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PubMed · 2762702

Immunization programs and human immunodeficiency virus.

Abstract

The emergence of human immunodeficiency virus (HIV) in epidemic form has implications for immunization programs. Infection with HIV, which is capable of infecting cells of the immune system and which can remain latent for many years, results in profound and progressive immunosuppression. As a consequence, vaccines may not elicit a protective response from HIV-infected individuals. Stimulation of the immune system may also be a cofactor for the progression of infection to AIDS, since stimulated lymphocytes are needed for the replication of HIV. HIV-positive individuals may also react differently to vaccines than do uninfected persons. The standard vaccines in use today are extremely safe. The possibility that the excellent safety profile of vaccines may be altered in HIV-positive patients must be considered. Since this virus can be transmitted through exposure to blood and blood products, mass immunization programs must take steps to minimize the possibility of accidental transmission of infection during a mass vaccination program. Finally, the problems and prospect for the testing and use of vaccines to prevent HIV are discussed.

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BibTeXRIS

J R La Montagne. Immunization programs and human immunodeficiency virus.. https://doi.org/10.1093/clinids%2F11.supplement_3.s639

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Analysis of dominant-negative effects of mutant Env proteins of human immunodeficiency virus type 1.

The Env protein of human immunodeficiency virus type 1 is assembled into a stable trimer, and oligomerization is required for maintenance of viral infectivity. This property of Env suggests that Env mutants may have a dominant-negative effect on virus infectivity. To investigate this possibility, we established a packaging cell line in which both wild-type and mutant Env proteins could be expressed simultaneously in a single cell. We analyzed the effects of two types of Env mutants: cytoplasmic tail-truncated TM mutants and a mutant defective in gp120/gp41 cleavage. The cytoplasmic tail-truncated proteins were found to be incorporated into virions by forming an oligomer with wild-type TM, but could not inhibit the wild-type function. In contrast, phenotypic mixing of cleavage-defective Env with the wild-type protein caused dramatic inhibition of infectivity, indicating that this mutant has a strong dominant-negative phenotype.

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