Using death to one's advantage: HIV modulation of apoptosis

ECU Author/Contributor (non-ECU co-authors, if there are any, appear on document)
TM Ross (Creator)
East Carolina University (ECU )
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Abstract: Infection by human immunodeficiency virus (HIV) is associated with an early immune dysfunction and progressive destruction of CD4+ T lymphocytes. This progressive disappearance of T cells leads to a lack of immune control of HIV replication and to the development of immune deficiency resulting in the increased occurrence of opportunistic infections associated with acquired immune deficiency syndrome (AIDS). The HIV-induced premature destruction of lymphocytes is associated with the continuous production of HIV viral proteins that modulate apoptotic pathways. The viral proteins such as Tat Env and Nef are associated with chronic immune activation and the continuous induction of apoptotic factors. Viral protein expression predisposes lymphocytes particularly CD4+ T cells CD8+ T cells and antigen-presenting cells to evolve into effectors of apoptosis and as a result to lead to the destruction of healthy non-infected T cells. Tat and Nef along with Vpu can also protect HIV-infected cells from apoptosis by increasing anti-apoptotic proteins and down- regulating cell surface receptors recognized by immune system cells. This review will discuss the validity of the apoptosis hypothesis in HIV disease and the potential mechanism(s) that HIV proteins perform in the progressive T cell depletion observed in AIDS pathogenesis. Originally published Leukemia Vol. 15 No. 3 Mar 2001

Additional Information

Leukemia. 15:3(March 2001) p. 332-341.
Language: English
Date: 2011
HIV (Viruses), AIDS, T cell depletion, Apoptosis

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