Early immune senescence in HIV disease

Seema Desai, Alan Landay

Research output: Contribution to journalReview articlepeer-review

172 Scopus citations

Abstract

Non-AIDS-defining co-morbidities that occur despite viral suppression and immune reconstitution using antiretroviral therapy depict early aging process in HIV-infected individuals. During aging, a reduction in T-cell renewal, together with a progressive enrichment of terminally differentiated T cells, translates into a general decline of the immune system, gradually leading to immunosenescence. Inflammation is a hallmark of age-associated comorbidities, and immune activation is a hallmark of HIV disease. Constant stimulation of the immune system by HIV or due to co-infections activates the innate and adaptive immune system, resulting in release of mediators of inflammation. Immune activation coupled with lack of anti-inflammatory responses likely results in accelerated aging in HIV disease. Dysfunctional thymic output, along with HIV-mediated disruption of the gastrointestinal barrier leading to microbial translocation, contributes to the circulating antigenic load driving early senescence in HIV disease.

Original languageEnglish (US)
Pages (from-to)4-10
Number of pages7
JournalCurrent HIV/AIDS Reports
Volume7
Issue number1
DOIs
StatePublished - Feb 2010
Externally publishedYes

Keywords

  • Activation
  • Inflammation
  • Microbial translocation
  • Senescene

ASJC Scopus subject areas

  • Virology
  • Infectious Diseases

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