Novel factors interfering with human immunodeficiency virus-type 1 replication in vivo and in vitro

Research output: Contribution to journalArticle

Abstract

The strategy of all retroviral infections is based on establishing an equilibrium between virus replication and proviral latency in the infected host. The human immunodeficiency virus-type 1 (HIV-1), belonging to the subfamily of lentiviridae, adds an additional level of sophistication to this general rule by encoding two regulatory genes (tat and rev) and four accessory genes (nef, vif, vpr and vpu); HIV-2, structurally similar to HIV-1 but characterized by lower pathogenicity in vivo, encodes another accessory gene, vpx. The function of these accessory genes has become clear in recent years: they serve as countermeasures to host-cell restriction factors that prevent or curtail the capacity of HIV to productively infect its target cells (typically, CD4+ T lymphocytes, macrophages and dendritic cells). Some of the best characterized restriction factors for HIV-1 are Tripartite Motif-5α (TRIM5α), preventing infection of nonhuman primates, although not being effective in humans, and apolipoprotein B mRNA-editing, enzyme-catalytic, polypeptide-like 3G (APOBEC 3G), counteracted by the viral accessory protein Vif. In addition, several other molecules are under scrutiny for their mechanism of action and potential exploitation as novel anti-HIV agents. This review will summarize the recently emerging knowledge on these novel factors and their potential relevance for the discovery of new anti-HIV agents targeting not only the replicative, but also the latent state of HIV infection.

Original languageEnglish
Pages (from-to)61-71
Number of pages11
JournalTissue Antigens
Volume81
Issue number2
DOIs
Publication statusPublished - Feb 2013

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Keywords

  • Epigenetics
  • Eradication
  • Human immunodeficiency virus
  • Human immunodeficiency virus cure
  • Restriction factors
  • STAT5
  • Transcription
  • TRIM22

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy
  • Genetics

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