Abstract

The presumed cause of AIDS is a retrovirus, HIV, the human immunodeficiency virus which infects lymphocytes and can be isolated from the blood of AIDS patients (1-3). However, only a small percentage of people infected with this virus have developed the full AIDS syndrome (4). Thus, a cofactor that enhances infection or disease expression by this virus is a possibility. Cytomegalovirus (CMV) is a logical cofactor candidate since nearly all adult AIDS cases are seropositive for CMV (5) and CMV infection causes immune dysfunction (6). In order to shed light on the possible role of CMV as a cofactor in the pathogenesis of AIDS, the studies will examine, in vitro, whether there are synergistic interelationships between these two viruses. Using peripheral blood mononuclear cells (PBMC) and cell lines our specific goals are to determine whether 1) HIV superinfection of cells pre-infected with CMV enhances HIV replication as compared to cells not preinfected with CMV; 2) CMV superinfection of HIV pre-infected cells enhances replication of HIV; 3) HIV superinfection of cells latently infected with CMV lead to reactivation and productive replication of CMV; 4) CMV superinfection of HIV infected cells enhances CMV replication.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Program Projects (P01)
Project #
3P01AI024286-05S1
Application #
3091764
Study Section
Special Emphasis Panel (SRC (01))
Project Start
1987-02-01
Project End
1992-06-30
Budget Start
1992-02-01
Budget End
1992-06-30
Support Year
5
Fiscal Year
1992
Total Cost
Indirect Cost

  Institution

Name
University of California San Francisco
Department
Type
Schools of Medicine
DUNS #
073133571
City
San Francisco
State
CA
Country
United States
Zip Code
94143

  Publications

Ng, V L; Hurt, M H; Herndier, B G et al. (1997) VH gene use by HIV type 1-associated lymphoproliferations. AIDS Res Hum Retroviruses 13:135-49
Murthy, K K; Cobb, E K; el-Amad, Z et al. (1996) Titration of a vaccine stock preparation of human immunodeficiency virus type 1SF2 in cultured lymphocytes and in chimpanzees. AIDS Res Hum Retroviruses 12:1341-8
Barnett, S W; Legg, H S; Sun, Y et al. (1996) Molecular cloning of the human immunodeficiency virus subtype 2 strain HIV-2UC2. Virology 222:257-61
Kaplan, L D; Shiramizu, B; Herndier, B et al. (1995) Influence of molecular characteristics on clinical outcome in human immunodeficiency virus-associated non-Hodgkin's lymphoma: identification of a subgroup with favorable clinical outcome. Blood 85:1727-35
Ng, V L; Hurt, M H; Fein, C L et al. (1994) IgMs produced by two acquired immune deficiency syndrome lymphoma cell lines: Ig binding specificity and VH-gene putative somatic mutation analysis. Blood 83:1067-78
Zingler, K; Littman, D R (1993) Truncation of the cytoplasmic domain of the simian immunodeficiency virus envelope glycoprotein increases env incorporation into particles and fusogenicity and infectivity. J Virol 67:2824-31
Barnett, S W; Quiroga, M; Werner, A et al. (1993) Distinguishing features of an infectious molecular clone of the highly divergent and noncytopathic human immunodeficiency virus type 2 UC1 strain. J Virol 67:1006-14
Herndier, B G; Shiramizu, B T; Jewett, N E et al. (1992) Acquired immunodeficiency syndrome-associated T-cell lymphoma: evidence for human immunodeficiency virus type 1-associated T-cell transformation. Blood 79:1768-74
Tang, S; Poulin, L; Levy, J A (1992) Lack of human immunodeficiency virus type 1 (HIV-1) replication and accumulation of viral DNA in HIV-1-infected T cells blocked in cell replication. J Gen Virol 73 ( Pt 4):933-9
Herndier, B G; Shiramizu, B T; McGrath, M S (1992) AIDS associated non-Hodgkin's lymphomas represent a broad spectrum of monoclonal and polyclonal lymphoproliferative processes. Curr Top Microbiol Immunol 182:385-94

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