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Journal of Virology, May 2003, p. 5749-5758, Vol. 77, No. 10
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.10.5749-5758.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Direct Relationship between Suppression of Virus-Specific Immunity and Emergence of Cytomegalovirus Disease in Simian AIDS

Amitinder Kaur,1* Nadine Kassis,1 Corrina L. Hale,1 Meredith Simon,2,{dagger} Michelle Elliott,2 Alicia Gomez-Yafal,3 Jeffrey D. Lifson,4 Ronald C. Desrosiers,5 Fred Wang,6 Peter Barry,7 Michael Mach,8 and R. Paul Johnson1,9

Divisions of Immunology,1 Pathology,2 Microbiology, New England Primate Research Center, Harvard Medical School, Southborough, Massachusetts 01772,5 Infectious Disease Unit and Partners AIDS Research Center, Massachusetts General Hospital, Charlestown, Massachusetts 02129,9 Therion Biologics, Cambridge, Massachusetts 02142,3 AIDS Vaccine Program, SAIC Frederick, Inc., National Cancer Institute—Frederick, Frederick, Maryland 21702,4 Department of Medicine, Brigham & Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115,6 Center for Comparative Medicine, University of California—Davis, Davis, California 95616,7 Institut Für Klinische Und Molekulare Virologie, Universitãt Erlangen-Nürnberg, D-91058 Erlangen, Germany8

Received 12 December 2002/ Accepted 21 February 2003

Although opportunistic infections like cytomegalovirus (CMV) are common sequelae of end-stage AIDS, the immune events leading to CMV reactivation in human immunodeficiency virus (HIV)-infected individuals are not well defined. The role of cellular and humoral CMV-specific immune responses in immune control of latent CMV infection was evaluated prospectively in a cohort of 11 simian immunodeficiency virus (SIV)-infected CMV-seropositive rhesus macaques, 6 of whom had histologic evidence of CMV disease at death. Macaques with CMV disease differed from macaques without CMV disease in having significantly higher levels of plasma SIV RNA and CMV DNA and significantly lower titers of anti-CMV binding antibodies (Abs) at the time of death. A significant decline in anti-CMV Abs and CMV-specific CD4+ and CD8+ T lymphocytes over time was observed in the macaques with CMV disease, but not in the macaques without CMV disease. Reduction in CMV-specific CD8+ T lymphocytes and anti-CMV neutralizing Abs was significantly correlated with a decline in CMV-specific CD4+ T lymphocytes. Although declines in CMV-specific T lymphocytes alone were sufficient for reactivation of low-level CMV viremia, high-level viremia (>1,000 copies of CMV DNA per ml of plasma) was observed when anti-CMV neutralizing and binding Abs had also declined. Thus, the occurrence of CMV reactivation-associated disease in AIDS is associated with suppression of both cellular and humoral CMV-specific immune responses. The underlying mechanism may be a dysfunction of memory B and CD8+ T lymphocytes associated with SIV-induced impairment of CMV-specific CD4+ T-cell help.

* Corresponding author. Mailing address: New England Primate Research Center, Harvard Medical School, One Pine Hill Dr., Southborough, MA 01772. Phone: (508) 624-8169. Fax: (508) 624-8172. E-mail: amitinder_kaur{at}hms.harvard.edu.

{dagger} Present address: Charles River Laboratories, Wilmington, MA 01887.

Journal of Virology, May 2003, p. 5749-5758, Vol. 77, No. 10
0022-538X/03/$08.00+0     DOI: 10.1128/JVI.77.10.5749-5758.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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