Targeting a foreign protein into virion particles by fusion with the Vpx protein of simian immunodeficiency virus

Article Abstract:

A foreign protein appears to be incorporated into the structure of the simian immunodeficiency virus (SIV) when fused to the SIV Vpx protein. The Vpx protein is a regulatory protein that is not always necessary for viral reproduction, but is commonly found packaged inside the viral particle. Researchers created a fusion protein by splicing the gene for the chloramphenicol acetyltransferase (CAT) enzyme to the gene for the Vpx protein. Biochemical analyses showed that fusion proteins were incorporated into viral particles. In addition, the activity of the CAT enzyme could still be detected in these viral particles. Delays in the reproduction of SIV containing these spliced genes appeared to be the result of the presence of the CAT gene, and not the fusion protein. The findings indicate that such fusion proteins might be used to study the functions of Vpx and other similar proteins, and may also be used in antiviral approaches.

Usage, Recombinant proteins

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Functional analysis of the vpx, vpr, and nef genes of the simian immunodeficiency virus

Article Abstract:

Certain regulatory genes in the simian immunodeficiency virus (SIV) appear to play different roles in viral replication depending on the context. SIV is similar to HIV. The effect on SIV replication of the vpx, vpr and nef regulatory genes was examined by exposing macaque peripheral blood mononuclear cells (PBMC) and human T cells to SIV mutations. When macaque PBMC were exposed to vpr-mutated SIV, impairment in viral replication depended on the source of the PBMC. When macaque PBMC were exposed to vpx-mutated SIV, viral replication was significantly reduced. When human T cells were exposed to single-gene mutated SIV, replication patterns were similar to those found in the wild-type virus. When human T cells were exposed to multiply-mutated SIV, viral replication was similar to that of single-gene mutant viruses. Replication was slightly delayed when MT-4 cells were exposed to multiply-mutated SIV.

Genetic aspects

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Effects of human immunodeficiency virus type 1 infection of programmed cell death in the presence or absence of Bcl-2

Article Abstract:

The death of CD4+ T cells during HIV infection does not appear to involve programmed cell death, a condition called apoptosis. This was demonstrated by infecting two T cell cultures with HIV. One of the cultures produced a protein called Bcl-2 that protects against apoptosis. The virus caused many of the cells in both cultures to die. But fewer than 12% died via apoptosis. The production of Bcl-2 by one culture did not protect the T cells from death by HIV.

Research, HIV (Viruses), HIV, Cell death, CD4 lymphocytes

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