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Long-lived intermediate states formed by glycoprotein catalysts are an essential part of the process used by influenza virus particles to infect cells.

Genome sequence data from 58 Mexican swine influenza A viruses resolves the spatial origin of the virus that originated the influenza pandemic of 2009.

The abundance and complex genetic diversity of swIAV were documented and the zoonotic potential evaluated.

Immunization with NY-ESO-1 S-FLU virus elicits a robust NY-ESO-1-specific CTL response and suppresses the NY-ESO-1-expressing tumour development and spontaneous metastasis.

Interferon-λ plays a decisive and previously underestimated role in limiting the spread of respiratory viruses from the nasal cavity to the lungs and it efficiently restricts virus transmission from infected individuals to naïve contacts.

During adaptation in dogs, H3N2 canine influenza viruses (CIVs) became to recognize human-like SAα2,6-Gal receptor, increased replication ability in human cells, acquired a 100% transmission rate via respiratory droplet in ferret model, and human population lacked immunity to H3N2 CIVs.

Important nonlinear links between infection, inflammation, and disease severity were revealed using experimentally validated mathematical models.

An analysis of influenza viruses from naturally infected people suggests a tight transmission bottleneck and little positive selection within hosts.

The local fitness landscape of an antigenic region in influenza neuraminidase was determined by combinatorial mutagenesis and next-generation sequencing.

Patterns of monocyte and dendritic cell mobilization and function during human respiratory viral infections are tissue-specific and pathogen-specific, and future studies must perform comparative investigations in blood and the site of infection for a comprehensive assessment of immune responses.