Viruses 2011, 3(5), 586-612; doi:10.3390/v3050586
Review

CD4+ T Cell Depletion in Human Immunodeficiency Virus (HIV) Infection: Role of Apoptosis

1 Unité Génomique Virale et Vaccination, CNRS URA 3015, Institut Pasteur, 28 rue du Dr Roux, 75015 Paris, France 2 Inserm UMRS 945, Université Pierre et Marie Curie, Hôpital Pitié Salpêtrière, Bâtiment CERVI, 83 Bd de l’hôpital, 75013 Paris, France
* Author to whom correspondence should be addressed.
Received: 24 March 2011; in revised form: 3 May 2011 / Accepted: 4 May 2011 / Published: 12 May 2011
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Abstract: Human immunodeficiency virus (HIV) infection is principally a mucosal disease and the gastrointestinal (GI) tract is the major site of HIV replication. Loss of CD4+ T cells and systemic immune hyperactivation are the hallmarks of HIV infection. The end of acute infection is associated with the emergence of specific CD4+ and CD8+ T cell responses and the establishment of a chronic phase of infection. Abnormal levels of immune activation and inflammation persist despite a low steady state level of viremia. Although the causes of persistent immune hyperactivation remain incompletely characterized, physiological alterations of gastrointestinal tract probably play a major role. Failure to restore Th17 cells in gut-associated lymphoid tissues (GALT) might impair the recovery of the gut mucosal barrier. This review discusses recent advances on understanding the contribution of CD4+ T cell depletion to HIV pathogenesis.
Keywords: apoptosis; HIV; viral proteins

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MDPI and ACS Style

Février, M.; Dorgham, K.; Rebollo, A. CD4+ T Cell Depletion in Human Immunodeficiency Virus (HIV) Infection: Role of Apoptosis. Viruses 2011, 3, 586-612.

AMA Style

Février M, Dorgham K, Rebollo A. CD4+ T Cell Depletion in Human Immunodeficiency Virus (HIV) Infection: Role of Apoptosis. Viruses. 2011; 3(5):586-612.

Chicago/Turabian Style

Février, Michèle; Dorgham, Karim; Rebollo, Angelita. 2011. "CD4+ T Cell Depletion in Human Immunodeficiency Virus (HIV) Infection: Role of Apoptosis." Viruses 3, no. 5: 586-612.

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