Cell-to-cell spread of the RNA interference response suppresses Semliki Forest virus (SFV) infection of mosquito cell cultures and cannot be antagonized by SFV.
In their vertebrate hosts, arboviruses such as Semliki Forest virus (SFV) (Togaviridae) generally counteract innate defenses and trigger cell death. In contrast, in mosquito cells, following an early phase of efficient virus production, a persistent infection with low levels of virus production is established. Whether arboviruses counteract RNA interference (RNAi), which provides an important antiviral defense system in mosquitoes, is an important question. Here we show that in Aedes albopictus-derived mosquito cells, SFV cannot prevent the establishment of an antiviral RNAi response or prevent the spread of protective antiviral double-stranded RNA/small interfering RNA (siRNA) from cell to cell, which can inhibit the replication of incoming virus. The expression of tombusvirus siRNA-binding protein p19 by SFV strongly enhanced virus spread between cultured cells rather than virus replication in initially infected cells. Our results indicate that the spread of the RNAi signal contributes to limiting virus dissemination.
Attarzadeh-Yazdi
Ghassem
G
The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Summerhall, Edinburgh, Scotland, United Kingdom.
Fragkoudis
Rennos
R
Chi
Yi
Y
Siu
Ricky W C
RW
Ulper
Liane
L
Barry
Gerald
G
Rodriguez-Andres
Julio
J
Nash
Anthony A
AA
Bouloy
Michèle
M
Merits
Andres
A
Fazakerley
John K
JK
Kohl
Alain
A
D000818:Animals; D002460:Cell Line; D006224:Cricetinae; D009033:Culicidae / Q000821:virology*; D015967:Gene Expression Regulation, Viral; D034622:RNA Interference; D012367:RNA, Viral / Q000235:genetics; D012672:Semliki forest virus / Q000235:genetics*; D014779:Virus Replication
D012367:RNA, Viral