Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

The cytosolic exonuclease TREX1 inhibits the innate immune response to human immunodeficiency virus type 1.

Nature immunology | Nov 20, 2010

http://www.ncbi.nlm.nih.gov/pubmed/20871604

Viral infection triggers innate immune sensors to produce type I interferon. However, infection of T cells and macrophages with human immunodeficiency virus (HIV) does not trip those alarms. How HIV avoids activating nucleic acid sensors is unknown. Here we found that the cytosolic exonuclease TREX1 suppressed interferon triggered by HIV. In Trex1(-/-) mouse cells and human CD4(+) T cells and macrophages in which TREX1 was inhibited by RNA-mediated interference, cytosolic HIV DNA accumulated and HIV infection induced type I interferon that inhibited HIV replication and spreading. TREX1 bound to cytosolic HIV DNA and digested excess HIV DNA that would otherwise activate interferon expression via a pathway dependent on the kinase TBK1, the adaptor STING and the transcription factor IRF3. HIV-stimulated interferon production in cells deficient in TREX1 did not involve known nucleic acid sensors.

Pubmed ID: 20871604 RIS Download

Mesh terms: Animals | Cell Line | Cells, Cultured | Cytosol | Exodeoxyribonucleases | HIV Infections | HIV-1 | HeLa Cells | Humans | Immunity, Innate | Interferons | Mice | Mice, Knockout | Phosphoproteins | Virus Replication

Research resources used in this publication

None found

Research tools detected in this publication

None found

Data used in this publication

None found

Associated grants

  • Agency: NIAID NIH HHS, Id: AI45587
  • Agency: NIAID NIH HHS, Id: P30 AI060354
  • Agency: NIAID NIH HHS, Id: R01 AI045587
  • Agency: NIAID NIH HHS, Id: R01 AI045587-10
  • Agency: NHLBI NIH HHS, Id: T32 HL066987

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.