Complete inhibition of SIVmac replication by its capsid mutants.
Mutations were introduced into a genomic region encoding the C-terminal portion of Gag capsid protein of pathogenic simian immunodeficiency virus (SIVmac239). All the mutants generated were defective for virion production and were non-infectious for monkey cells. They all efficiently suppressed the replication of wild type SIVmac in monkey cells. These results were in good agreement with those obtained for human immunodeficiency virus type 1, showing the importance of SIV/monkey model system for studies on Gag.
Department of Virology, School of Medicine, University of Tokushima, Japan.
R
R
Shimano
R
R
Inubushi
K
K
Amano
T
T
Ogasawara
H
H
Akari
A H
AH
Koyama
M
M
Kawamura
A
A
Adachi
D000818:Animals; D002213:Capsid / Q000235:genetics*; D002461:Cell Line, Transformed; D015500:Chloramphenicol O-Acetyltransferase / Q000235:genetics / Q000378:metabolism; D004279:DNA, Viral / Q000235:genetics; D003673:Defective Viruses / Q000235:genetics; D005057:Eukaryotic Cells / Q000166:cytology / Q000378:metabolism / Q000821:virology; D006367:HeLa Cells; D006801:Humans; D008253:Macaca mulatta; D016297:Mutagenesis, Site-Directed; D009154:Mutation; D012194:RNA-Directed DNA Polymerase / Q000378:metabolism; D015302:Simian Immunodeficiency Virus / Q000235:genetics*; D014779:Virus Replication
D004279:DNA, Viral; D015500:Chloramphenicol O-Acetyltransferase; D012194:RNA-Directed DNA Polymerase