Effects of endocytosis inhibitory drugs on rubella virus entry into VeroE6 cells.
It has been suggested that infectious entry of rubella virus (RV) is conducted by receptor mediated endocytosis. To explore the cellular entry mechanism of RV, inhibitory effects of drugs affecting various endocytic pathways on RV entry into VeroE6 cells were analyzed. Results showed that RV infectious entry into VeroE6 cells is mediated by clathrin-dependent endocytosis and not by caveolae-mediated endocytosis. Moreover, chemical inhibition of macropinocytosis such as treatments of amiloride, actin and microtubule-disrupting drug significantly reduced RV infection. Considering that macropinocytosis is inducible endocytosis by cellular stimulations, clathrin-mediated endocytosis is likely to be a major route of RV infectious entry.
Kee
Sun-Ho
SH
Department of Microbiology, College of Medicine, The Institute for Viral Diseases, Medical Science Research Center, Korea University, Seoul.
Cho
Eun-Jin
EJ
Song
Jin-Won
JW
Park
Kwang Sook
KS
Baek
Luck Ju
LJ
Song
Ki-Joon
KJ
D000818:Animals; D002522:Chlorocebus aethiops; D002746:Chlorpromazine / Q000494:pharmacology; D002966:Clathrin / Q000378:metabolism*; D003599:Cytoskeleton / Q000187:drug effects / Q000378:metabolism; D004705:Endocytosis / Q000187:drug effects*; D005372:Filipin / Q000494:pharmacology; D015739:Nocodazole / Q000494:pharmacology; D010873:Pinocytosis / Q000187:drug effects; D012412:Rubella virus / Q000187:drug effects / Q000472:pathogenicity*; D014709:Vero Cells
D002966:Clathrin; D005372:Filipin; D015739:Nocodazole; D002746:Chlorpromazine