Talk:Simian immunodeficiency virus

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Comments[edit]

This article appears to be a direct copying from an article in Nature. See [[1]]

Thanks, I'll try to fix it. AxelBoldt 23:07, 30 Dec 2004 (UTC)

Origins[edit]

Someone might want to take a stab at adding some of this data on origins... [2] work of Dr. Beatrice Hahn of the University of Alabama at Birmingham. Maybe someone can find the original scientific article to cite as well. Don't have time right now, myself... Isoxyl 21:14, 25 May 2006 (UTC)

There is a contradiction in this text: in the first paragraph - "The most likely route of transmission from monkeys to humans involves the contact with the blood of hunted animals" and then later on: "The monkey SIV strains do not infect humans and HIV-1 does not infect monkeys".

The short answer: There is no evidence that if you take a strain of SIV and infect a human with it, that it will cause any pathogenecity. But we can tell by how genetically similar the virus are that SIV and HIV are related, so transmission had to occur at some point. In order to jump species, the virus must have mutated. In fact, there were many jumps across species. Many strains of HIV are more closely related to strains of SIV then HIV, indicated that multiple transmission events happened. The most likely route of transmission was through bushmeat. Read any paper out of Beatrice Hahn's lab (there are many) for specific details.

speculation about pathogenicity[edit]

I substantially cut and merged these two paragraphs:

SIV monkey strains are transmitted sexually and usually do not cause AIDS in their natural hosts, SMs and African Green Monkeys (AGMs). Scientists suggest that this lack of response is evidence that SMs and AGMs have evolved together for a long time. One potential explanation for this unusual induction of tolerance is that SIV successfully incorporates itself into a system that protects the gametes and the developing monkey in utero from potential immune responses during the very early stages of pregnancy. This model is known as the eutherian fetoembryonic defense system (eu-FEDS) hypothesis. Evidence in favor of this paradigm is that the very mild immune response that AGMs and SMs mount against SIV closely mirrors the maternal immune response to the developing eutherian.
Immunological studies have shown that AGMs and SMs infected with SIV carry large viral loads and display similar levels of infection and subsequent apoptosis of CD4+ T cells observed in human patients infected with HIV-1. However, these natural hosts do not progress to AIDS. Instead, this weak immune response against SIV in AGMs and SMs appears to spare them from the chronic immunopathologies observed in humans and non-natural (heterologous) host species. These immunopathologies are of course almost always fatal if not treated.

My problems with the above:

  1. This theory about immune response during pregnancy has been mentioned in (as far as I can tell) a total of three published papers sharing the same author, who is also the editor who added the link. The theory may be a good one but I don't think it's accepted or notable; see Talk:Eutherian fetoembryonic defense system (eu-FEDS) hypothesis.
  2. No "evidence" is presented here. Plenty of hosts have mild immune responses to plenty of viruses. It is hardly unusual for a virus to be well adapted to a particular host in which it does not cause disease.
  3. The claim in the second paragraph is quite confusing and, I think, misleading. I can see how a host could have a high viral load and weak immune response without the virus being pathogenic to that host. But if you have high levels of destruction of CD4+ cells, don't you by definition have immunopathology? Maybe this is not what the editor meant to say. Compare this paper which suggests that a high level of immune activation can contribute indirectly to the loss of CD4+ cells, but certainly does not say that the monkeys who do lose their T-cells are not getting sick. ←Hob 05:49, 27 October 2006 (UTC)

I'm still having disagreements with User:Clarkgf about material in Eutherian fetoembryonic defense system (eu-FEDS) hypothesis, but I would like to keep discussion of the SIV article on the appropriate talk page as much as possible, so I'm copying part of Clarkgf's latest response here:

Are you claiming that the rate of CD4+ T-cell destruction does not correlate with the development of AIDS at all? In my (limited) understanding, that is very far from being a consensus viewpoint; that doesn't mean it can't be discussed on WP, but it shouldn't just be tossed off as if it is common knowledge, and you will definitely want to confer with editors on the AIDS and HIV articles as well. "References coming" is not a very useful approach when editors raise questions like this. ←Hob 02:26, 31 October 2006 (UTC)

The increased turnover of naive CD4+ T cells is not the cause of AIDS, as outlined in a recent review article. [3]. In the abstract to this review, the following correct phrase is included:
"Recent attempts to understand HIV-1 pathogenesis have set aside the view that CD4+ T-cell depletion is effected solely by HIV-1-mediated killing in favor of a more complete explanation that also includes T-cell dynamics and, more specifically, chronic immune activation as a central factor in HIV-1 pathogenesis."
You see, the experts acknowledge two major problems with CD4+ T cell destruction. First, the rate of decline of CD4+ T cells is too slow for the real culprit to be the overt destruction of naïve CD4+ T cells (the major cell population that is affected by cytolysis). Another major problem is that no one has ever demonstrated that there is any difference in the cytopathicity of SIV for CD4+ T cells in their natural hosts. As previously outlined, essentially complete tolerance is observed in the natural hosts even as CD4+ T cell destruction mirrors what occurs in HIV-1 infected patients. And that is why this very simple explanation is so problematic, and why unfortunately the current AIDS article is incorrect based on our current scientific understanding. Even in encyclopedias, we need to be accurate.--Clarkgf 15:41, 1 November 2006 (UTC)

My response:

I am well aware that direct killing of infected CD4+ T cells is no longer thought to be the major mechanism in HIV pathogenesis; I never said it was, and the AIDS and HIV articles don't say so either - they just say that there are both direct and indirect mechanisms, including some degree of destruction by cytotoxic T cells (your points about the destructive effects of immune system activation in HIV disease are, as far as I know, fairly uncontroversial at this point). None of which is to say that your hypothesis is wrong with regard to SIV - just that this particular argument, as you presented it in the article, is partly based on attacking an oversimplified straw-man notion, and lumping together the general problem of CD4+ T cell loss with questions about specific mechanisms in a misleading way... and in any case, that kind of speculation about recent research just doesn't belong here. ←Hob 22:10, 4 November 2006 (UTC)

Rename[edit]

There is less difference between SIV and HIV-1 than their is between HIV-1 and HIV-2 yet SIV retains a seperate name. One must realize the virus was orginally classed as a subtype of HIV-1. Almost immediately the press reported Africans got AIDS from having sex with monkeys and African nations demanded a retraction. Partly in response this virus which was always considered a subtype of HIV-1 was renamed. This makes NO sense. If one has rabies you don't rename it. It's rabies regardless if it's in a dog, skunk or human being. —Preceding unsigned comment added by 4.142.96.186 (talkcontribs)

Did you read the SIV article? Whether it's more closely related to HIV-1 or HIV-2 depends on which strain of SIV you're talking about. The science has come a long way since the virus was first discovered. Regardless of what you think "makes sense", this is the terminology scientists are using. Wikipedia is here to summarize current knowledge, not to second-guess it. ←Hob 22:30, 4 November 2006 (UTC)

The above poster is correct. Sorry if a virus is closer genetically than it's the same virus. So SIV is in fact at best only a subtype of HIV2 or HIV2 is part of SIV subtype.

It is illogical and it is political not science, the Wikipeida is here to teach people not to give in to political correctness. This is like saying a chimpanzee is a subtype of Humans. SIV is a type of HIV or you cannot say that HIV1 and HIV2 are the related or else you could say Eboloa is a Marburg virus, just because someone decided to call it that.

Actually, if you do not consider HIV and SIV to be to seperate viruses, then HIV would be a subtype of SIV. HIV-1 and HIV-2 are more closely related to strains of SIV then they are to each other (SIVcpz and SIV sm respecivily).

Hello, I don't see any discussion about the origin of HIV possibly coming from the use of chimps in the making of the polio vaccine. My reference is based on freedocumentaries.org, The Origin of HIV. Very interesting, sad and indicative of bad human behavior. Cinshif (talk) 14:43, 13 April 2009 (UTC)

perhaps it's because HIV predates the polio virus: see Worobey M, Gemmel M, Teuwen DE, et al. (October 2008). "Direct evidence of extensive diversity of HIV-1 in Kinshasa by 1960". Nature 455 (7213): 661–4.96.54.53.165 (talk) 00:58, 19 September 2010 (UTC)

Possible inaccuracy[edit]

The article under footnote 12 doesn't seem to say that it would take humans about 32k years to adapt to HIV (which seems extreme)- only that the virus could become nonlethal in that time period, not humans literally becoming no longer affected by it. As in, HIV itself would become nonlethal in that time period, as opposed to humans taking that long to no longer suffer it's effects. —Preceding unsigned comment added by Mannoro (talkcontribs) 05:53, 19 September 2010 (UTC)