Mechanisms of HIV-1 escape from immune responses and antiretroviral drugs

Research output: Contribution to journalArticle

Abstract

Despite the fact that HIV-1 induces vigorous antiviral immune responses, viral replication is never completely controlled in infected individuals. Recent studies have provided insight into the mechanisms by which focused immune pressure directed at particular B or T cell epitopes leads to the rapid appearance of escape mutations. Even if anti-HIV-1 immune responses could be enhanced to the point where they inhibit viral replication to the same extent as certain combinations of antiretroviral drugs, eradication would be unlikely because of the persistence of the virus in an extremely stable latent reservoir in resting memory CD4+ T cells.

Original languageEnglish (US)
Pages (from-to)470-476
Number of pages7
JournalCurrent Opinion in Immunology
Volume16
Issue number4
DOIs
StatePublished - Aug 2004

Fingerprint

HIV-1
B-Lymphocyte Epitopes
T-Lymphocyte Epitopes
Drug Combinations
Pharmaceutical Preparations
Antiviral Agents
Viruses
T-Lymphocytes
Pressure
Mutation

Keywords

  • acquired immunodeficiency syndrome
  • AIDS
  • CTL
  • cytotoxic T lymphocyte
  • env
  • HAART
  • highly active antiretroviral therapy
  • HIV
  • HIV-1 envelope
  • human immunodeficiency virus
  • IκB
  • inhibitor of κB
  • major histocompatibility complex
  • MHC
  • nAb

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Mechanisms of HIV-1 escape from immune responses and antiretroviral drugs. / Bailey, Justin; Blankson, Joel N; Wind-Rotolo, Megan; Siliciano, Robert F.

In: Current Opinion in Immunology, Vol. 16, No. 4, 08.2004, p. 470-476.

Research output: Contribution to journalArticle

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