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Wednesday, October 24, 2007 8:44:18 AM
"immune cell activity after massive apoptosis during AHI"
they, (Haynes etc.), state that
"The nature of the innate response in AHI and its interaction with the adaptive response
may be among the factors involved in determining the set point of plasma viremia"
and
"A key implication of this hypothesis is the suggestion that innate responses may be harnessed to form an
important component of vaccine-elicited protective immunity, a setting in which
rapid triggering of effector functions following exposure to HIV or HIV-infected
cells is likely to be critical."
so in CHAVI 012,
"It is proposed to characterize the
innate effector mechanisms activated in primary HIV infection and explore their
role in control of early virus replication; and to address whether HIV impairs
aspects of innate immunity in AHI to promote its persistence. This will facilitate
the design of vaccination strategies to target key effector pathways and/or
circumvent infection-associated impairments in innate functions."
what are those ' key effector pathways' / 'infection-associated impairments in innate functions' ?
"Acutely expressed cytokines and apoptotic microparticles
hypothesized to play a key role in AHI pathogenesis will be
assayed.
The CHAVI panel of cytokines including alpha IFN, TNF alpha, IL10,
TGF-beta, as well as a Luminex panel of T and B regulatory cytokines, and
plasma microparticles will be quantitated."
http://72.14.209.104/search?q=cache:BCKueWKqWTIJ:www.chavi.org/wysiwyg/downloads/CHAVI_012_protocol_v1.pdf+%22CHAVI+012%22&hl=en&ct=clnk&cd=1&gl=us&client=firefox-a
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j
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