Henju Marjuki

TL;DR: The results demonstrate that T-705 induces a high rate of mutation that generates a nonviable viral phenotype and that lethal mutagenesis is a key antiviral mechanism of T-707.

TL;DR: Investigation of the function of PI3K during influenza virus infection revealed that it appears to regulate a very early step during viral entry, a perfect example of a seemingly antiviral signalling component that is misused by the virus to support effective replication.

TL;DR: These findings suggest that changes optimizing receptor specificity and interaction of viral polymerase components with host cellular factors are the major mechanisms that contribute to the optimal competitive advantage of pandemic influenza viruses in mice.

TL;DR: It is shown that hemagglutinin membrane accumulation and its tight association with lipid-raft domains trigger activation of the MAPK cascade via protein kinase Cα activation and induces RNP export, which may represent an auto-regulative mechanism that coordinates timing of R NP export to a point when all viral components are ready for virus budding.

TL;DR: It is shown that V‐ATPase activity is elevated during infection of cell monolayers with IAV, as measured by intracellular pH change, via a mechanism mediated by extracellular signal‐regulated kinase (ERK) and phosphatidylinositol 3‐kinase (PI3K).