TY - JOUR
T1 - Immunopathogenesis of acute AIDS virus infection
AU - Picker, Louis J.
N1 - Funding Information:
This work was supported by the National Institutes of Health (grants RO-AI054292 and P51-RR00163).
PY - 2006/8
Y1 - 2006/8
N2 - The pathogenesis of chronic HIV infection has long been envisioned as a slow process of immune degradation ultimately leading to overt immune deficiency and AIDS. However, recent studies suggest that the massive viral replication of acute infection initiates the pathogenic process, significantly degrading the immune system and setting up a sequence of events that years later leads to final decompensation and AIDS. The central player of the disease process appears to be the CD4+ effector memory T cell population that resides in the extra-lymphoid immune effector sites of the body (e.g. gut, lung and genital tract), and has a crucial role in maintaining immune competence at the tissue-external environment interface. HIV and its monkey counterpart SIV specifically target these CCR5-expressing T cells, significantly depleting them in acute infection and, in AIDS-susceptible species (humans, Asian macaques), initiating and maintaining a state of hyperactivation that undermines their regeneration. With time, uncontrolled viral replication leads to loss of these cells in tissue below a crucial threshold, resulting in increased susceptibility to opportunistic infection.
AB - The pathogenesis of chronic HIV infection has long been envisioned as a slow process of immune degradation ultimately leading to overt immune deficiency and AIDS. However, recent studies suggest that the massive viral replication of acute infection initiates the pathogenic process, significantly degrading the immune system and setting up a sequence of events that years later leads to final decompensation and AIDS. The central player of the disease process appears to be the CD4+ effector memory T cell population that resides in the extra-lymphoid immune effector sites of the body (e.g. gut, lung and genital tract), and has a crucial role in maintaining immune competence at the tissue-external environment interface. HIV and its monkey counterpart SIV specifically target these CCR5-expressing T cells, significantly depleting them in acute infection and, in AIDS-susceptible species (humans, Asian macaques), initiating and maintaining a state of hyperactivation that undermines their regeneration. With time, uncontrolled viral replication leads to loss of these cells in tissue below a crucial threshold, resulting in increased susceptibility to opportunistic infection.
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U2 - 10.1016/j.coi.2006.05.001
DO - 10.1016/j.coi.2006.05.001
M3 - Review article
C2 - 16753288
AN - SCOPUS:33745363316
SN - 0952-7915
VL - 18
SP - 399
EP - 405
JO - Current opinion in immunology
JF - Current opinion in immunology
IS - 4
ER -