Early immune senescence in HIV disease.
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.
Desai
Seema
S
Department of Immunology/Microbiology, Rush University Medical Center, 1735 W. Harrison Street, Room 660 Cohn, Chicago, IL, 60612, USA. seema_n_desai@rush.edu
Landay
Alan
A
D000163:Acquired Immunodeficiency Syndrome / Q000188:drug therapy / Q000276:immunology; D000375:Aging / Q000276:immunology*; D023241:Antiretroviral Therapy, Highly Active; D015488:HIV Antigens / Q000502:physiology; D015658:HIV Infections / Q000188:drug therapy / Q000276:immunology* / Q000503:physiopathology*; D006801:Humans; D007107:Immune System / Q000503:physiopathology*; D018836:Inflammation Mediators / Q000276:immunology; D008213:Lymphocyte Activation; D008875:Middle Aged; D013601:T-Lymphocytes / Q000276:immunology; D014779:Virus Replication
D015488:HIV Antigens; D018836:Inflammation Mediators