Engagement of ICAM-3 provides a costimulatory signal for human immunodeficiency virus type 1 replication in both activated and quiescent CD4+ T lymphocytes: implications for virus pathogenesis.
Human immunodeficiency virus type 1 (HIV-1) replication is regulated by several extracellular signals. We demonstrate that intercellular adhesion molecule 3 (ICAM-3) acts as a costimulating molecule to increase HIV-1 transcription and viral production, a process allowing productive infection of quiescent CD4+ T lymphocytes. The present work suggests an important role for ICAM-3 in HIV-1 replication.
Barat
Corinne
C
Laboratory of Human Immuno-Retrovirology, Research Center in Infectious Diseases, RC709, CHUL Research Center, 2705 Laurier Boulevard, Quebec City, Quebec, Canada G1V 4G2.
Gervais
Philippe
P
Tremblay
Michel J
MJ
D015703:Antigens, CD / Q000378:metabolism*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000502:physiology / Q000821:virology*; D015815:Cell Adhesion Molecules; D015497:HIV-1 / Q000472:pathogenicity* / Q000502:physiology; D006801:Humans; D008213:Lymphocyte Activation; D014158:Transcription, Genetic; D014779:Virus Replication
D015703:Antigens, CD; D015815:Cell Adhesion Molecules; C483616:ICAM3 protein, human