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Virol Res J 2017 Volume 1 Issue 3
International Virology Conference
October 30-31, 2017 | Toronto, Canada
M
any enveloped viruses utilize cholesterol-rich lipid
rafts at the plasma membrane for virus assembly and
production. However, the functional role of cholesterol
in virus formation and infectivity is unclear. In this study,
we investigated the effects of FDA approved cholesterol-
reducing agents on raft formation and the production
of infectious parainfluenza virus (PIV), influenza A virus
(IAV) and respiratory syncytial virus (RSV) in human airway
cells. Depletion of cholesterol with the agents, especially
when combined, significantly decreased production of
all infectious viruses. Depletion of cellular cholesterol
reduced cell surface accumulation of PIV glycoproteins
and inhibited virus assembly and release. In contrast,
depletion of cellular cholesterol did not decrease IAV and
RSV surface glycoproteins accumulation, and virus particles
were efficiently released from the cells. However, the
released virus particles were less stable due to abnormal
virion density and decreased cholesterol content in the viral
membrane. Replenishing the virus released from the treated
cells with cholesterol rescued virus stability and infectivity.
Collectively, our findings suggest that cholesterol is critical
for PIV assembly, and maintaining the stability of infectious
IAV and RSV particles. Our data suggests that cholesterol
is an attractive target for antiviral agents against various
clinically important respiratory viruses.
e:
shringkhala_bajimaya@urmc.rochester.eduInhibition of respiratory virus infection by cholesterol reducing agents
Shringkhala Bajimaya, Tsuyoshi Hayashi, Tünde Frankl, Peter Bryk, Brian Ward
and
Toru Takimoto
University of Rochester Medical Center, USA