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HIV's Effect On White Blood Cells Questioned By New Research?


HIV's Effect On White Blood Cells Questioned By New Research

http://www.sciencedaily.com/releases/200...

"Science Daily 鈥?Scientists have refuted a longstanding theory of how HIV slowly depletes the body's capacity to fight infection, in new research.

The researchers were looking at T helper cells, a class of white blood cells which recognise infection and co-ordinate the body's immune defences. They are attacked by HIV, and their numbers gradually decline in HIV positive patients. It has long been a major puzzle why this process of depletion is so slow, often taking 10 years or more.

One popular theory has been the "runaway" hypothesis, which says that T cells infected by HIV produce more HIV virus particles, which activate more T cells, that in turn become infected, leading to an uncontrolled cycle of T cell activation, infection, HIV production and cell destruction.

However, this new study in PLoS Medicine shows that this theory cannot explain the very slow pa

However, this new study in PLoS Medicine shows that this theory cannot explain the very slow pace of depletion that occurs in HIV infection. The research team used a mathematical model of the processes by which T cells are produced and eliminated to show that if the runaway theory was correct, then T helper cell numbers would fall to very low levels over a number of months, not years"

Now, who was saying that VERY same thing YEARS ago? Could it have been Peter Duesberg???

The rest of the article can be read at Sciencedaily.com

The article being questioned here is:

Yates A, Stark J, Klein N, Antia R, Callard R.
Understanding the Slow Depletion of Memory CD4(+) T Cells in HIV Infection.
PLoS Med. 2007 May 22;4(5):e177
PMID: 17518516

ABSTRACT:

BACKGROUND: The asymptomatic phase of HIV infection is characterised by a slow decline of peripheral blood CD4(+) T cells. Why this decline is slow is not understood. One potential explanation is that the low average rate of homeostatic proliferation or immune activation dictates the pace of a "runaway" decline of memory CD4(+) T cells, in which activation drives infection, higher viral loads, more recruitment of cells into an activated state, and further infection events. We explore this hypothesis using mathematical models. METHODS AND FINDINGS: Using simple mathematical models of the dynamics of T cell homeostasis and proliferation, we find that this mechanism fails to explain the time scale of CD4(+) memory T cell loss. Instead it predicts the rapid attainment of a stable set point, so other mechanisms must be invoked to explain the slow decline in CD4(+) cells. CONCLUSIONS: A runaway cycle in which elevated CD4(+) T cell activation and proliferation drive HIV production and vice versa cannot explain the pace of depletion during chronic HIV infection. We summarize some alternative mechanisms by which the CD4(+) memory T cell homeostatic set point might slowly diminish. While none are mutually exclusive, the phenomenon of viral rebound, in which interruption of antiretroviral therapy causes a rapid return to pretreatment viral load and T cell counts, supports the model of virus adaptation as a major force driving depletion.

====

Duesberg claims that HIV is totally harmless, and only drug abusers experience any decline in CD4+ T-cells over time.
He has been proven wrong in many ways, but he insists on repeating his lies.

No, what he's been saying is utter rot. Spme of his supporters will seize on anything which sounds similar to the untrained mind, out of context to try to support his twaddle.

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