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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.edu

Inhibition 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