Influenza virus infection causes global inhibition of host protein synthesis in infected cells. This host shutoff is thought to allow viruses to escape from the host antiviral response, which restricts virus replication and spread. Although the mechanism of host shutoff is unclear, a novel viral protein expressed by ribosomal frameshifting, PA-X, was found to play a major role in influenza virus-induced host shutoff.
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Sendai virus (SeV) is a pneumotropic murine pathogen in the Paramyxoviridae family, which includes many clinically important human pathogens. It is an enveloped negative-strand RNA virus and encodes 6 major structural proteins: two glycoproteins (HN and F), the matrix (M) protein, the nucleoprotein (NP), and the phosphoprotein (P) and large (L) proteins, which make up the polymerase complex.
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Influenza A viruses are negative-sense, single-stranded, segmented RNA viruses that infect a wide range of hosts, including humans and many avian species. One mechanism for the instigation of a pandemic is direct infection of humans with an avian virus that contains mutations allowing it to easily infect and spread among humans.
Learn more about Role of Influenza Polymerase in Host Adaptation