Silke Stertz

Missorting of LaCrosse virus nucleocapsid protein by the interferon-induced MxA GTPase involves smooth ER membranes.

Interferon-induced, antiviral human MxA protein localizes to a distinct subcompartment of the smooth endoplasmic reticulum.

The intracellular sites of early replication and budding of SARS-coronavirus.

Induction of MxA gene expression by influenza A virus requires type I or type III interferon signaling.

The antiviral potential of interferon-induced cotton rat Mx proteins against orthomyxovirus (influenza), rhabdovirus, and bunyavirus.

The Mx GTPase family of interferon-induced antiviral proteins.

Influenza A virus strains differ in sensitivity to the antiviral action of Mx-GTPase.

Human host factors required for influenza virus replication.

Protection of mice against lethal challenge with 2009 H1N1 influenza A virus by 1918-like and classical swine H1N1 based vaccines.

Oseltamivir-resistant variants of the 2009 pandemic H1N1 influenza A virus are not attenuated in the guinea pig and ferret transmission models.

Pandemic 2009 H1N1 vaccine protects against 1918 Spanish influenza virus.

Uncovering the global host cell requirements for influenza virus replication via RNAi screening.

Serum- and glucocorticoid-regulated kinase 1 is required for nuclear export of the ribonucleoprotein of influenza A virus.

Glycosylations in the globular head of the hemagglutinin protein modulate the virulence and antigenic properties of the H1N1 influenza viruses.

Emergence of a C-terminal seven-amino-acid elongation of NS1 in around 1950 conferred a minor growth advantage to former seasonal influenza A viruses.

Entry of influenza A virus: host factors and antiviral targets.

Prolidase is required for early trafficking events during influenza A virus entry.

Swine interferon-inducible transmembrane proteins potently inhibit influenza A virus replication.

Correction for lanz et Al., Swine interferon-inducible transmembrane proteins potently inhibit influenza a virus replication.

A Potent Anti-influenza Compound Blocks Fusion through Stabilization of the Prefusion Conformation of the Hemagglutinin Protein.

Cathepsin W Is Required for Escape of Influenza A Virus from Late Endosomes.

Recent strategies and progress in identifying host factors involved in virus replication.