Virological and immunological impact of tuberculosis on human immunodeficiency virus type 1 disease.
Unlike other opportunistic infections associated with human immunodeficiency virus (HIV) type 1, tuberculosis (TB) occurs throughout the course of HIV-1 infection, and, as a chronic infection, its impact on viral activity is sustained. In dually infected subjects, HIV-1 load and heterogeneity are increased both locally and systemically during active TB. Studies over the past decade have indicated that Mycobacterium tuberculosis (MTB) infection supports HIV-1 replication and dissemination through the dysregulation of host cytokines, chemokines, and their receptors. Furthermore, concentrations of HIV-1 inhibitory chemokines are limited during TB and at sites of MTB infection. Cumulatively, these data indicate that TB provides a milieu of continuous cellular activation and irregularities in cytokine and chemokine circuits that are permissive of viral replication and expansion in situ. I address new research that has identified the basis for the augmentation of HIV-1 replication during TB and discuss potential immunotherapies to contain viral expansion during TB.
Toossi
Zahra
Z
Department of Medicine, University Hospitals of Cleveland, Case Western Reserve University, Cleveland, Ohio 44106-4984, USA. zxt2@po.cwru.edu.
D017088:AIDS-Related Opportunistic Infections / Q000276:immunology / Q000382:microbiology / Q000503:physiopathology; D015658:HIV Infections / Q000150:complications / Q000276:immunology* / Q000503:physiopathology* / Q000821:virology; D015497:HIV-1 / Q000235:genetics / Q000472:pathogenicity / Q000502:physiology*; D006801:Humans; D009169:Mycobacterium tuberculosis / Q000276:immunology / Q000472:pathogenicity; D014397:Tuberculosis, Pulmonary / Q000150:complications* / Q000276:immunology / Q000503:physiopathology; D014779:Virus Replication