However, their functions during the influenza A virus infection process remain unclear.

Background: During March 2009 a novel Influenza A virus emerged in Mexico.

Avian influenza A viruses often do not propagate efficiently in mammalian cells.

Thirty-four chinchillas were inoculated intranasally with either influenza A virus or sterile saline.

Pandemic influenza A virus (IAV) remains a significant threat to global health.

Water birds are the natural host of influenza A viruses.

Our data indicate that NA alone among viral proteins limits influenza A virus superinfection.

Sulfonic acid polymers exert selective inhibitory effects on RSV and influenza A virus replication.

In summary, this study establishes a quantitative biochemical correlate for influenza A virus transmission.

However, to what extent sumoylation is exploited by influenza A virus is not fully understood.

Taken together, these findings indicate that autophagy is actively involved in influenza A virus replication.

However, little is known about the regulatory role of autophagy in influenza A virus replication.

Rapid antigenic evolution in the influenza A virus hemagglutinin precludes effective vaccination with existing vaccines.

Novel antivirals are needed to supplement existing control strategies for influenza A virus (IAV).

It was recently reported that influenza A virus proteins interact extensively with the host sumoylation system.

By comparison, the influenza A virus has been found to survive on surfaces for 17 days.