HIV and AIDS: Settled Science or Unresolved Debate?|
Objections to the Claim that Questioning = Denial
My point in objecting to analogies between AIDS and the Holocaust is that the cast of mind that makes such analogies tends to disregard the line separating truth from fiction; it is a mind that may consciously or cynically blur definitive differences between events and situations. Whether it does this through zealousness or another motivational spur is a secondary concern. What concerns me most is that this sort of mind seems basically unbalanced, and, as such, untrustworthy in matters unrelated to AIDS and the Holocaust. Here again is the first paragraph from “Deadly Quackery,” the Op Ed piece by John Moore and Nicoli Nattrass discussed earlier in this column:
“HIV causes AIDS. This is not a controversial claim but an established fact, based on more than 20 years of solid science. It is as certain as the descent of humans from apes and the falling of dropped objects to the ground.”
After 25 years of investigating AIDS (it is no longer 20 years), is AIDS science as
settled as Moore/Nattrass imply? Consider the following short excerpts culled from recent articles in the peer-reviewed literature.
Excerpts one and two are from the abstract and conclusion of a review titled “HIV-1 pathogenesis,” published in Nature Medicine, Volume 9/Number 7/July 2003. The author, Mario Stevenson, was part of the Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA, at the time of publication.
[Abstract] “Despite considerable advances in HIV science in the past 20 years,
reason why HIV-1 infection is pathogenic is still debated and the goal of eradicating
HIV-1 infection remains elusive. A deeper understanding of the interplay between HIV-1 and its host and why simian immunodeficiency virus (SIV) is nonpathogenic in some natural hosts may provide a few answers.”
[Conclusion] “There is a general misconception that more is known about HIV-1
than about any other virus, and that all of the issues regarding HIV-1 biology and pathogenesis have been resolved.
On the contrary, what we know represents only a thin veneer on the surface of what needs to be known.
Despite the effectiveness of antiviral therapy, there is room for improvement, and new drug targets need to be identified.”
The third excerpt consists of a single sentence from the conclusion of a paper titled “Pathogenesis of HIV infection: what the virus spares is as important as what it destroys,” published in Nature Medicine, (online), March 6, 2006. The lead author, Zvi Grossman, is at the National Institute of Allergies and Infectious Diseases, National Institutes of Health, Bethesda, MD. Grossman is also in the Department of Physiology and Pharmacology, Sackler Faculty of Medicine, University of Tel Aviv, Israel.
“The pathogenic and physiologic processes leading to AIDS remain a conundrum.”
Excerpts four through eight are from an editorial titled “Explaining, predicting, and treating HIV-associated CD4 cell loss: after 25 years still a puzzle,” published in the Journal of the American Medical Association, September 27, 2006. W. Keith Henry, the lead author, is with the HIV Program, Hennepin County Medical Center and the University of Minnesota, Minneapolis. This editorial comments on a report in the same issue of JAMA, titled “Predictive value of plasma HIV RNA level on rate of CD4 T-Cell decline in untreated HIV infection,” by Rodriguez, B, et al.
“The provocative main finding from their study [Rodriguez et al] was that the
presenting plasma HIV RNA load predicted no more than 10% of the observed CD4 cell loss in
patients with chronic untreated HIV infection.
“What factor(s) explain the other 90%? Twenty-five years into the HIV epidemic,
a complete understanding of what drives the decay of CD4 cells – the essential event of HIV disease –
is still lacking.
“The findings presented by Rodriguez et al provide support to those who favor
nonvirological mechanisms as the predominant cause of CD4 cell loss.
“The study by Rodriguez et al may have several important clinical implications.
The first and most straightforward is that baseline measurements of viral load alone
should have less of a role in driving decisions on when to start antiretroviral
therapy for an individual patient; these initial viral load levels cannot predict
how rapidly the disease will progress.
“The sustainability of the current paradigm for the more than 40 million HIV-infected individuals and the more than 4 million new HIV infections per year is at best questionable.”
Note: All of the articles quoted above accept HIV as the cause of AIDS. All agree
that antiretroviral therapy can be effective in stemming progression of the condition. But compare the information cautiously put forward in these scientific articles with the glib assertion of Moore/Nattrass at the beginning of “Deadly Quackery” that everything about HIV science is “solid”; the Op Ed piece by M/N reads like unabashed propaganda.
For an AIDS clinician’s perspective on what’s been learned about treatment after 25 years,
I recommend Abigail Zuger’s review in The New York Times titled
“A Long Life?
A Death Sentence? AIDS Still Offers No Easy Answers” (Science Times, June 6, 2006). Zugar, an MD, has been in “the AIDS business long term” (her words). It’s unusual to find the disturbing drawbacks and uncertainties of AIDS therapy discussed so candidly anywhere in the pages of the Times.