Cutting Edge: Experimentally Induced Immune Activation in Natural Hosts of Simian Immunodeficiency Virus Induces Significant Increases in Viral Replication and CD4+ T Cell Depletion

Chronically SIVagm-infected African green monkeys (AGMs) have a remarkably stable nonpathogenic disease course, with levels of immune activation in chronic SIVagm infection similar to those observed in uninfected monkeys and with stable viral loads for long periods of time. In vivo administration of...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2008-11, Vol.181 (10), p.6687-6691
Main Authors: Pandrea, Ivona, Gaufin, Thaidra, Brenchley, Jason M, Gautam, Rajeev, Monjure, Christopher, Gautam, Aarti, Coleman, Clint, Lackner, Andrew A, Ribeiro, Ruy M, Douek, Daniel C, Apetrei, Cristian
Format: Article
Language:English
Subjects:
Adjuvants, Immunologic
Animals
CD4-Positive T-Lymphocytes - immunology
CD4-Positive T-Lymphocytes - virology
Cercopithecus aethiops
Chronic Disease
Diphtheria Toxin - immunology
Flow Cytometry
Interleukin-2 - immunology
Lipopolysaccharides - immunology
Lymphocyte Activation - immunology
Recombinant Fusion Proteins - immunology
Simian Acquired Immunodeficiency Syndrome - immunology
Simian Acquired Immunodeficiency Syndrome - virology
Simian Immunodeficiency Virus - immunology
Viral Load
Virus Replication - immunology
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Summary:Chronically SIVagm-infected African green monkeys (AGMs) have a remarkably stable nonpathogenic disease course, with levels of immune activation in chronic SIVagm infection similar to those observed in uninfected monkeys and with stable viral loads for long periods of time. In vivo administration of LPS or an IL-2/diphtheria toxin fusion protein (Ontak) to chronically SIVagm-infected AGMs triggered increases in immune activation and subsequently of viral replication and depletion of intestinal CD4(+) T cells. Our study indicates that circulating microbial products can increase viral replication by inducing immune activation and increasing the number of viral target cells, thus demonstrating that immune activation and T cell proliferation are key factors in AIDS pathogenesis.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.181.10.6687