       Document 0342
 DOCN  M9630342
 TI    Activation of virus replication after vaccination of HIV-1-infected
       individuals.
 DT    9603
 AU    Staprans SI; Hamilton BL; Follansbee SE; Elbeik T; Barbosa P; Grant RM;
       Feinberg MB; Gladstone Institute of Virology and Immunology, San
       Francisco,; California 94141, USA.
 SO    J Exp Med. 1995 Dec 1;182(6):1727-37. Unique Identifier : AIDSLINE
       MED/96096446
 AB    Little is known about the factors that govern the level of HIV-1
       replication in infected individuals. Recent studies (using potent
       antiviral drugs) of the kinetics of HIV-1 replication in vivo have
       demonstrated that steady-state levels of viremia are sustained by
       continuous rounds of de novo infection and the associated rapid turnover
       of CD4+ T lymphocytes. However, no information is available concerning
       the biologic variables that determine the size of the pool of T cells
       that are susceptible to virus infection or the amount of virus produced
       from infected cells. Furthermore, it is not known whether all CD4+ T
       lymphocytes are equally susceptible to HIV-1 infection at a given time
       or whether the infection is focused on cells of a particular state of
       activation or antigenic specificity. Although HIV-1 replication in
       culture is known to be greatly facilitated by T cell activation, the
       ability of specific antigenic stimulation to augment HIV-1 replication
       in vivo has not been studied. We sought to determine whether vaccination
       of HIV-1-infected adults leads to activation of virus replication and
       the targeting of vaccine antigen-responsive T cells for virus infection
       and destruction. Should T cell activation resulting from exposure to
       environmental antigens prove to be an important determinant of the
       steady-state levels of HIV-1 replication in vivo and lead to the
       preferential loss of specific populations of CD4+ T lymphocytes, it
       would have significant implications for our understanding of and
       therapeutic strategies for HIV-1 disease. To begin to address these
       issues, HIV-1-infected individuals and uninfected controls were studied
       by measurement of immune responses to influenza antigens and
       quantitation of virion-associated plasma HIV-1 RNA levels at baseline
       and at intervals after immunization with the trivalent influenza
       vaccine. Influenza vaccination resulted in readily demonstrable but
       transient increases in plasma HIV-1 RNA levels, indicative of activation
       of viral replication, in HIV-1-infected individuals with preserved
       ability to immunologically respond to vaccine antigens. Activation of
       HIV-1 replication by vaccination was more often seen and of greater
       magnitude in individuals who displayed a T cell proliferative response
       to vaccine antigens at baseline and in those who mounted a significant
       serologic response after vaccination. The fold increase in viremia, as
       well as the rates of increase of HIV-1 in plasma after vaccination and
       rates of viral decline after peak viremia, were higher in individuals
       with higher CD4+ T cell counts.(ABSTRACT TRUNCATED AT 400 WORDS)
 DE    Adult  Antibodies, Viral/BIOSYNTHESIS  Human  HIV Infections/*IMMUNOLOGY
       Immunophenotyping  Influenza Vaccine/*IMMUNOLOGY  Lymphocyte
       Transformation  Polymerase Chain Reaction  RNA, Viral/ANALYSIS  Support,
       Non-U.S. Gov't  T-Lymphocytes/*IMMUNOLOGY  Time Factors
       Vaccination/*ADVERSE EFFECTS  *Virus Replication  CLINICAL TRIAL
       JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

