Key result
Influenza virus ribonucleoprotein complexes gain preferential access to host cell export machinery by tethering to host-cell chromatin at sites of Ran regeneration.
Population
HeLa, A549, and MDCK cells infected with influenza virus (WSN strain, rWSN-PB2-Strep, WSN-NEP20/21, SC35M)
Comparison
Infection with influenza virus and treatment… vs Mock-infected cells or untreated infected cells
Design
Preclinical
Authors
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May identify novel influenza antiviral targets; extends mechanistic insights in animal models but leaves open human translation.
Influenza viruses hijack the host cell nuclear export machinery by targeting vRNP export complexes to dense chromatin sites where RanGTP is regenerated by Rcc1.
Chase et al. (2011) studied Influenza virus infection. Influenza virus infection vs. Mock infection was evaluated on vRNP export complex composition and chromatin association. Influenza virus ribonucleoprotein complexes gain preferential access to host cell export machinery by tethering to host-cell chromatin at sites of Ran regeneration.
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