Banana beats anti-HIV drugs

But when I turned the page, I was riveted. Gallo had deleted a statement by Popovic saying: 'Despite intensive research efforts, the causative agent of AIDS has not yet been identified.'

(images in book - scanned copies of the words as typed by Popovic and changed by Gallo)

This was totally unexpected. Nothing I read had led me to expect this. No one had mentioned these deleted words. Not Crewdson, not any of the investigators, no history of AIDS science. No one had reported these words, let alone their deletion by Gallo.

The evidence that HIV kills T-Cells Popovic's paper calls HTLV-3 a 'cytopathic' retrovirus; that is, one that causes degeneration or disease in cells. But when I searched for any evidence in his paper to support this, I could only find the observation that AIDS patients typically have low numbers of ‘Helper' (DC4) T-Cells - with the implied inference that this was because the AIDS virus had killed them. It is widely known in science that many factors can diminish the numbers of these cells - such as chronic drug addiction, severe malnutrition and Chronic Fatigue Syndrome. Sometimes even healthy people have low numbers. As I have noted, in 2001 Nature reported that it still was not known how HIV could kill T-cells.

In 2006 a paper by Benigno Rodriquez reported that HIV can't be killing more than 4% to 6% of the CD4 cells lost in AIDS cases - in other words not enough by itself to cause AIDS.

Popovic noted in his paper that there was a CD4-CD8 ‘reverse ratio', before Gallo deleted it. Popovic meant by this that when Helper CD4 T-Cells cells fall in number, the population of Killer CD8 T-cells goes up commensurately, and vice versa. We now know our immune system can change CD4s into CD8s as needed. It needs only a very small surface change to them. This too might explain why sometimes there are fewer CD4 cells.

It may simply be that we need more CD8s. In some frustration I have since searched for earlier papers in which Gallo or Popovic might have proved LAV, renamed as HTLV-3, able to kill or as cytopathic - but there are none, utterly none. The Institut Pasteur likewise seems not to have proved this. Neither had Popovic or Gallo proved their own virus, HTLV3, able to kill T-Cells.

Techniques such as polymerase chain reaction (PCR) have enabled scientists to demonstrate that a much larger proportion of CD4+ T cells are infected than previously realized, particularly in lymphoid tissues. Robert Gallo, a preeminent HIV virologist, suggests that as many as 3% of CD4+ T cells show signs of HIV invasion.[citation needed] Macrophages and other cell types are also infected with HIV and serve as reservoirs for the virus.

Although the fraction of CD4+ T cells that is infected with HIV at any given time is never high (only a small subset of activated cells serve as ideal targets of infection), several groups have shown that rapid cycles of death of infected cells and infection of new target cells occur throughout the course of disease.[35]

Furthermore, like other viruses, HIV is able to suppress the immune system by secreting proteins that interfere with it. For example, HIV's coat protein, gp120, sheds from viral particles and binds to the CD4 receptors of otherwise healthy T cells; this interferes with the normal function of these signalling receptors. Another HIV protein, Tat, has been demonstrated to suppress T cell activity. This behavior is not significantly different in quality from, say, the influenza viruses, which are well-known to secrete immunosuppressive proteins which can slow down the antiviral immune response.

Infected lymphocytes express the Fas ligand, a cell-surface protein that triggers the death of neighboring uninfected T cells expressing the Fas receptor.[36] This "bystander killing" effect shows that great harm can be caused to the immune system even with a limited number of infected cells.