Key result
Influenza virus selectively translates its own mRNAs in a cap-dependent manner while blocking host cellular protein synthesis at both the initiation and elongation stages.
The study elucidates the molecular mechanisms by which influenza virus selectively translates its own mRNAs while shutting off host protein synthesis.
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Provides mechanistic basis for viral host shutoff; leaves open translation to antiviral strategies or human disease models.
In cells infected by influenza virus type A, host protein synthesis undergoes a rapid and dramatic shutoff. To define the molecular mechanisms underlying this selective translation, a transfection/infection protocol was developed utilizing viral and cellular cDNA clones. When COS-1 cells were transfected with cDNAs encoding nonviral genes and subsequently infected with influenza virus, protein expression from the exogenous genes was diminished, similar to the endogenous cellular genes. However, when cells were transfected with a truncated influenza viral nucleocapsid protein (NP-S) gene, the NP-S protein was made as efficiently in influenza virus infected cells as in uninfected cells, showing that the NP-S mRNA, although expressed independently of the influenza virus replication machinery, was still recognized as a viral and not a cellular mRNA. Northern blot analysis demonstrated that the selective blocks to nonviral protein synthesis were at the level of translation. Moreover, polysome experiments revealed that the translational blocks occurred at both the initiation and elongation stages of cellular protein synthesis. Finally, we utilized this transfection/infection system as well as double infection experiments to demonstrate that the translation of influenza viral mRNAs probably occurred in a cap-dependent manner as poliovirus infection inhibited influenza viral mRNA translation.
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Garfinkel et al. (1992) studied Influenza virus type A infection. Transfection with truncated influenza viral nucleocapsid protein (NP-S) gene vs. Nonviral genes / uninfected cells was evaluated on Protein expression and translation mechanism. Influenza virus selectively translates its own mRNAs in a cap-dependent manner while blocking host cellular protein synthesis at both the initiation and elongation stages.
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