Safeguard against DNA sensing

The role of TREX1 in HIV-1 infection and autoimmune diseases

Maroof Hasan, Nan Yan

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Innate immune recognition is crucial for host responses against viral infections, including infection by human immunodeficiency virus 1 (HIV-1). Human cells detect such invading pathogens with a collection of pattern recognition receptors that activate the production of antiviral proteins, such as the cytokine interferon-type I, to initiate antiviral responses immediately as well as the adaptive immune response for long-term protection. To establish infection in the host, many viruses have thus evolved strategies for subversion of these mechanisms of innate immunity. For example, acute infection by HIV-1 and other retroviruses have long been thought to be non-immunogenic, signifying suppression of host defenses by these pathogens. Studies in the past few years have begun to uncover a multifaceted scheme of how HIV-1 evades innate immune detection, especially of its DNA, by exploiting host proteins. This review will discuss the host mechanisms of HIV-1 DNA sensing and viral immune evasion, with a particular focus on TREX1, three prime repair exonuclease 1, a host 3' exonuclease (also known as DNase III).

Original languageEnglish (US)
Article numberArticle 193
JournalFrontiers in Microbiology
Volume5
Issue numberAPR
DOIs
StatePublished - 2014

Fingerprint

Virus Diseases
Autoimmune Diseases
HIV-1
spleen exonuclease
DNA
Antiviral Agents
Infection
Immune Evasion
Pattern Recognition Receptors
Interferon Type I
Viral DNA
Adaptive Immunity
Retroviridae
Innate Immunity
Proteins
Cytokines
Viruses

Keywords

  • Autoimmune diseases
  • DNA sensing
  • HIV
  • Innate immunity
  • Trex1

ASJC Scopus subject areas

  • Microbiology
  • Microbiology (medical)

Cite this

Safeguard against DNA sensing : The role of TREX1 in HIV-1 infection and autoimmune diseases. / Hasan, Maroof; Yan, Nan.

In: Frontiers in Microbiology, Vol. 5, No. APR, Article 193, 2014.

Research output: Contribution to journalArticle

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