Macrophages as a Source of HIV during Opportunistic Infections

The source of increasing viremia that characterizes the latter stages of human immunodeficiency virus (HIV) disease has remained a paradox because it occurs at a time when lymphoid tissue is quantitatively and qualitatively impaired, and the patients' CD4 T lymphocytes are steadily declining. H...

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Bibliographic Details
Published in:Science (American Association for the Advancement of Science) 1997-06, Vol.276 (5320), p.1857-1861
Main Authors: Orenstein, Jan M., Fox, Cecil, Wahl, Sharon M.
Format: Article
Language:English
Subjects:
Adult
AIDS
AIDS-Related Opportunistic Infections - virology
AIDS/HIV
Anatomy
Biological and medical sciences
Dendritic Cells - virology
Development and progression
Giant cells
HIV
HIV 1
HIV infection
HIV infections
HIV Infections - virology
HIV-1 - isolation & purification
HIV-1 - physiology
Human immunodeficiency virus
Humans
Immunodeficiencies
Immunodeficiencies. Immunoglobulinopathies
Immunopathology
In Situ Hybridization
Infections
Lymph nodes
Lymph Nodes - virology
Lymphocytes
Macrophages
Macrophages - virology
Male
Medical research
Medical sciences
Microscopy, Electron
Mycobacterium avium
Mycobacterium avium complex
Mycobacterium avium-intracellulare Infection - virology
Patients
Phagocytes
Physiological aspects
Pneumocystis carinii
Pneumonia, Pneumocystis - virology
RNA, Viral - analysis
T lymphocytes
Virus Replication
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Summary:The source of increasing viremia that characterizes the latter stages of human immunodeficiency virus (HIV) disease has remained a paradox because it occurs at a time when lymphoid tissue is quantitatively and qualitatively impaired, and the patients' CD4 T lymphocytes are steadily declining. Here, macrophages, both infected and uninfected with common opportunistic pathogens of HIV disease such as Mycobacterium avium complex and Pneumocystis carinii, were identified as highly productive sources of HIV in coinfected lymph nodes. These observations indicate that tissue macrophages are not only infected with HIV, but that common pathogens of HIV disease can dramatically increase their production of virus. Thus, prevention or successful treatment of opportunistic coinfections, or both, potentially benefits the patient twofold by limiting the pathology caused by opportunistic infection and by controlling induction of HIV replication.
ISSN:0036-8075
1095-9203
DOI:10.1126/science.276.5320.1857