AMCON SET TO TAKE OVER BEN BRUCE COMPANIES

The reason there’s no vaccine for HIV/AIDS, the National
Institutes of Health explains, is because HIV has “unique
ways of evading the immune system, and the human body
seems incapable of mounting an effective immune
response against it.” A recently published animal study
further clarifies the problem by showing how vaccines
designed to protect against HIV backfire, leading to an
increase, not decrease, in new infections. Specifically, it is
the higher number of activated CD4+ T cells which may be
a possible cause for spiking rates of new infection among
those already vaccinated.
“The virus infects the very cells of the immune system that
any vaccine is supposed to [activate],” Dr. Guido Silvestri,
senior author and chief of microbiology and immunology at
Yerkes National Primate Research Center, stated in a press
release . The vaccines meant to prevent disease seem to
make the target larger and therefore easier to hit.
Killer Cells and Their Helpers
T cells are a type of white blood cells that send signals to
activate the body’s immune response whenever they detect
an intruder, such as bacteria or viruses. T cells always
work in pairs, and so scientists place them in two large
categories based on their function (and the molecules
found on their surfaces). CD4+ T cells, referred to as
helper T cells, lead the fight by identifying an infection,
while CD8+ T cells go in for the kill. It's an effective
partnership, the basis of the immune system.
However, this essential system breaks down in the
presence of auto-immune diseases like AIDS. When a
person becomes infected with HIV, the virus attacks CD4+
T cells and then uses the stolen parts of their machinery to
multiply itself and spread throughout the body. When trying
to develop a vaccine for AIDS, many scientists have
decided to use CD4 + T cells as a potential target because
of this key role in both HIV and SIV (simian
immunodeficiency virus) infection.
For Silvestri’s research project, he and his co-authors
evaluated five different strategies for immunizing 36
rhesus macaques against SIV. After being given an initial
shot of one of the five different vaccines, each of the
monkeys received booster shots at 16 weeks and then
again at 32 weeks. Next, the monkeys were exposed to a
low-dose of SIV. In general, the researchers found none of
the vaccines prevented an SIV infection. Oddly, all the
immunized monkeys had detectable levels of circulating
"killer" T cells — the CD8+ T cells — but these cells did not
prevent infection. That said, at the beginning of their
infections, the vaccinated animals showed a lower than
expected initial viral load or level of SIV in their blood. What
was the researchers’ most important finding? The monkeys
had higher levels of activated CD4+T cells in their rectal
mucosal tissues before becoming infected.
“The possibility that certain immunization regimens
designed to protect against HIV infection and AIDS result in
increased risk of virus transmission is not just a theoretical
concern, because three recent large-scale clinical trials …
have shown a trend toward higher infection rates in
vaccinated individuals than in placebo recipients,” noted the
authors in their conclusion.
Source: Carnathan DG, Wetzel KS, Yu J, et al. Activated
CD4+CCR5+ T cells in the rectum predict increased SIV
acquisition in SIVGag/Tat-vaccinated rhesus macaques.
PNAS. 2014