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Cell Death in HIV Pathogenesis and Its Modulation by Retinoids
Author(s) -
SZONDY ZSUZSA,
TÓTH RÉKA,
SZEGEZDI ÉVA,
REICHERT UWE,
ANCIAN PHILIPPE,
FÉSÜS LÁSZLÓ
Publication year - 2001
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2001.tb03905.x
Subject(s) - apoptosis , pathogenesis , immunology , cd8 , programmed cell death , immunodeficiency , lymphocyte , t lymphocyte , biology , cytotoxic t cell , cell , human immunodeficiency virus (hiv) , virus , t cell , lentivirus , cancer research , virology , viral disease , immune system , in vitro , genetics
A bstract : Patients infected with the human immunodeficiency virus exhibit a progressive decline in the CD4 T‐cell number, resulting in immunodeficiency and increased susceptibility to opportunistic infections and malignancies. Although CD4 T cell production is impaired in patients infected with HIV, there is now increasing evidence that the primary basis of T cell depletion is accelerated apoptosis of CD4 and CD8 T cells. The rate of lymphocyte apoptosis in HIV infection correlates inversely with the progression of the disease: it is low in long‐term progressors and in patients undergoing highly active antiretroviral therapy. Interestingly, only a minor fraction of apoptotic lymphocytes are infected by HIV, indicating that the enhanced apoptosis does not necessarily always serve to remove the HIV + cells and results from mechanisms other than direct infection. Thus, understanding and influencing the mechanisms of HIV‐associated lymphocyte apoptosis may lead to new therapies for HIV disease. In this paper the potential effects of retinoids on CD4 T cell apoptosis is discussed.