form [the Basic Reproductive Ratio] tells us whether a population is at risk from a given disease.”

    If we assume, for example, that the average person can survive for 21 sexually-active years with an HIV infection, (they must be sexually active for at least 21 of their remaining years, regardless of how long they actually survive since it is by definition impossible to transmit STDs while you are celibate,) then that would give HIV a basic reproductive ratio of 1, according to the 4.8/100 person years estimated in the study you cite.

    However, a basic reproductive ratio of 1 means that the disease will neither spread nor dissipate — in order to spread, HIV has to have a BRR>1, which means that it either has to be significantly more transmissible than demonstrated by Vincenzi, or infected individuals must survive, on average, much longer than 21 years, and remain sexually active for more than 21 of their remaining years. If the average HIV-infected individual is sexually active for less than 21 of his remaining years, then the basic reproductive ratio of HIV would be less than 1, and the epidemic would peter out on its own.

    Thus, what Vincenzi actually proved was that HIV is not sexually transmissible enough to sustain an epidemic.

    And that’s if we go with the basic underlying assumption that HIV is sexually transmitted at all, since the conclusion of this study is based entirely on that assumption.

    What if, for example, we weren’t discussing HIV, but athsma or diabetes or any number of other diseases that are not transmissible at all, but which may be caused or triggered by factors that a couple may share, regardless of their sexual activity, such as environment, diet, lifestyle, stress levels, etc.?

    If this very same study had been done with couples in which one partner was athsmatic or diabetic and the other weren’t, how many of the non-diseased spouses would develop the same disease per 100 person-years? Would it be greater or less than 4.8? I submit that it would probably be equal to or greater than that tiny figure, simply because of the other factors that a couple share in common.

    …And yet, we know that athsma and diabetes are in no way transmissible, sexually or otherwise. Thus, HIV has not been proven by Vincenzi to be more transmissible than athsma or diabetes. The best that Vincenzi could do was to assume sexual transmissibility and to quantify based upon that assumption, but when you do the math, it becomes obvious that if anything, Vincenzi proved that HIV isn’t sexually transmissible enough to sustain an epidemic.

    — Gos
    gos@nerosopeningact.com
    “Nobody here but us heretics…”

  • invalid-0

    Gos, you’re just handwaving. The Lancet study was the work of the ART Cohort Collaboration, if you want to see a list of all the publications they have showing the beneficial impact of ART on survival just look at their website:

    http://www.art-cohort-collaboration.org

    The “treatment response” study you cited was comparing different cohorts that started in different calendar years, with the most recent being 2003. If you can suggest a way that they could have followed people out into the future in order to get the longer term follow up data you’re asking for, please say so. In reality, in order to get multiple years of follow up from 2003, it’s necessary to wait for the years to actually happen. The most that they could include in the Lancet study was a supplemental analysis looking at two years of ART in the different calendar years (with the most recent period being 2001, for obvious reasons). Here is the mortality data from that analysis:

    1995/96: total number=1232 / number of deaths=53 (4.3%)
    1997: 4785 / 151 (3.2%)
    1998: 4583 / 144 (3.1%)
    1999: 3699 / 109 (3.0%)
    2000: 3203 / 99 (3.1%)
    2001: 2783 / 69 (2.5%)

    The differences aren’t large enough to be statistically significant, but it looks to me like the data is going in the same direction as the surrogate markers.

    You also specifically wrote in your first post that the Rodriguez study evaluated clinical endpoints, it did not.

    I have no idea what you’re trying to do with the Vincenzi study…the risk is 4.8% per person-year (95 percent confidence interval, 2.5 to 8.4). You should have quoted the rest of the abstract:

    “The risk of transmission increased with advanced stages of HIV infection in the index partners (P less than 0.02) and with genital infection in the HIV-negative partners (P less than 0.04). Withdrawal to avoid ejaculation in the vagina had a protective effect in uninfected women (P less than 0.02). Consistent use of condoms for heterosexual intercourse is highly effective in preventing the transmission of HIV.”

    Don’t think any of those things significantly increase or lessen the risk of asthma or diabetes, do they? And the original list of cites contains multiple independent studies showing that viral load correlates with risk of HIV transmission.

  • invalid-0

    These are the data on AIDS events from the Lancet “treatment response” study.

    After one year of ART:

    1995–96 total n=1096 / # AIDS events=103 (9%) adjusted HR=1•07 95% CI=(0•84–1•36)
    1997 4460 / 287 (6%) 1•30 (1•09–1•54)
    1998 (reference) 4222 / 222 (5%) 1 1
    1999 3328 / 192 (6%) 1•07 (0•88–1•30)
    2000 2873 / 204 (7%) 1•18 (0•97–1•43)
    2001 2421 / 172 (7%) 1•23 (1•00–1•50)
    2002–03 1656 / 105 (6%)1•35 (1•06–1•71)

    After two years of ART (from Web Table #3, which Peter Duesberg has not put on his website).

    1995–96 1096 / 135 (12%) 1•10 (0•89–1•36)
    1997 4460 / 356 (8%) 1•24 (1•06–1•45)
    1998 (reference) 4222 286 (7%) 1 1
    1999 3328 / 245 (7%) 1•07 (0•90–1•27)
    2000 2873 / 248 (9%) 1•15 (0•97–1•36)
    2001 2421 / 199 (8%) 1•25 (1•04–1•50)

    In every calendar period, far fewer AIDS events occurred in the second year of ART than the first. How is that consistent with ART use increasing the risk of AIDS? It’s just the opposite.

    The slightly increased risk of experiencing an AIDS event during the first or second year or ART for people that started in 02/03 vs. 1998 (based on the adjusted hazard ratio) is entirely accounted for by an increase in the number of people with TB:

    Tuberculosis

    1995–96 total n=1096 / # events=8 (0•7%) adjusted HR=0•73 (0•33–1•63)
    1997 4460 27 (0•6%) 0•97 (0•57–1•63)
    1998 4222 29 (0•7%) 1 1
    1999 3328 34 (1•0%) 1•50 (0•91–2•48)
    2000 2873 38 (1•3%) 1•69 (1•04–2•75)
    2001 2421 28 (1•2%) 1•48 (0•87–2•50)
    2002–03 1656 26 (1•6%) 2•94 (1•70–5•08)

    Other AIDS defining conditions

    1995–96 1096 94 (9%) 1•09 (0•84–1•40)
    1997 4460 261 (6%) 1•34 (1•11–1•61)
    1998 4222 195 (5%) 1 1
    1999 3328 160 (5%) 1•01 (0•82–1•25)
    2000 2873 170 (6%) 1•12 (0•91–1•37)
    2001 2421 146 (6%) 1•19 (0•96–1•48)
    2002–03 1656 81 (5%) 1•15 (0•88–1•50)

    Whatever happened with your care sounds truly horrible Gos, but it doesn’t mean that HIV doesn’t cause AIDS or that it’s OK to try and twist the results of studies to fit your biases.

  • invalid-0

    Richard Jefferys wrote: “The differences aren’t large enough to be statistically significant, but…”

    ‘Out of the mouths of babes and…’

    But nothing. There’s no phrase in the English language which can truthfully follow the word “but” in that sentence. (And “…it looks to me”, since it denotes purely subjective interpretation, is an exceptionally poor choice of words, to follow the word “but”.) The differences aren’t large enough to be statistically significant. Period. In your own words.

    Which means that while ARVs do have a measurable effect on indirect surrogate markers such as CD4 count and so-called “viral load”, there is no statistically significant health benefit to antiretroviral therapy measured by the very research you yourself are citing as proof of the benefit of ARVs.

    Now, this leaves the consistency of the findings, making it so that it looks to you like the numbers are at least consistent enough to suggest some long-term benefit that hasn’t been measured yet.

    The reason for my concern is this: According to Why Most Published Research Findings Are False (Ioannidis JPA, PLoS Medicine Vol. 2, No. 8, e124 doi:10.1371/journal.pmed.0020124), claimed research findings may often be simply accurate measures of the prevailing bias. The author goes on to suppose the existence of a research field for which no true scientific findings exist, reminding us, “History of science teaches us that scientific endeavor has often in the past wasted effort in fields with absolutely no yield of true scientific information, at least based on our current understanding. In such a ‘null field,’ one would ideally expect all observed effect sizes to vary by chance around the null in the absence of bias. The extent that observed findings deviate from what is expected by chance alone would be simply a pure measure of the prevailing bias.”

    From my research of scores of articles similar to the Vincenzi study you cited, I’ve found that research findings in the field of HIV research consistently range from zero to statistically insignificant, yet are consistently interpreted as though they show significant support for the prevailing (and indeed the researchers’ own) bias (or as I like to pronounce it, “bee-ess”.)

    Richard Jefferys wrote: “You also specifically wrote in your first post that the Rodriguez study evaluated clinical endpoints, it did not.”

    Ummmm…specifically when did I do that?

    Now, I will concede that I misspoke about the Rodriguez study. In my earlier post, I said, “…But at least HAART increases CD4 count, right? Yes, it does, but according to a study published only a month later in JAMA (http://jama.ama-assn.org/cgi/content/abstract/296/12/1498) higher CD4 counts have very little correlation (a single-digit percentage of correlation in all cases) to eventual progression to AIDS.”

    I must admit that when I wrote that paragraph, I wasn’t looking at the article at the moment. I should have said, “…But at least HAART reduces viral load, right? Yes, it does, but according to …JAMA… lower viral loads have very little correlation (4%-6% — a single-digit percentage of correlation), to eventual progression…” etc. [corrected text emphasized]

    However, I hardly think this slip of the tongue (as it were) helps your case, since the corrected version is even more damaging to the very idea that HIV causes AIDS, since if it did, viral load would be an excellent prognosticator of CD4 decline and progression to AIDS, and Rodriguez proved that it is not, and went so far as to conclude, “Other factors, [other than viral load] as yet undefined, likely drive CD4 cell losses in HIV infection.” [emphasis mine]

    ‘Out of the mouths of babes and HIV researchers…’

    Richard Jefferys wrote: “Whatever happened with your care sounds truly horrible Gos, but it doesn’t mean that HIV doesn’t cause AIDS or that it’s OK to try and twist the results of studies to fit your biases.”

    Thanks for your concern, it was truly horrible.

    However, my own personal experience aside, I think I’m making a good case that the results of HIV studies are twisted enough on their own, by professional persons paid to do so, who don’t need the help of an amateur like me.

    — Gos
    gos@nerosopeningact.com
    “Nobody here but us heretics…”

  • invalid-0

    Richard Jefferys wrote: “I have no idea what you’re trying to do with the Vincenzi study…the risk is 4.8% per person-year (95 percent confidence interval, 2.5 to 8.4).”

    It’s not suprising that you have no idea what I’m trying to do with the Vincenzi study, since you’re misrepresenting the risk by a factor of 10,000%. This is a copy/paste from the article itself: “the rate of seroconversion was 4.8 per 100 person-years“.[emphasis mine] Not per person-year; per 100 person-years.

    And at that, I have to ask myself, when we’re talking about person-years, how does that translate in terms of couple-years? Is it equivalent to a couple-year, or are there 2 person years in 1 couple-year? If the latter is the case, then everything I said earlier goes double. In my earlier post, I assumed the former, in order to be conservative, but as I break the problem down to its simplest terms for you to digest, I want you to consider that I am assuming that 100 person-years is equal to 100 couple-years, despite the fact that (since it takes two to tango) it is more reasonable to assume that 100 couple-years is equal to 200 person-years. It is thus quite possible that everything I’m about to point out goes doubly in my favor.

    Here we go:

    100 person-years / 4.8 = 20.833 person-years per transmission with regular sexual frequency and inconsistent or no condom use

    Thus, in order for HIV to have a Basic Reproductive Ratio of 1 or more, (which is, according to the laws of mathematical biology, absolutely necessary to sustain an epidemic,) the average HIV-infected person would have to survive AND remain sexually active for at least 20.833 years.

    While this is not generally considered to be outside the realm of possibility, I think that most would agree that to expect the average HIV-positive person to survive for long enough to have significantly more than 20.833 sexually-active years (plus any number of celibate years) is a bit of a stretch, if we’re assuming that sooner or later, he’s going to get AIDS and die. Thus, we cannot stretch very far beyond the 21-sexually-active-year-mark to get a Basic Reproductive Ratio that’s significantly higher than 1 (which would be required for the epidemic to spread, rather than remaining stable, as it would if the BRR were exactly 1.)

    In fact, if we assume that the average HIV-positive person has fewer than 21 sexually-active years left once he becomes infected, then the Basic Reproductive Ratio would be less than 1, and the epidemic would peter out.

    Now, if we assume that there are 2 couple-years per person year, then everything above is doubled — which would mean it takes nearly 42 years of regular sexual activity for a single case of transmission to occur, which would mean that a person infected in his mid-thirties would have to live to be at least 75 years of age and maintain consistent sexual regularity throughout, in order to infect at least one other person. I don’t think I need to tell you what that does to the Basic Reproductive Ratio, or what that means.

    But I’m more than content to let it ride at a 1:1 ratio of couple-years to person-years, (despite the fact that it seems wrong to me) since even the more conservative interpretation shows HIV to have a Basic Reproductive Ratio that is, at best, 1 or possibly slightly more (though still not significantly enough to support a spreading epidemic,) and at worst, a BRR of zero.

    — Gos
    gos@nerosopeningact.com
    “Nobody here but us heretics…

  • invalid-0

    Jefferies, You Said:

    “In every calendar period, far fewer AIDS events occurred in the second year of ART than the first. How is that consistent with ART use increasing the risk of AIDS? It’s just the opposite”.

    Of course the second year of ART was lower than the first year. The first year being 1995 and some of those patients were still succumbing to the effects from the prior AZT monotherapy.

    Those who survived the monotherapy and transition to other drugs (which by the way still contained AZT but at a lower dose) still succumbed to immune systems damaged by the drugs, but slightly lesser due to the lesser AZT being administered. But deadly and toxic nonetheless!

    It always fascinates me how the advocates proclaim the benefits of ART drugs, simply because they are overall about a third as toxic than pure high dosages of AZT monotherapy. What kind of twisted logic and thinking is that?

  • invalid-0

    You haven’t even begun to grasp what the study is about. These are multiple large cohorts of individuals, each separate cohort started ART in a different calendar period. Data is provided on what happened to each separate cohort during their first two years on ART. The second-year difference in AIDS events occurs in every cohort in every calendar period, e.g. out of the cohort of 2,421 people that started ART in 2001, 172 experienced AIDS events during their first year of ART, 27 experienced AIDS events during their second year of ART.

    Here is the breakdown for each calendar period:

    1995–96 total n=1096 / # AIDS events= 1st yr 103 2nd yr 32
    1997 4460 / 1st yr 287 2nd yr 69
    1998 (reference) 4222 / 1st yr 222 2nd yr 64
    1999 3328 / 1st yr 192 2nd yr 53
    2000 2873 / 1st yr 204 2nd yr 44
    2001 2421 / 1st yr 172 2nd yr 27

  • invalid-0

    Gos wrote:

    “Which means that while ARVs do have a measurable effect on indirect surrogate markers such as CD4 count and so-called “viral load”, there is no statistically significant health benefit to antiretroviral therapy measured by the very research you yourself are citing as proof of the benefit of ARVs.”

    That is a complete and utter lie, and it’s preceded by some desperate quote-mining. I’ve explained that the Lancet study (which you cited as showing ART does not work) does not show what you claim it shows. Thankfully, people can read the paper themselves. The study shows that people that started ART in 2002/3 have slightly better viral loads and CD4 counts *after one year of ART* than those that started in 95/96 *after one year of ART*, but because relatively few people die during the *first year of ART* the decline in mortality *after one year of ART* (from 2.2% of people that started in 95/96 to 1.3% of people that started in 2002/3) is not statistically significant. You’re arguing that the difference in surrogate markers should have translated into a bigger improvement in survival after one year of ART than the improvement from 97.8% for the 1232 people that started in 95/96 to 98.7% for the 1932 people that started in 2002/3. I wish that survival was 100% in these cohorts but given that a proportion of people in cohorts this size will have started ART with very advanced disease I think that’s unrealistic.

    See also the data above on AIDS events in this paper, which also give the lie to your claims.

    You asked for sexual transmission cites (saying that the Padian study was an “exemplar” of the ones you’d seen – another falsehood), then complained that I posted too many of them, then used one piece of incidence data to try and show (as far as I can tell, anyway) that HIV can’t spread by calculating a basic reproductive ratio based on the idea (derived from data expressed as person-years) that someone has to live 21 years for one transmission event to occur…

    There were 121 couples who used condoms inconsistently who were followed for an average of 20 months, 12 infections occurred. In other words, 9.9% of the couples. And you’re suggesting that I’m wrong to translate the person-year data into a risk of an infected person transmitting to their uninfected partner in this study that came out to be ~4.8% per year? That this is a 10,000% misrepresentation of the risk? How so?

  • invalid-0

    Also, if you’re still attempting to suggest that the inability of a single viral load measurement to predict six month change in peripheral blood CD4 count renders these surrogate markers meaningless, a study that did evaluate clinical endpoints found that:

    “Median HIV-1 RNA explained 51% and 58% of the variability in AIDS and death, and median CD4 cell count explained 29% and 35% of the variability in AIDS and death, respectively.” (JAMA.2007; 297: 2349-2350).

    I mentioned this study before, but you ignored it. Rodriguez et al note that immune activation is likely a better predictor of the rate of peripheral CD4 T cell decline, they are not the first researchers to suggest this.

    J Immunol. 2002 Sep 15;169(6):3400-6.
    CD4 T cell depletion is linked directly to immune activation in the pathogenesis of HIV-1 and HIV-2 but only indirectly to the viral load.
    Sousa AE, Carneiro J, Meier-Schellersheim M, Grossman Z, Victorino RM.

    Clinical Immunology Unit/Institute of Molecular Medicine, Faculty of Medicine of Lisbon, Lisbon, Portugal.

    The causal relationships among CD4 cell depletion, HIV replication, and immune activation are not well understood. HIV-2 infection, “nature’s experiment” with inherently attenuated HIV disease, provides additional insights into this issue. We report the finding that in HIV-2 and HIV-1 patients with a comparable degree of CD4 depletion the imbalance in the relative sizes of the naive and memory T cell populations and the up-regulation of CD4 and CD8 cell activation markers (HLA-DR, CD38, CD69, Fas molecules) are similar, even though the viral load in the plasma of HIV-2-infected patients is two orders of magnitude lower than in HIV-1 patients and HIV-2 patients are known to have slower rates of CD4 T cell decline and a better clinical prognosis. Moreover, we found a similar increase in the frequency of cycling CD4 T cells (Ki67+), which was in strong correlation with the expression of activation markers. Finally, the level of T cell anergy, as assessed by the proliferative responses to CD3 stimulation and to a panel of microbial Ags, proved to be comparable in HIV-1 and HIV-2 patients with a similar degree of CD4 depletion despite large differences in viral load. Our data are consistent with a direct causal relationship between immune activation and CD4 cell depletion in HIV disease and an only indirect relation of these parameters to the virus replication rate. Invoking the concept of proximal immune activation and virus transmission, which links efficient transmission of virus to local cell activation and proliferation in response to Ags and inflammation, we propose an integrative interpretation of the data and suggest that strongly elevated immune activation induces CD4 cell depletion and not vice versa, with potential implications for the choice of treatment strategies.

  • invalid-0

    Richard Jefferys wrote: “… this is a 10,000% misrepresentation of the risk? How so?”

    You said that Vincenzi showed a transmission risk of 4.8 per person-year — the study itself shows a risk of 4.8 per 100 person years, or 4.8% per person-year.

    Whether expressed as a percentage or an incidence per 100 couple-years is irrelevant, because either way the outcome remains the same — at a rate of 4.8% per person year, it would take 20.833 person-years for a single instance of transmission to occur. (100% / 4.8% = 20.833 or 100 person-years / 4.8 = 20.833 person years per transmission) Given that all groups reported at least *some* sexual frequency, this means that these 20.833 years have to be sexually active years, since the virus cannot be passed on sexually during a period of celibacy.

    Richard Jefferys wrote: “…then [Gos] used one piece of incidence data to try and show (as far as I can tell, anyway) that HIV can’t spread by calculating a basic reproductive ratio based on the idea (derived from data expressed as person-years) that someone has to live 21 years for one transmission event to occur…”

    Well at least we understand each other thus far…{cracks knuckles}…now let’s get to work simplifying an elementary rule of epidemiology.

    The Basic Reproductive Ratio determines whether or not an epidemic can be sustained in a totally susceptible population. If it is 1, then the epidemic will neither grow nor shrink. If it is greater than 1, then the epidemic will grow, and if it is less than 1, then the epidemic will stall and die.

    If it takes 20.833 (let’s call it 21 — it’s close enough,) sexually active person-years to transmit it, then the basic reproductive ratio can only be 1 if the average HIV-positive individual has 21 or more sexually-active years before he dies (and considering the long periods of celibacy that often come with being seropositive as a result of social stigma, he may have to live quite a while for that to occur.) If the average HIV-infected person does not have at least that many sexually-active years left at the point he becomes infected, the BRR drops below 1 and the epidemic meets the fate of the Stegosaurus.

    Given the findings of the Vincenzi study, it is therefore impossible for an epidemic of sexually-transmitted HIV to increase in size, unless the average infected individual survives long enough to have 21 sexually-active years.

    …As to whether the average infected person lives long enough to have 21 sexually-active years + whatever number of celibate years they may have + long enough to bring the BRR of HIV significantly higher than 1, I leave that as an exercise for the reader, but since we’re talking about a bare minimum of 25 ~ 30 years or more that the average infected person would have to live after infection in order to spread it sexually to enough people to sustain the epidemic, how do you explain HIV spreading in Africa the way it did, if it’s killing people there in only 5 or 10 years, maybe even less? According to the sexual transmissibility demonstrated by Vincenzi, that’s not nearly long enough for the average infected person to spread the virus to even one other person, on sexual transmissibility alone. Are you about to try to tell me that millions of Africans spent the 1970s shooting smack with dirty needles and/or engaging in rampant bi- and heterosexual anal sex?

    And if the average infected person is living 25 years or more, we can’t credit ARVs, since the vast, vast majority of HIV-positives in the world aren’t taking ARVs, and in fact most don’t even have access to ARVs — not to mention the fact that this still wouldn’t explain how HIV managed to spread back when the life-expectancy of an infected person was much shorter.

    So take your pick, either infected persons do not live long enough to spread the virus to enough people to sustain the epidemic, or they’re living long enough (without ARVs in the vast majority of cases) to make us wonder whether it is HIV that eventually kills them at all. (After all, if we say that the average person lives 25 years after getting their first gray hair, that doesn’t mean that it’s having gray hair that killed them.)

    And we also have to remember that if the average is 25 years or more, then that means that nearly half live significantly longer. Again, this by itself doesn’t conclusively prove that HIV doesn’t cause AIDS, but again, it is definitely enough to make you seriously wonder.

    I have to tell you, after I got finished explaining this to you the first time, my daughter walked up and asked, “Whatcha writing, Daddy?” So I explained it to her, and she got it the very first time I explained it, and I know she got it because we had a discussion in which it was clearly apparent that she understood perfectly that HIV cannot spread unless its hosts live long enough, on average, to spread it to more than one other person. I will admit that I dumbed it down for her, but she’s a 10-year-old; you’re not.

    Richard Jefferys wrote: “You asked for sexual transmission cites …, then complained that I posted too many of them, then used one piece of incidence data…”

    You did post too many — do you honestly expect any onlooker to this conversation to check each and every one of them to make sure that they were legit? Hell, I picked the very first one off the list, and found that the single highest quote of incidence data contained therein was insufficient to support an epidemic. Do you honestly expect me to spend the next month or more discussing each of these articles in turn at a rate of 1 per day, to show you how each in turn assumes sexual transmission rather than proving it?

    Volume does not equal proof. If the proof is contained in any one of those articles, then citation of that one article should be sufficient. If you cannot find the proof in this mountain of articles you listed, don’t expect me to dive in and find it for you.

    Now, I’m not an academic myself, but a friend of mine who read your “citations” told me that he’d have been laughed out of grad school for pulling a stunt like that, simply listing 3 dozen or so citations with no explanation of their relevance to the discussion, not a word of context, and any number of which are likely to be irrelevant or even contradictory. He says what you did shows an utter lack of understanding of basic academic standards.

    …As for that “one piece of incidence data”, that was the highest quoted incidence anywhere in the article — should I have used any other than the highest, or perhaps the average of all incidence data in it, instead? If I had my argument would be significantly stronger against the possibility of a sustained HIV epidemic — I used the highest figure to prove that even in the worst-case scenario demonstrated by this study, HIV could not do much more than remain stable as a sexually-transmitted epidemic, and would likely tend to die off rather than spread in populations (such as third-world countries) where sexual transmission is more or less its only mode of transportation, and/or the average life expectancy of an infected person is significantly lower than 21 years after infection.

    What we’re talking about, therefore, is an epidemic that is mathematically impossible, if we are to assume that the Vincenzi incidence estimate is correct.

    — Gos
    gos@nerosopeningact.com
    “Nobody here but us heretics…”

  • invalid-0

    Nice attempt at a dodge, but here is exactly what you wrote (quoting me accurately this first time):

    “Richard Jefferys wrote: “I have no idea what you’re trying to do with the Vincenzi study…the risk is 4.8% per person-year (95 percent confidence interval, 2.5 to 8.4).”

    It’s not suprising that you have no idea what I’m trying to do with the Vincenzi study, since you’re misrepresenting the risk by a factor of 10,000%.”

    But thanks for the retraction. I’m sorry that it took me a while to realize what you were doing with the basic reproductive ratio, it’s just so bizarre: what you’re doing is calculating what the reproductive ratio would be if every infected person was in a long term monogamous relationship with just one other uninfected person!

    So your attempt at an argument entirely falls apart.

    To correctly calculate the basic reproductive ratio you need to use the risk of transmission per contact and the estimated number of contacts per infected person.

    You also write:

    “Volume does not equal proof. If the proof is contained in any one of those articles, then citation of that one article should be sufficient. If you cannot find the proof in this mountain of articles you listed, don’t expect me to dive in and find it for you.”

    But the Ioannidis paper in PLoS Medicine you cited says:

    “most research questions are addressed by many teams, and it is misleading to emphasize the statistically significant findings of any single team. What matters is the totality of the evidence.”

    Every single one of those papers demonstrates sexual transmission of HIV. You never even addressed why condom use or withdrawal prior to ejaculation would reduce the risk of transmission, or why so many of those studies independently confirm that viral load correlates with risk of transmission.

  • invalid-0

    It wasn’t a dodge, it was an attempt at a ram, but an unfair one, and for that you have my apologies — I just re-read the original post, and noticed the % sign that I hadn’t picked up on before.

    Richard Jefferys wrote: “I’m sorry that it took me a while to realize what you were doing with the basic reproductive ratio, it’s just so bizarre: what you’re doing is calculating what the reproductive ratio would be if every infected person was in a long term monogamous relationship with just one other uninfected person!”

    The only thing that’s bizarre is the way you’re flailing to introduce irrelevancies into the discussion in order to avoid addressing the point. Do you honestly believe that when an infected person has sex with an uninfected person, it matters whether they are in a long-term monogamous relationship or whether they’re two strangers who met at a glory hole and didn’t even take off their shirts?

    The issue of long-term monogamy is irrelevant — it’s all about the number of unprotected sexual encounters that occur between serodiscordant people. In order to spread HIV to one other person, the average HIV-positive would have to live long enough to have unprotected sex as many times as the average couple in non-consistent condom users’ group would have had if they’d maintained the same unprotected sexual frequency for 20 years and 10 months. (And I must say that you’re plainly a helluva lot more intelligent than this, so I can only take your continued insistence on not understanding the relevance or irrelevance of these variables as obfuscation.)

    Richard Jefferys wrote: “But the Ioannidis paper in PLoS Medicine you cited says: ‘most research questions are addressed by many teams, and it is misleading to emphasize the statistically significant findings of any single team. What matters is the totality of the evidence.'”

    Let’s say I told you I was gonna show you a picture, and then proceeded to dump an entire box of puzzle pieces in front of you, and tell you that if you wanted to see the picture, you’d have to put it together yourself…

    If you’re gonna cite three dozen articles, you have to contextualize each and every one of them. I’m not going to dive into this mountainous pile of research that you’ve dumped on my desk, with absolutely no idea of the context in which you’re presenting each citation, to try to figure out what you’re trying to prove with each and every citation. If you think each of these articles conclusively proves anything, then you have to explain how each paper proves a specific point that you’re trying to make. I’m not gonna do your homework for you, you have to do it yourself, or you’ve proven nothing and accomplished nothing other than giving yourself Carpal Tunnel Syndrome from copying and pasting.

    Richard Jefferys wrote: “Every single one of those papers demonstrates sexual transmission of HIV.”

    Hmmmm….

    I once had a long-term relationship with an athsmatic. Interestingly, only a few years later, I developed athsma myself. Does that mean that my experience demonstrates sexual transmission of athsma?

    What if I’d been a subject in such a study at the time — provided the study was large enough and long enough, do you think maybe there might not be other couples like us in the group, in which one had athsma and the other later developed it? Sure there would, such phenomena make up the statistical noise floor in any large study.

    How many do you think would “seroconvert” to “athsma-positive” status during the course of such a large, long study? Considering the number of athsma-triggering factors that a couple might share, such as pets, living environment, smoking habits, etc., we’d probably expect, in the case of athsma, that it would probably far more common than one might initially think, for an athsmatic to be in a long-term relationship with a non-athsmatic who later develops athsma. Do you think it might be as high as, say, 4.8% per person-year? I think it probably would, but that’s my own opinion, and you are entitled to yours on this specific matter.

    If such a study were done to study the sexual transmissibility of athsma, and such cases were to be documented, would this prove athsma to be sexually transmissible? No.

    Thus, though I haven’t examined those dozens of other of your “citations”, I can say that the very first of your list doesn’t prove sexual transmissibility at all, and in fact the very highest risk incidence estimated by the study in the highest-risk group is so small that it arguably falls well within the statistical noise floor demonstrated by the imaginary “athsma sexual transmission study” above.

    Thus, Vincenzi has proven HIV, at worst, to be no more or less sexually “transmissible” than athsma.

    To add insult to injury, if we take that highest incidence rate and do the math, it very strongly appears that HIV couldn’t have a BRR much greater than 1 as a sexually-transmitted epidemic, if it were greater than one at all.

    Now, we’ve discussed the Basic Reproductive Ratio, but haven’t discussed Actual Reproductive Ratio yet. ARR is always lower than BRR, because BRR assumes a totally-susceptible population, and no viral epidemic starts with a totally-susceptible population, not to mention the fact that as a viral epidemic progresses, the population becomes less and less susceptible, so that as that happens, the gap between ARR and BRR continue to widen.

    So even if the BRR were 1 or slightly greater, ARR would still likely be less than 1 and dropping, decades after the initial outbreak, and HIV would be bound for extinction. Thus, not only does Vincenzi not prove sexual transmission, the paper strongly suggests that HIV, if we assume (as Vincenzi does) that it is transmissible, it still isn’t contagious enough as an STD to sustain an epidemic — at least not in the absence of other factors such as rampant IV drug use to spread it around faster, which leaves us at a loss to explain (among many other things) the alleged heterosexual pandemic in Africa.

    Richard Jefferys wrote: “You never even addressed why condom use or withdrawal prior to ejaculation would reduce the risk of transmission,…”

    Well, once the numbers proved statistically impotent to support the very idea of HIV as a sexually-transmitted epidemic, it seemed about as pointless to address the researchers’ interpretation of statistically meaningless phenomena as to discuss what color to paint a car that has a piston rod sticking out of the side of the engine.

    But, since you insist, let’s go there…

    First of all, according to Vincenzi, “Subjects in both groups received identical, intensive instruction on the prevention of HIV-1 infection and condom use and were offered free condoms and voluntary, confidential serologic testing for HIV-1 and counseling by trained project counselors.”

    Now, this is a ubiquitous practice by researchers, to offer “safe sex” counseling as part of the program. What it does, in practice, is to motivate subjects to exaggerate or outright lie about their sexual practices.

    Now, maybe not all of them will lie, but a certain rather large percentage will, rather than endure another sermon about safe sex from the counselor, and virtually all of them will be people who don’t use condoms and lie about it, rather than the other way around, no?

    Now, what happens when a couple has lied and there’s a seroconversion? Suddenly, they ‘fess up (or perhaps make up another lie about having “one time” neglected to use a condom while drunk,) and BAM, they go from the “safe sex” to the “unsafe sex” column, while five or a dozen more couples just like them that also lied and didn’t seroconvert continue to maintain the lie. This has the effect of shoving all or nearly all seroconversions to the “unsafe sex” column, so that at the end of it all, it looks like those who use condoms avoid getting HIV, when what really made the difference wasn’t who actually used condoms or practiced withdrawal, but merely who reported doing so, after having been very carefully “coached”, as it were, on the answers that the counselors would expect, and maintaining the lie until and unless a seroconversion occurred.

    Richard Jefferys wrote: “You never … addressed why … so many of those studies independently confirm that viral load correlates with risk of transmission.”

    I’ll address that, if you can explain for me why the inventor of the PCR technique itself views the viral load PCR test for HIV to be meaningless.

    Actually, I’m kidding about that, but seriously, which of those studies shows risk incidence rates high enough to be considered statistically significant?

    I’ve already demonstrated nine ways to sunday that Vincenzi — the very first “citation” on your list — did not do so, but merely proves that a large group of people, carefully counseled to give a specific answer, will give that answer even if it’s not true, until they feel themselves already caught in a lie, and that by filtering statistically insignificant bits of the data stream through this bias machine, it is possible to make it appear that HIV is sexually-transmissible at first glance, but that by taking a closer look at the numbers, it is possible to see that the data thus generated is still too small and statistically insignificant to support the larger idea of HIV as a growing sexually-transmitted epidemic.

    Now, having spent 3 days doing so, I’m not going to spend the next 105 days explaining why the other 35 of your citations is equally bereft of proof. If even one of the studies you cite shows a risk instance higher than we might conceivably see in the aforementioned hypothetical athsma experiment, then cite it and we’ll debate its merits, but I’m not going to sit here for the next three months and debate all 3 dozen of your “citations”, if even a large fraction of them are as devoid of the proof you claim as Vincenzi has already proven to be.

    — Gos

  • invalid-0

    …Are you still searching desperately for the reference in that pile of “citations” that demonstrates a risk incidence statistically significant enough to prove HIV to be more contagious than athsma?

    Don’t bother. For two reasons:

    #1: I’m pretty sure you won’t find it. I will admit that the last time I myself looked for such a reference was a few years ago, and I’m sure hundreds of studies have been published since then, but I’m also pretty sure that if any study had been published which documented HIV to be more contagious than any previous study had, it would have been all over the headlines: “HIV More Contagious Than Previously Thought.” Have you seen any such headlines? Me neither. So I’m pretty sure that no such study exists (though I could be wrong.)

    #2: Even if you did find one such study, you said yourself, by way of quoting Ioannidis, “‘most research questions are addressed by many teams, and it is misleading to emphasize the statistically significant findings of any single team. What matters is the totality of the evidence.'”

    Thus, even if you did manage to find one such study, you’d still need to prove that the totality of the “evidence” you presented by way of those 3 dozen “citations” demonstrates an average risk incidence for unprotected sex that is as high as this one study, and of course that’s mathematically impossible if that study is on the high end of the spectrum.

    And then, I’m sure that if we assume that you yourself have actually read each and every one of these studies, that you hand-picked those that showed some seroconversions, unlike, for example, Padian, which demonstrated no seroconversions in 282 couple-years (564 person-years, to compare it apples-for-apples with Vincenzi.) Thus, if there were studies that you excluded from your list because they demonstrated no seroconversions, then you have to re-include them for the purposes of averaging, and that’ll bring your average even lower. By the time you get finished evaluating “the totality of the evidence”, you’ll be lucky if you come back with an average risk incidence as high as Vincenzi’s estimate, which I’ve already demonstrated to be too statistically insignificant to be accepted as proof that HIV is more contagious than athsma.

    — Gos
    gos@nerosopeningact.com
    “Nobody here but us heretics…”

  • invalid-0

    Gos, you haven’t even understood your own argument. To calculate a reproductive ratio you need risk of transmission per contact and an average number of susceptible contacts for each infected person. The Vincenzi paper doesn’t give you a per contact risk estimate, and in your attempt to derive a reproductive ratio from it you assumed that each infected person comes into contact with only one susceptible contact (thereby wrongly suggesting that an infected person can’t infect more than one other susceptible contact).

  • invalid-0

    It isn’t me who doesn’t understand the argument, and once again, you aren’t failing to understand, you are refusing to understand, by injecting irrelevancies into the argument.

    First of all, the risk incidence does not need to be expressed in terms of risk per contact in order to calculate a reproductive ratio — all that’s needed is to make sure that the risk incidence is expressed the same way on both sides of any comparison. In mathematics, there are always many different ways to express any given value (as exemplified by the earlier-demonstrated fact that 4.8% per person year is equal to 4.8 per 100 person-years.)

    Second of all, while Vincenzi does not baldly state a risk per transmission, the paper does give us enough data to calculate this figure for ourselves.

    The Vincenzi paper reports a median sexual frequency for couples not using condoms consistently of 2-3 per week. Let’s split the difference and call it 2.5/week — that’s 130 sexual contacts per year.

    4.8% / 130 = 0.036923% risk per contact (approx)

    Expressed another way:

    100% / 0.036923% = 1 risk per 2708 contacts (approx)

    Let’s check that figure:

    2708 / 130 contacts per year = 20.83 years for a couple to have sex 2708 times. Thus, the figures check out, since we’ve already demonstrated earlier that the average couple in the group would have had to have sex for 20.83 years in order to have 1 statistical risk of transmission.

    Thus, Vincenzi suggests a per-contact risk of 0.036923%, or 1 risk per 2708 sexual contacts.

    Richard Jefferys wrote: “…in your attempt to derive a reproductive ratio from [Vincenzi] you assumed that each infected person comes into contact with only one susceptible contact (thereby wrongly suggesting that an infected person can’t infect more than one other susceptible contact).”

    Having already explained this, I’m going to be very short in explaining it a second time: When an infected person has sex with a susceptible person, it does not matter whether they are married or strangers, it only matters that one is infected and the other susceptible, and that they have sex. One infected person could have sex with 1 susceptible person 2708 times, or he could have sex once each with 2708 different susceptible partners — statistically, it does not matter. The only sense in which his number of partners becomes relevant is in that it’s impossible for him to transmit the virus to multiple partners if he only has one (which is no help to your argument, since this means that he has to have multiple partners in order to have a reproductive ratio greater than 1.) Assuming multiple susceptible partners, the average infected person has to have sex with a susceptible person an average of 2708 times for each susceptible partner that he infects, in order to be statistically consistent with the 4.8%/person-year figure reported by Vincenzi.

    And in the same vein, I’d like to address another irrelevancy you tried to introduce earlier, when you said, “what you’re doing is calculating what the reproductive ratio would be if every infected person was in a long term monogamous relationship with just one other uninfected person!” [emphasis mine]

    Not “every”, just the average, and you’re definitely smart enough to know better, so there’s no excuse for you to make such a ridiculous statement. (I was going to use the word “specious” instead, to soften the blow, but then I remembered that in order to be specious, a statement has to at least appear to be correct, and yours doesn’t meet that requirement.)

    As any sixth-grader knows, the word “average” doesn’t mean that every member of a group has to be identical, it just means that for every one that falls on one side of the average, there must be one or more who fall equidistantly on the other side. Thus, for each infected person who transmits the virus in only one sexual contact, there must be another who has sex more than 5400 times before transmitting it, or two others who have sex an average of more than 4000 times each, or an endless number of combinations of three or more others, in order to arrive at an average of 2708. (I can’t believe I’m explaining the law of averages to a grown man!)

    And again, it doesn’t matter whether this sex occurs with one susceptible partner or many (outside the fact that he has to have multiple partners in order to infect multiple partners.) He still has to have sex the same average number of times in order to transmit the virus to an average of one or more people, and he still has to transmit the virus to an average of one or more people in order to sustain an epidemic.

    Jeez Louise, what’s next, are you going to say that each and every HIV-positive has to live in a house with as many bedrooms as the couples in the Vincenzi study, in order for the Vincenzi estimate to be relevant to the reproductive ratio of HIV?

    You’re far more intelligent than this, so I can only assume that your insistence on continuing to inject such obvious irrelevancies is an act of desperation. What’s the matter, you still can’t find a single study which demonstrates an incidence risk statistically significant enough to suggest that HIV is more contagious than athsma, even after checking all 3 dozen of your own “citations”?

    — Gos
    gos@nerosopeningact.com
    “Nobody here but us heretics…”

  • invalid-0

    Hey Richard! Guess what? I found an article in your “citations” that actually shows a high enough transmission risk incidence to conceivably suggest that HIV might be more contagious than athsma:

    http://content.nejm.org/cgi/content/abstract/342/13/921 (free full text with registration)
    Quinn TC, Wawer MJ, Sewankambo N, Serwadda D, Li C, Wabwire-Mangen F, Meehan MO, Lutalo T, Gray RH.
    Viral load and heterosexual transmission of human immunodeficiency virus type 1. Rakai Project Study Group.
    N Engl J Med. 2000 Mar 30;342(13):921-9.

    I thought I was in real trouble for a minute there, then I read the article, and nearly fell out of my chair laughing.

    Remember what you were saying earlier about the Vincenzi study? As I recall, it went a little something like: “You never even addressed why condom use or withdrawal prior to ejaculation would reduce the risk of transmission…”

    OK — now here’s where it gets a little funny, but the punch line is yet to come:

    According to Quinn et al, “On bivariate analysis, there were no significant differences in the risk of infection among HIV-1–negative partners according to the level of formal education, history of travel outside the district within the previous year, the number of sexual partners within the past year (one vs. two or more), or condom use or nonuse.”

    Wait, say that again? “On bivariate analysis, there were no significant differences in the risk of infection among HIV-1–negative partners according to … condom use or nonuse”?!

    But wait, there’s more, and hold on to your seats, ’cause this one’s a screamer…

    If you look at the table which breaks it all down, what you find is that condom use appears to nearly double the transmission risk, from 11.2%~11.5%(median 11.35%) per person-year to 16.2%~24.2%(median 20.2%) per person year. In fact, in the case of couples whose HIV-positive partner reported condom use, the transmission rate more than doubled, from 11.2%/py to 24.2%/py.

    Now, if I should have to explain why Vincenzi shows that 100% of seroconversions occur among couples that report inconsistent or no use of condoms, (which I did,) then you should have to explain how condoms could possibly double the transmission rate. (In fact, the incidence among condom users in Quinn et al is more than 5 times the incidence among condom non-users reported in Vincenzi.[24.2%/py vs 4.8%/py])

    Actually, I’m gonna let you off the hook on that one, because I think that the one thing you and I agree on is that condoms could not possibly increase transmission risk.

    However, the fact that the difference apparently made by condoms is one of the greater differences documented in the article (as much as 216%) strongly suggests an extremely high statistical noise floor for this whole study. In fact, given that the median transmission rate for condom users is almost twice the overall transmission rate of 11.8%/py, it would seem that that if the condom users’ transmission rate is an example of the statistical noise floor, then most of the risk estimates (including the overall estimate) are well below the statistical noise floor, and as we both know, that which is below the statistical noise floor is statistically insignificant.

    Another thing I’d like to call your attention to the interpretation of this data by the researchers. Compare the statements “Transmission rates were not significantly affected by … condom use or nonuse,” and “Transmission rates appeared to virtually double with condom use.” Not very similar statements, are they? If the latter was what the data overwhelmingly appeared to show, why was the former statement the one reported in the article?

    …Is that the sound of data being cherry-picked? Did a bull just do his business nearby, or is that the distinct odor of researchers selectively interpreting their findings to fit their own and the prevailing biases?

    No, wait — it’s the smell of someone being burned. Oh S#$%, it’s you! mwoooHAHAHAHA!

    Go Gosmer, itsya birfday – Go Gosmer, itsya birfday…

    — Gos
    gos@nerosopeningact.com
    “Nobody here but us heretics…”

  • invalid-0

    Shall I continue through your little list of “citations”, one by one?

    (…I could, y’know.)

    And there’s a reason that I can and that I know for a fact that I can tear each and every one of them into little pieces and dance on the pieces, and it’s very, very simple: The overwhelming evidence is that the HIV/AIDS hypothesis is exactly what Ioannidis refers to as a “null field” — a field “with absolutely no yield of true scientific information”. A field in which thousands of researchers selectively interpret statistically insignificant data that “[varies] by chance around the null,” but NOT “in the absence of bias.” Thus, as defined by Ioannidis, HIV research is nothing more than a measure of the prevailing bias and the bias of individual researchers.

    …So of course it appears that the vast bulk of published studies agree (except where they are more mutually-contradictory than any two sections of the Bible,) but that’s not because they’re measuring a statistically measurable phenomenon other than random chance filtered through bias (pronounced “bee-ess”.)

    — Gos
    gos@nerosopeningact.com
    “Nobody here but us heretics…”

  • invalid-0

    Whether expressed as a percentage or an incidence per 100 couple-years is irrelevant, because either way the outcome remains the same — at a rate of 4.8% per person year, it would take 20.833 person-years for a single instance of transmission to occur.

    There is just so much wrong with your argument that it is hard to know where to start.

    You are assuming that a) the risk per contact is constant for different people and at different satges of HIV infection and b) the infection is spread by monogamous couples.

    The papers that Richard cited show that a) is not true. The risk of transmission varies markedly with factors such as the stage of infection. Risk of infection is markedly higher during acute infection when viral load is highest. Any study that involves discordant couples in a stable monogamous relationship obviously excludes the acute infection period.

    It should also be obvious that monogamous couples do not create epidemics of STDs. STDs are generally spread by a small proportion of the population that have a larger number of sexual contacts and sexual partners. This forms a strongly interconnected network of sexual contacts. People who have sex with people that have multiple partners are themselves likely to have multiple partners. People that become infected with HIV are likley to have multiple partners and are likely to infect another person during the acute infection stage.

    A number of the papers that Richard cited also used genetic sequencing to confirm transmission so your quip about asthma being sexually transmitted is rather silly. The papers definitely demonstrate that HIV is being sexually transmitted.

    The silly naively simplistic mathematical games are the equivalent of proving that bumblebees can’t fly with a few simplistic equations. You only have to look at a bumblebee flying to see that it does fly. No amount of silly theoretical calculations will change this simple fact.

    HIV is sexually transmitted. No amount of silly theoretical calculations will change this simple fact.

  • invalid-0

    I’m glad you’re amusing yourself Gos. There’s actually a sort of meta-commentary on this thread on the “AIDS Myth Exposed” message board:

    http://groups.msn.com/aidsmythexposed/general.msnw?action=get_message&mview=0&ID_Message=29926&LastModified=4675631770500812840

    http://groups.msn.com/aidsmythexposed/activism.msnw?action=get_message&mview=0&ID_Message=30264&LastModified=4675632830389315271

    Your first salvo in this thread made several claims, all false:

    1. Nancy Padian’s study is an exemplar of sexual transmission studies; it is not, as a handful of citations demonstrates (this was just a list I’d quickly pulled from PubMed several months ago for different reasons, if you want more, click on any of the links and then hit the “related articles” link to the right). You then attempted to attack the first citation by claiming the transmission risk was too low to sustain a reproductive ratio greater than 1…by calculating the reproductive ratio incorrectly. Now you’re attempting to attack the second citation by focusing on a statistically insignificant difference between the people that reported zero vs. any condom use in the past year (the Vincenzi study compared consistent vs. inconsistent use during the study). There’s actually a precedent for people with less exposure prior to joining the study having increased risk of becoming infected during prospective follow-up: in a study of 741 couples discordant for HSV-2, 27 partners became infected. People whose partner had been HSV-2 infected for more than 2 years prior to the study were less likely to acquire infection than people whose partners had been infected less than 2 years. Any guesses as to what might explain this phenomenon?

    Also, while focusing on this statistically insignificant result from the Quinn study, you failed to explain the robustly significant correlations between viral load levels and risk of transmission.

    2. You made a false claim about the ART Cohort Collaboration treatment response study in the Lancet, made one half-hearted attempt at defending your claim, then gave up and didn’t mention it again.

    3. You made a false claim about the Rodriguez study in JAMA, also made a half-hearted attempt at defending it, then didn’t mention that study again, either.

    So, if blustering challenges are what interests you, here are mine:

    Figure out how many partners and instances of sexual intercourse per year would be required to sustain a reproductive ratio greater than one with a per contact risk of 0.03.

    Explain how the Lancet ART Cohort Collaboration study shows that ART does not reduce mortality and increases the risk of AIDS, as you claimed in your original post.

    Explain how the Rodriguez study shows viral load does not predict progression to AIDS, as you claimed in your original post.