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Journal of Virology, June 2001, p. 5151-5158, Vol. 75, No. 11
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.11.5151-5158.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Reduction of Simian-Human Immunodeficiency Virus 89.6P Viremia in Rhesus Monkeys by Recombinant Modified Vaccinia Virus Ankara Vaccination

Dan H. Barouch,1,* Sampa Santra,1 Marcelo J. Kuroda,1 Jörn E. Schmitz,1 Ronald Plishka,2 Alicia Buckler-White,2 Alicia E. Gaitan,3 Rebekah Zin,3 Jae-Hwan Nam,4 Linda S. Wyatt,4 Michelle A. Lifton,1 Christine E. Nickerson,1 Bernard Moss,4 David C. Montefiori,3 Vanessa M. Hirsch,2 and Norman L. Letvin1

Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 022151; Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Rockville, Maryland 208522; Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 208924; and Duke University Medical Center, Durham, North Carolina 277103

Received 8 December 2000/Accepted 3 March 2001

Since cytotoxic T lymphocytes (CTLs) are critical for controlling human immunodeficiency virus type 1 (HIV-1) replication in infected individuals, candidate HIV-1 vaccines should elicit virus-specific CTL responses. In this report, we study the immune responses elicited in rhesus monkeys by a recombinant poxvirus vaccine and the degree of protection afforded against a pathogenic simian-human immunodeficiency virus SHIV-89.6P challenge. Immunization with recombinant modified vaccinia virus Ankara (MVA) vectors expressing SIVmac239 gag-pol and HIV-1 89.6 env elicited potent Gag-specific CTL responses but no detectable SHIV-specific neutralizing antibody (NAb) responses. Following intravenous SHIV-89.6P challenge, sham-vaccinated monkeys developed low-frequency CTL responses, low-titer NAb responses, rapid loss of CD4+ T lymphocytes, high-setpoint viral RNA levels, and significant clinical disease progression and death in half of the animals by day 168 postchallenge. In contrast, the recombinant MVA-vaccinated monkeys demonstrated high-frequency secondary CTL responses, high-titer secondary SHIV-89.6-specific NAb responses, rapid emergence of SHIV-89.6P-specific NAb responses, partial preservation of CD4+ T lymphocytes, reduced setpoint viral RNA levels, and no evidence of clinical disease or mortality by day 168 postchallenge. There was a statistically significant correlation between levels of vaccine-elicited CTL responses prior to challenge and the control of viremia following challenge. These results demonstrate that immune responses elicited by live recombinant vectors, although unable to provide sterilizing immunity, can control viremia and prevent disease progression following a highly pathogenic AIDS virus challenge.

* Corresponding author. Mailing address: Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Research East Room 113, 330 Brookline Ave., Boston, MA 02215. Phone: (617) 667-2042. Fax: (617) 667-8210. E-mail: dan_barouch{at}hotmail.com.

Journal of Virology, June 2001, p. 5151-5158, Vol. 75, No. 11
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.11.5151-5158.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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