A CHALLENGE TO THE AIDS ESTABLISHMENT
By Peter Duesberg
Bio/Technology Nov. 1987
Acquired Immune Deficiency Syndrome (AIDS) has become a cause celebre
for journals, companies, and scientists, and the "deadly AIDS virus"
has been sold to the public as the cause of AIDS with the confidence and
authority that is usually derived from absolute scientific proof. The bases
of the virus-AIDS hypothesis are that this retrovirus was originally isolated
from an immune-deficient patient, that 80%-90% of AIDS patients have antibody
to the virus, and that there is a reasonable correlation between anti-viral
antibodies and persons in high-risk groups for the disease. The hypothesis
is appealing because it appears to fit a 100-year-old tradition of triumphs
in medicine that proved viral and bacterial parasites to be the causes
of contagious disease. But this appearance is deceptive.
Three criteria need to be met before a virus can be said to function
as a pathogen. It must be biochemically active. It must infect or intoxicate
more cells than the host can regenerate or spare. And the host must be
genetically and immunologically permissive. Yet almost none of the accumulated
data on the "Human Immunodeficiency Virus" (HIV) demonstrate
that the virus satisfies any of these criteria.
HIV is latent and inactive, not only in the 1-2 million Americans who
test positive for antibody to the virus, but also in the 10,000 who annually
develop AIDS and the 5,000 who die from it. Yet all other pathogenic viruses
are known to be meta-bolically active when they cause disease. Latency
is the mechan-ism by which parasites typically survive as passengers in
HIV also fails to meet the second criterion since it actively infects
fewer than .01% of susceptible lymphocytes and since 5% of T cells are
regenerated during the 2 days it takes the virus to infect the cell. Moreover,
it is truly paradoxical that HIV is said to cause AIDS only after an asymptomatic
incuba-tion period of at least 5 years, although antiviral immunity is
induced within a few weeks. Ever since Jenner discovered the principle
of vaccination, anti-viral immunity (the basis of the AIDS test) has been
considered the ultimate weapon against rather than an indication for, future
Consistent with the presence of antiviral antibody, there is very little
direct evidence for the presence of the virus in per-sons with AIDS. There
is not one report of a virus titer from an AIDS patient. Indeed, virus
can only be isolated from 50% of symptomatic and asymptomatic carriers,
and then only by tech-niques originally designed to activate latent viruses.
The methods are to grow millions of cells in culture, away from the immune
system and as yet unknown suppressors of the host, until at least one previously
latent virus becomes active. This will then be multiplied by adding uninfected
cells until a detectable titer is reached. Thus isolating virus from 50%
of AIDS patients implies that 50% carried less than one latent virus in
several million cells.
In fact, viral genomes have only been detected in about 15% of persons
who test positive for HIV antibody; in these persons, about one proviral
genome is found in 100-1000 susceptible lym-phocytes. In other words, 85%
of antibody-positive persons carry either less provirus than this or none
at all. Moreover, most of these proviruses are dormant since only one in
10,000-100,000 susceptible cells express viral RNA in both symptomatic
and asymptomatic carriers. In contrast, the titers of other known retroviruses
are between 10 to the fourth power to 10 to the tenth power infectious
units per ml of serum or tissue when they function as pathogens.
The virus-AIDS hypothesis also totally fails to explain how the virus
depletes T-helper cells, and why it takes at least 3-5 years to do so.
Unlike all other animal viruses, retroviruses need mitosis to initiate
infection. Moreover, no HIV gene remains inactive during replication, which
takes about 1-2 days, as with all other retroviruses. Thus HIV would be
expected to kill T cells and cause AIDS when it first infects an organism
and not 5 years later when it is biochemically inactive and suppressed
by antiviral immunity. The 5-year latency presents proponents of the hypothesis
with two bizarre options: either old T cells die 5 years after infection,
or the offspring must die in the 50th generation, given a one-month
generation time for the average T cell.
Nevertheless, killing of T cells within weeks, not years, after infection
has been observed in cell culture-in apparent agreement with the claim
that the virus kills T cells. But this type of killing is fundamentally
different from the unconditional cell lysis achieved by true cytocidal
viruses. It involves cell fusion mediated via HIV antigens on the surface
of infected cells, and is conditional on the cells and virus isolates used.
Further, it does not occur in chronically infected human T-cell lines that
grow indefinitely in culture yet produce more virus than any other system,
nor has it ever been observed in blood taken from an AIDS patient. In fact,
limited cell killing by fusion is a common feature of retroviruses, none
of which have as yet been claimed to cause AIDS.
It seems clear from the foregoing that the virus-AIDS hypothesis fails
to make a case for sufficiency. It offers no explanation for why less than
1% of antibody-positive persons develop AIDS and why the mean latency between
infection and disease is 5 years, whereas antiviral immunity is established
in a few weeks. A latent period for pathogenicity that exceeds the latent
period for immunity is unambiguous evidence for a co-factor or another
causative agent altogether. Finally, the hypothesis cannot support a claim
that the virus is even neces-sary for AIDS in view of the fact that it
is barely present and consistently latent even in persons with the disease.
Since the transmission of AIDS depends on frequent contacts involving the
exchange of cells, the case for a viral cause remains open.*