| Summary: | 碩士 === 國防醫學院 === 解剖學研究所 === 84 === HIV (human immunodeficiency virus)is the etiologic agent of
AIDS worldwide. The increase of HIV-1 infections in Taiwan
have been reported monthly by the Department of Health, the
Executive Yuan, R.O.C. There were 1102 HIV-1 seropositive
cases by May 1996. Entry of HIV into CD4-positive cells is
mediated by the specific binding of the viral envelope
protein, gp120, and the cell surface CD4 molecules.
Infection of HIV-1 subsequently lead to the disappearance of
CD4 molecules from the plasma membrane, a phenomenon refered
to as receptor mwdiated down-modulation. It is known that
three HIV gene products, Nef, Vpu, and gp120/160, were
involved. However, the mechanism of CD4 down-modulation by
Nef and Vpu remains unknown. In this study, we intend
to identify the intracellular locations of CD4 and
investigate the relationships between these viral proteins by
immunocytochemistry and electron microscopy in vitro. CD4+
cells were applied: Jurkat and HPBALL T cells transfected
with enf gene; peripheral blood mononuclear cells (PBMC)
infected wuth HIV-1 strain of wild type or Vpu mutants.
Viral protein transfections and HIV-1 infections were
performed in Dr. Ratner's Laboratory at Washington
University Medical School. This semiquantitative results
of immunocytochemistry and statistic assays showed that (1).
Nef down-modulation CD4 molecules by binding CD4 on the
cell surface and then drag CD4 into the cytoplasm. (2).
The decrease of CD4 number in the cytoplasm and plasma
membrane are related to the presence of Vpu. Vpu may cause CD4
down-modulation by degrading CD4 in rER. (3). The assembly of
Gag protein into the viral particles is not influenced by Vpu.
|
|---|
