作者: Andrew D. Badley , André A. Pilon , Alan Landay , David H. Lynch
关键词: Cytotoxic T cell 、 Acquired immunodeficiency syndrome (AIDS) 、 T lymphocyte 、 Biology 、 Virus 、 Chemokine receptor CCR5 、 Virology 、 Lentivirus 、 Immunology 、 Viral replication 、 Immune system
摘要: Infection with the human immunodeficiency virus (HIV) is associated a progressive decrease in CD4 T-cell number and consequent impairment host immune defenses. Analysis of T cells from patients infected HIV, or vitro demonstrates significant fraction both uninfected dying by apoptosis. The many mechanisms that contribute to HIV-associated lymphocyte apoptosis include chronic immunologic activation; gp120/160 ligation receptor; enhanced production cytotoxic ligands viral proteins monocytes, macrophages, B cells, CD8 HIV-infected kill cells; direct infection target resulting Although HIV results apoptosis, under some circumstances resting macrophages does not result apoptosis; this may be critical step development reservoirs. Recent therapies for effectively reduce lymphoid peripheral replication, enhance cellular competence; however, they do alter Further understanding regulation disease required develop novel immune-based aimed at modifying HIV-induced benefit HIV.