Open AccessThis article is
- freely available
CD4+ T Cell Depletion in Human Immunodeficiency Virus (HIV) Infection: Role of Apoptosis
Unité Génomique Virale et Vaccination, CNRS URA 3015, Institut Pasteur, 28 rue du Dr Roux, 75015 Paris, France
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
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
Citations to this Article
Cite This Article
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.
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.
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.