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Journal of Virology, October 1998, p. 7772-7784, Vol. 72, No. 10
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Effect of Immune Activation on the Dynamics of Human Immunodeficiency Virus Replication and on the Distribution of Viral Quasispecies

Mario A. Ostrowski,1,* David C. Krakauer,2 Yuexia Li,1 Shawn J. Justement,1 Gerald Learn,3 Linda A. Ehler,1 Sharilyn K. Stanley,1 Martin Nowak,2 and Anthony S. Fauci1

Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland1; Department of Zoology, University of Oxford, United Kingdom2; and Department of Microbiology, University of Washington, Seattle, Washington3

Received 17 February 1998/Accepted 7 July 1998

Virus replication in a human immunodeficiency virus (HIV)-infected individual, as determined by the steady-state level of plasma viremia, reflects a complex balance of viral and host factors. We have previously demonstrated that immunization of HIV-infected individuals with the common recall antigen, tetanus toxoid, disrupts this steady state, resulting in transient bursts of plasma viremia after immunization. The present study defines the viral genetic basis for the transient bursts in viremia after immune activation. Tetanus immunization was associated with dramatic and generally reversible shifts in the composition of plasma viral quasispecies. The viral bursts in most cases reflected a nonspecific increase in viral replication secondary to an expanded pool of susceptible CD4+ T cells. An exception to this was in a patient who harbored viruses of differing tropisms (syncytium inducing and non-syncytium inducing [NSI]). In this situation, immunization appeared to select for the replication of NSI viruses. In one of three patients, the data suggested that immune activation resulted in the appearance in plasma of virus induced from latently infected cells. These findings illustrate certain mechanisms whereby antigenic stimulation may influence the dynamics of HIV replication, including the relative expression of different viral variants.

* Corresponding author. Mailing address: Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, NIH, Bldg. 10, Rm. 6A11, Bethesda, MD 20892. Phone: (301) 402-2618. Fax: (301) 402-4122. E-mail: mostrowski{at}nih.gov.

Journal of Virology, October 1998, p. 7772-7784, Vol. 72, No. 10
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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