Wednesday, July 22, 2009

Chimpanzees get AIDS too

This is really more the area of Tara or ERV but I still thought I'd comment on this piece of news.

African primates can be infected with over 40 different simian immunodeficiency viruses (SIVs). These diseases are related to two diseases which infects our particular species of primates, Homo sapiens, human immunodeficiency virus types 1 and 2 (HIV-1 and HIV-2) - indeed the two types of HIV are the result of SIVs crossing the species barrier.

HIV is considered an epidemic with more than 30 million people suffering from it worldwide (source - .pdf). As people hopefully know, HIV 1 and 2 will, if not treated by medicine, result in acquired immune deficiency syndrome (AIDS), which is fatal. 2 million people died from AIDS in 2007.

HIV and AIDS is one of the top prioritized areas of medical studies, and both the evolution of HIV from SIV and the connection between HIV and AIDS are well understood. This doesn't, however, keep some people from either claiming that HIV/AIDS is man-made, or that AIDS doesn't exist.

One of the arguments used by both groups is that SIV doesn't lead to AIDS in primates - the one group to argue that HIV couldn't have evolved from SIV, the other to argue that AIDS is not real.

Neither group makes sense. The lack of development of AIDS in SIV carrying primates is by no means evidence of there being no SIV-HIV connection, nor evidence of there being no HIV-AIDS connection.

Still, this matters even less now. Researchers have found out that some primates can get AIDS.

Nature has a new paper by Beatrice Hahn et al.

Increased mortality and AIDS-like immunopathology in wild chimpanzees infected with SIVcpz (link takes you to the abstract, the paper is behind a paywall)

African primates are naturally infected with over 40 different simian immunodeficiency viruses (SIVs), two of which have crossed the species barrier and generated human immunodeficiency virus types 1 and 2 (HIV-1 and HIV-2)1, 2. Unlike the human viruses, however, SIVs do not generally cause acquired immunodeficiency syndrome (AIDS) in their natural hosts3. Here we show that SIVcpz, the immediate precursor of HIV-1, is pathogenic in free-ranging chimpanzees. By following 94 members of two habituated chimpanzee communities in Gombe National Park, Tanzania, for over 9 years, we found a 10- to 16-fold higher age-corrected death hazard for SIVcpz-infected (n = 17) compared to uninfected (n = 77) chimpanzees. We also found that SIVcpz-infected females were less likely to give birth and had a higher infant mortality rate than uninfected females. Immunohistochemistry and in situ hybridization of post-mortem spleen and lymph node samples from three infected and two uninfected chimpanzees revealed significant CD4+ T-cell depletion in all infected individuals, with evidence of high viral replication and extensive follicular dendritic cell virus trapping in one of them. One female, who died within 3 years of acquiring SIVcpz, had histopathological findings consistent with end-stage AIDS. These results indicate that SIVcpz, like HIV-1, is associated with progressive CD4+ T-cell loss, lymphatic tissue destruction and premature death. These findings challenge the prevailing view that all natural SIV infections are non-pathogenic and suggest that SIVcpz has a substantial negative impact on the health, reproduction and lifespan of chimpanzees in the wild.


In other words, there is a non-trivial health cost in being infected with SIVcpz.

This is not a trivial finding. As Nature makes clear in it's news release on the story (Wild chimpanzees get AIDS-like illness) this will impact future research.

The results suggest that it will not be possible to find the key to HIV immunity in the chimpanzee genome, as scientists had hoped. However, the study, published in Nature, sets the stage for researchers to gain insight into how HIV and SIV cause disease in their hosts by studying the responses of different primates to the viruses. Wild monkeys that have coexisted with SIV for a long time — such as sooty mangabeys and African green monkeys — seem to have evolved the ability to control SIV, and so do not become ill when exposed to the virus. The new paper, however, shows that chimpanzees — which, like humans, were exposed to SIV more recently — are sickened by the virus.


NY Times also writes about this study: Chimpanzees Do Die From Simian AIDS, Study Finds

Update: Carl Zimmer has written a great blog post about this.

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Saturday, October 25, 2008

HIV testing of pregnant women

While looking around over at PLoS One, I came across this study.

Rapid Testing May Not Improve Uptake of HIV Testing and Same Day Results in a Rural South African Community: A Cohort Study of 12,000 Women by Mkwanazi et al.

Personally, I found the title confusing, but what it tries to convey is the fact that the availability of rapid HIV testing has not led to more people wanting to get tested, contrary to what one might have believed.

Background

Rapid testing of pregnant women aims to increase uptake of HIV testing and results and thus optimize care. We report on the acceptability of HIV counselling and testing, and uptake of results, before and after the introduction of rapid testing in this area.

Methods and Principal Findings

HIV counsellors offered counselling and testing to women attending 8 antenatal clinics, prior to enrolment into a study examining infant feeding and postnatal HIV transmission. From August 2001 to April 2003, blood was sent for HIV ELISA testing in line with the Prevention of Mother-to-Child Transmission (PMTCT) programme in the district. From May 2003 to September 2004 women were offered a rapid HIV test as part of the PMTCT programme, but also continued to have ELISA testing for study purposes. Of 12,323 women counselled, 5,879 attended clinic prior to May 2003, and 6,444 after May 2003 when rapid testing was introduced; of whom 4,324 (74.6%) and 4,810 (74.6%) agreed to have an HIV test respectively. Of the 4,810 women who had a rapid HIV test, only 166 (3.4%) requested to receive their results on the same day as testing, the remainder opted to return for results at a later appointment. Women with secondary school education were less likely to agree to testing than those with no education (AOR 0.648, p<0.001), as were women aged 21–35 (AOR 0.762, p<0.001) and >35 years (AOR 0.756, p<0.01) compared to those >20 years.

Conclusions

Contrary to other reports, few women who had rapid tests accepted their HIV results the same day. Finding strategies to increase the proportion of pregnant women knowing their HIV results is critical so that appropriate care can be given.


The study is interesting for several reasons. Not only did it find that rapid test results are not helping getting more women to get tested, it also shows that young women (below 21 years old) are more likely to get tested, and that educated women are less likely to get tested. Also, in the time period observed, there has been a general downward trend in getting tested.

All of this makes it sound like that targeted promotion of HIV tests to educated women and/or women above 20 could be at least as efficient as ensuring rapid test results.

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Wednesday, November 21, 2007

The future of AIDS treatment

MSNBC has an article, Finding the way again after failed AIDS vaccine, about the future of HIV/AIDS treatment, after the recent failure of a new vaccine by Merck (not only didn't it help people, it seemed like the vaccination might make it easier for people to get infected by HIV).

The MSNBC article raises some good point, especially at the end, where Robert Bazell writes

But meanwhile we do know that treatment works well for those who are infected, and old-fashioned prevention efforts keep people from getting infected in the first place. Perhaps it is time to re-think the priorities.


I think Bazell is both right and wrong. Yes, we should up-prioritize research into treatments, and focus on proper sex-ed (which is most assuredly not abstinence-only sex-ed). On the other hand, it is also necessary to find a cure for HIV, and we shouldn't cut back on that. Instead, we could cut back on many other less urgent, or directly wasteful, things (think what kind of resources an end to the Iraq war would free).

Another thing we need to educate people on, is what causes HIV/AIDS, so AIDS-denialists are rejected as the idiots they are. Now, too much credence is made to their dangerous ideas by far too many people, including people in positions of power.

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Wednesday, August 22, 2007

A few short notes

Few of my readers are probably unaware of this, but PZ Myers has been sued over some unfavorable book reviews of Stuart Pivar's LifeCode: The Theory of Biological Self Organization. Blake Stacey has more, with plenty of links. The Panda's Thumb also has a good post on it. PZ is keeping quiet about the case for now.

My take on this is that Pivar has absolutely no case, since he cant demonstrate neither financial loss, nor even that it's libel. As people probably know, truth is the best defense against libel lawsuits. One of Pivar's points is related to a prominent scientist (Neil deGrasse Tyson) withdrawing his endorsement of the book, but it's clear from the scientist's own statements that he has never endorsed the book, even though Pivar claims this.
For other good arguments against the lawsuit, see the comments at The Panda's Thumb




Tara Smith, of Aetiology has written an article about HIV Denial in the Internet Era together with Steven Novella. It has been published by PLoS Medicine.

I some times participate in the HIV-AIDS debates over at Aetiology, but I have burned out on hearing the same denialist arguments again and again, so it's very little I venture into those threads these days.




Last of all, an article that some might find interesting - I know that some will agree with it's basic message.

Science and mysticism: a tainted embrace

Scientists who indulge mystical and religious fantasies in the interest of popularisation are betraying their professional calling, says Yves Gingras

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Thursday, August 02, 2007

ERV takes on Behe

Abbie, who writes the great blog Endogenousretrovirus, and comments under the handle ERV or SA Smith, has written a great post in which she explains how woefully wrong Michael Behe is in his newest book.

Michael Behe, please allow me to introduce myself...

In short, Abbie's post demolishes the whole premise for Behe's book.

The post will go up on The Panda's Thumb as well, so it will reach the wide audience it deserves.

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Sunday, April 22, 2007

Scientific American defends Duesberg article

Or rather the choice to bring the article.

When Pariahs Have Good Ideas

Even mentioning the name Peter Duesberg inflames strong feelings, both pro and con. After gaining fame in 1970 as the virologist who first identified a cancer-causing gene, in the 1980s he became the leading scientific torchbearer for the so-called AIDS dissidents who dispute that HIV causes the immunodeficiency disorder. To the dissidents, Duesberg is Galileo, oppressed for proclaiming scientific truth against biomedical dogma. A far larger number of AIDS activists, physicians and researchers, however, think Duesberg has become a crank who refuses to accept abundant proof that he is wrong. To them, he is at best a nuisance and at worst a source of dangerous disinformation on public health.


I think this can be said to be a fairly reasonable summary, except the don't mention the fact that Duesberg's claims flies in the face of all evidence. It could also have been good if the Scientific Amercian had explained why Duesberg is competely and utterly wrong.

Readers may therefore be shocked to see Duesberg as an author in this month's issue. He is not here because we have misgivings about the HIV-AIDS link. Rather Duesberg has also developed a novel theory about the origins of cancer, one that supposes a derangement of the chromosomes, rather than of individual genes, is the spark that ignites malignant changes in cells. That concept is still on the fringe of cancer research, but laboratories are investigating it seriously. Thus, as wrong as Duesberg surely is about HIV, there is at least a chance that he is significantly right about cancer. We consider the case worthy of bringing to your attention, with the article beginning on page 52.


Wouldn't Medical Hypothesis be a more suitable place for Duesberg's article than Scientific American? At least until there is some evidence of his hypothesis?

Thousands of scientific papers appear in technical journals every month; why do some rate more fame and journalistic attention? It helps for science news to have dramatic relevance to human affairs: Is there strong new hope for curing a disease, transforming the economy, building a better mousetrap? Alternatively, reporters and editors may gravitate toward new science that easily inspires the public's sense of wonder, as so many astronomy stories do. And reports that appear in certain major scientific journals tend to get more play because those publications have a self-fulfilling reputation for releasing the most noteworthy papers. (It doesn't hurt that those journals have particularly strong public relations departments, too.)

When we look at submitted manuscripts from scientists, we consider it a reassuring sign when the authors forthrightly acknowledge both their collaborators and their competitors and note potential conflicts of interest before we ask. If we see that they are describing the science of their rivals fairly, we can have more confidence that they are being similarly candid about their own work. (Still, the old nuclear disarmament treaty maxim applies: trust, but verify.) We typically steer away from controversial ideas too new to have much supporting evidence. Those that have lasted for years and accumulated some substantiation have earned consideration. Our judgments are imperfect, but they tend to mirror those of the scientific community.


Since there doesn't seem to be any evidence yet for Duesberg's ideas, I fail to see why they then included the article. And what in Duesberg's recent track record shows that he has any ability to evaluate scientific work done by others? Or by himself for that matter?

Blots on a researcher's history often should bear on regard for his or her new work. Scientists who have intentionally published fraudulent papers, as the stem cell researcher Woo Suk Hwang so notoriously did two years ago, may be irredeemably tainted. But to dismiss a scientist solely for holding some wrong or controversial views risks sweeping away valuable nuggets of truth. We respect the opinions of any readers who may criticize our choice to publish Duesberg in this case but hope they will nonetheless evaluate his ideas about cancer on their own merits.


It's not the fact that Duesberg holds wrong or controversial views that should keep him away from the journal's pages, but the fact that he demonstrately cannot recognize flaws in his own science. His "research" on HIV/AIDS has been shown to be wrong numerous times, and yet he persists in insisting on it, and even try to affect African policy on the issue. Something which not only endangers people, but which my surely have resulted in unnecessary deaths.

By bringing an article by Duesberg, Scientific American lends credibility to Duesberg - not only on the hypothesis discussed in the article, but also on his other dangerous ideas. That's why the article should not have been brought, unless there is some evidence of his ideas being right.

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Wednesday, April 04, 2007

HIV/AIDS findings

While looking for a different paper in the Journal of Infectious Diseases, I came across an article and a editiorial commentry that I found interesting, especially when combined.

The editorial commentry takes a look at the effects of highly active antiretroviral therapy (HAART) for HIV on HIV infections, while the paper takes a more general look at the dynamics of the spreading of HIV in Quebec.

The editorial, Primary HIV Infection, Phylogenetics, and Antiretroviral Prevention, makes clear that while HAART has been effective in prolonging the lives of HIV-infected people, it has done nothing to stop the spreading of HIV at all.

Over the past 10 years, the world has witnessed one of the most significant chronic disease interventions ever seen—that of highly active antiretroviral therapy (HAART) for HIV infection. Morbidity and mortality have plummeted in those areas of the world with unrestricted access to these drugs [1], and HIV/AIDS has been transformed from an almost certain death sentence to, for those receiving treatment, a long-term, manageable disease, with a potentially normal life expectancy. By contrast, this success has not been matched by reductions in HIV transmissions over the same period. Indeed, current surveillance data suggest that transmissions are increasing in resource-rich communities—particularly among men who have sex with men (MSM) [2], in addition to the large epidemics ongoing within the resource-poor world. Such increases represent a public health failure. The inevitable outcome of widespread HAART use in the midst of increasing HIV transmission—namely, transmission of drug-resistant viruses—has now become a worldwide reality [3–5].

The suboptimal impact of safe sex messages over the past 20 years suggests that more innovative and effective preventive strategies are required. More research is necessary to uncover the dynamics and drivers of transmission within different communities and risk groups, to inform an evidence base for such interventions.


As the editorial makes clear, to do this, we have to know something about the dynamics of the spreading of HIV, which leads us to the paper, High Rates of Forward Transmission Events after Acute/Early HIV-1 Infection by Brenner et al, which describes the pattern of the spreading of HIV in Quebec, with a focus on how large a part of it happens by people who are newly infected. And the paper reaches a pretty important conclusion.

Early infection accounts for approximately half of onward transmissions in this urban North American study. Therapy at early stages of disease may prevent onward HIV transmission.


In other words, if we can stop the infection at its early stage, half of the spreading can be stopped (if Quebec is representative in that aspect). That's pretty important, since most of the focus has been on preserving the health of infected people, and find a complete cure. None of these aspects should be ignored, but there should certainly be a focus on stopping the spreading of the virus as well.

The paper I was looking for was this one: Highly Attenuated Rabies Virus–Based Vaccine Vectors Expressing Simian-Human Immunodeficiency Virus89.6P Env and Simian Immunodeficiency Virusmac239 Gag Are Safe in Rhesus Macaques and Protect from an AIDS-Like Disease by McKenna et al.

It basicly describes how an rabies vaccination seemed to protect four test animals against an AIDS-like disease. ScienceDaily described it here.

Obviously a lot more research has to go into this, before it can even be considered for human trials, but the findings are interesting, and has the potential for being a major break-through in combating HIV/AIDS.

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