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

被引:14
作者
Park, IW
Kondo, E
Bergeron, L
Park, J
Sodroski, J
机构
[1] DANA FARBER CANC INST, DIV HUMAN RETROVIROL, BOSTON, MA 02115 USA
[2] HARVARD UNIV, SCH MED, DEPT PATHOL, BOSTON, MA USA
[3] HARVARD UNIV, SCH PUBL HLTH, DEPT CANC BIOL, BOSTON, MA 02115 USA
关键词
HIV-1; Bcl-2; programmed cell death; apoptosis; Jurkat cell; HTLV-III/LAV ENVELOPE; T4; MOLECULE; FAS ANTIGEN; B-CELLS; HIV; GLYCOPROTEIN; EXPRESSION; RETROVIRUS; SURVIVAL; CYTOPATHICITY;
D O I
10.1097/00042560-199608010-00001
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The effect of human immunodeficiency virus (HIV-I) infection on the programmed cell death of CD4 + lymphocytes was studied by using Jurkat cells stably expressing high levels of the Bcl-2 protein (Jurkat-Bcl2) or control cells (Jurkat-P). Both Jurkat-Bcl2 and Jurkat-P cells exhibited surface CD4 expression adequate to support HIV-I infection. We observed no differences between HIV-l-infected Jurkat Bcl2 cells and control cells with respect to kinetics of virus replication, protein expression, and processing. Severe cytopathic effects, which were typical of acute HIV-I infection and consisted of syncytium formation followed by single-cell lysis, were observed in both cell types. However, several lines of evidence, such as cell viability analysis by trypan blue dye exclusion, chromosomal DNA laddering, and morphologic analysis by acridine orange/ethidium bromide or Giemsa staining, indicated that HIV-1 did not induce a significant amount of programmed cell death in either cell type. These results suggest that apoptosis is at most a minor element in HIV-l-induced cytopathicity in Jurkat lymphocytes.
引用
收藏
页码:321 / 328
页数:8
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