Cholesterol dependence of HTLV-I infection.
Cholesterol-rich plasma membrane microdomains are important for entry of many viruses, including retroviruses. Depletion of cholesterol with 2-hydroxypropyl-beta-cyclodextrin inhibits entry of human T cell leukemia virus type I (HTLV-1) and HTLV-I envelope pseudotyped lentivirus particles. Using a soluble fusion protein of the HTLV-I surface envelope protein with the immunoglobulin Fc domain, the HTLV-I receptor was found to colocalize with a raft-associated marker and to cluster in specific plasma membrane microdomains. Depletion of cholesterol did not alter receptor binding activity, suggesting a requirement for cholesterol in a postbinding virus entry step.
Wielgosz
Matthew M
MM
Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
Rauch
Daniel A
DA
Jones
Kathryn S
KS
Ruscetti
Frank W
FW
Ratner
Lee
L
D000073738:2-Hydroxypropyl-beta-cyclodextrin; D000818:Animals; D002460:Cell Line; D002462:Cell Membrane / Q000378:metabolism; D002784:Cholesterol / Q000378:metabolism*; D015368:Human T-lymphotropic virus 1 / Q000235:genetics / Q000378:metabolism / Q000472:pathogenicity*; D006801:Humans; D016086:Lentivirus / Q000235:genetics; D021962:Membrane Microdomains / Q000378:metabolism*; D011991:Receptors, Virus / Q000378:metabolism; D014162:Transfection; D014759:Viral Envelope Proteins; D014771:Virion / Q000235:genetics / Q000378:metabolism / Q000472:pathogenicity*; D047392:beta-Cyclodextrins
C080823:HTLV-I receptor; D011991:Receptors, Virus; D014759:Viral Envelope Proteins; D047392:beta-Cyclodextrins; D000073738:2-Hydroxypropyl-beta-cyclodextrin; D002784:Cholesterol