Cell cycle dependence of foamy retrovirus infection.
In common with oncoviruses but unlike the lentivirus human immunodeficiency virus type 1, foamy (spuma) viruses require host cell proliferation for productive infection. We show that human immunodeficiency virus type 1 replicates in RD-CD4 cells regardless of the growth arrest condition of the cells, while murine leukemia virus is unable to infect growth-arrested RD-CD4 cells or cells progressing through a partial cell cycle that includes S phase but not mitosis. Human foamy virus, like murine leukemia virus, does not productively infect G1/S or G2 growth-arrested cells. Two other foamy viruses, simian foamy virus type 1, isolated from a macaque, and simian foamy virus type 6, isolated from a chimpanzee, also fail to establish productive infection in G1/S-arrested cells.
D000818:Animals; D016590:Aphidicolin / Q000494:pharmacology; D015496:CD4-Positive T-Lymphocytes / Q000821:virology; D002453:Cell Cycle / Q000187:drug effects / Q000528:radiation effects; D002455:Cell Division; D002460:Cell Line; D016193:G1 Phase; D016195:G2 Phase; D015497:HIV-1 / Q000472:pathogenicity / Q000502:physiology*; D006801:Humans; D009052:Leukemia Virus, Murine / Q000502:physiology; D008251:Macaca / Q000821:virology; D002679:Pan troglodytes / Q000821:virology; D013045:Species Specificity; D016092:Spumavirus / Q000302:isolation & purification / Q000472:pathogenicity / Q000502:physiology*; D014779:Virus Replication
D016590:Aphidicolin