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HIV may be weakening

  1. Sep 30, 2005 #1

    Ivan Seeking

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    http://seattletimes.nwsource.com/html/nationworld/2002530417_hiv30.html
     
  2. jcsd
  3. Sep 30, 2005 #2

    Chronos

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    Hopeful thinking, my guess.
     
  4. Sep 30, 2005 #3

    Moonbear

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    I'd agree with the last sentence in the article. It's interesting, but with only 12 samples, it's far from conclusive. And, if the findings hold up, there's also no guarantee that at the rate this virus mutates that it won't become stronger again. It might also be a result of human behavior. A weaker strain might be spread more readily because the infected people aren't aware of their infection as quickly or don't get as sick, while the stronger strains may still be out there ready to take hold if people get careless, but the people currently infected by those strains are too sick to spread it or are taking more precautions because they are more aware of their symptoms.
     
  5. Sep 30, 2005 #4
    It sounds like evolution at work
     
  6. Sep 30, 2005 #5

    DocToxyn

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    Would that be "survival of the weakest"? :wink:
     
  7. Oct 1, 2005 #6

    selfAdjoint

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    It's no advantage to a pathogen to kill off its host population. There's a lot of evolutionary thinking that suggests the most lethal ones evolve moderation over time, to permit the infected population to breed and transmit the parasite to newer generations.
     
  8. Oct 2, 2005 #7
    Self Adjoint - your response is interesting in light of my question.

    I have a 'friend' on another forum who is anti-vaccination. He argues that vaccines are introduced (typically) as a disease is in its decline anyway.

    Why would a disease "decline"? (Self Adjoint, your answer applies.)

    This article could easily be used as an argument that if a vaccine were developed for AIDS, that it was not really helping at the peak of the pandemic anyway - and that the disease would "disappear" on its own anyway.... or at least become a non-virulent form.

    The whole thing just sounds funny. And I'm not particularly articulate at the moment, which doesn't help.
     
  9. Oct 2, 2005 #8

    Moonbear

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    It's not so much that it would "decline" as become a less acutely lethal disease, but instead be more of a chronic disease. If you kill your host too quickly, there isn't much chance for spread, especially with something like HIV that requires fairly intimate contact to spread (it would be different for an airborne disease that can spread through dense populations quickly).

    I don't think that's what the article is saying. Of course, a lot of the diseases that vaccines are developed for are also not immediately lethal in most people, but they can lead to chronic health problems or disfigurement (think Polio...many kids died from it, but many others survived, yet wound up in a wheelchair or leg braces for life).

    The problem with this article though, is that HIV is not an immediately lethal disease anyway. It is a chronic illness and has a sufficiently long time from acquiring the virus to conversion to AIDS and eventually death, even before medications were available, that it could spread quite readily, so the argument that the weaker strains would have a survival advantage in terms of keeping the host alive longer doesn't really hold up very well.

    The difficulty in creating a vaccine to HIV lies in how rapidly it mutates to new strains. That's another reason I'm a bit skeptical about these findings. It doesn't look at a pattern, more of just a snapshot in only a few patients, so when the virus is known to rapidly mutate, how much weight can you give to a strain that is weaker when it's just one of so many out there (and if they weren't testing all the same strain, then your N is really even less than 12).
     
  10. Oct 5, 2005 #9

    marcus

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    Here is Eric Arts homepage at Case Western Reserve

    http://p450.case.edu/faculty/faculty.asp?arts

    it does not look to me like he has updated his list of publications to include the article in AIDS journal that is being discussed here

    however it shows earlier articles that he and co-workers have published in AIDS and in other journals

    I would be interested to hear if anyone comes across the actual article

    (the article itself may make several of the points made in this thread----e.g. that the sample is too small and the finding preliminary, that one might expect the pathogen to evolve into a less lethal form if this were to allow it to spread more widely in the population, as has happened in other cases, and that this is not necessarily something to get real happy about----and the article might have interesting references to other work)

    Anyway hope to hear more. Thanks to Ivan Seeking for catching this one!
     
    Last edited: Oct 5, 2005
  11. Oct 5, 2005 #10

    marcus

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    Ah! here is something interesting

    http://www.aidsonline.com/pt/re/aids/currenttoc.htm


    this is an online version of the AIDS Journal!

    (probably it is pay-per-view, :yuck:, but it may still give information)

    It shows the 14 October issue TOC, with the Eric Arts article at the top

    Replicative fitness of historical and recent HIV-1 isolates suggests HIV-1 attenuation over time.
    Kevin K Ariën; Ryan M Troyer; Youssef Gali; Robert L Colebunders; Eric J Arts; Guido Vanham
     
    Last edited: Oct 5, 2005
  12. Oct 5, 2005 #11

    marcus

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    the PDF text was not free, however
    the abstract was free, so here it is:
    ===============================


    http://www.aidsonline.com/pt/re/aids/abstract.00002030-200510140-00001.htm

    Replicative fitness of historical and recent HIV-1 isolates suggests HIV-1 attenuation over time.
    AIDS. 19(15):1555-1564, October 14, 2005.
    Arien, Kevin K a; Troyer, Ryan M b; Gali, Youssef a; Colebunders, Robert L c; Arts, Eric J b; Vanham, Guido a,d
    Abstract:
    Background: Changes in virulence during an epidemic are common among pathogens, but still unexplored in the case of HIV-1. Here we used primary human cells to study the replicative fitness of primary HIV-1 isolates from untreated patients, comparing historical (1986-1989) and recent samples (2002-2003).

    Methods: Head-to-head dual virus infection/competition assays were performed in both peripheral blood mononuclear cells and human dendritic cell/T-cell co-cultures with pairs of 12 carefully matched historical and recent HIV-1 isolates from untreated patients. Sensitivity to inhibition by lamivudine (3TC) and TAK-779 of historical and recent R5 HIV-1 isolates was measured in a subset of samples.

    Results: Overall, the historical HIV-1 out-competed the recent HIV-1 isolates in 176 of 238 competitions and in 9 of 12 competitions carefully matched for CD4 cell count. The mean relative replicative fitness (W) of all historical HIV-1 strains was significantly greater than that of recent HIV-1 isolates (W1986-1989 = 1.395 and W2002-2003 = 0.545, P < 0.001 (t test)). The more fit viruses (mean W > 1) from 1986-1989 appeared less sensitive to TAK-779 and 3TC than did the less fit (mean W < 1) 2002-2003 viruses.

    Conclusions: These findings suggest that HIV-1 replicative fitness may have decreased in the human population since the start of the pandemic. This 'attenuation' could be the consequence of serial bottlenecks during transmission and result in adaptation of HIV-1 to the human host.
     
    Last edited: Oct 5, 2005
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