Influenza virus gene expression and replication

Influenza virus gene expression and replication represent the coordinated biological processes required for the viral life cycle within a host cell (Reid et al., 2021; PMID: 33432168). This cycle begins with viral entry mediated by Hemagglutinin and subsequent uncoating via the M2 ion channel (Pielak & Chou, 2011; PMID: 21115317). The core of this process is the replication of the segmented negative-sense RNA genome and the transcription of viral mRNA, both performed by the viral RNA-dependent RNA polymerase (RdRp) complex consisting of PA, PB1, and PB2 subunits (Te Velthuis & Fodor, 2016; PMID: 27109529). A unique feature of influenza transcription is "cap-snatching," where the PA subunit cleaves host pre-mRNAs to provide primers for viral mRNA synthesis (Reid et al., 2021; PMID: 33432168). Therapeutic strategies target various stages of this cycle: M2 inhibitors (Amantadine) block uncoating, PA endonuclease inhibitors (Baloxavir marboxil) halt transcription, and Neuraminidase inhibitors (Oseltamivir) prevent the release of progeny virions (Hayden et al., 2018; PMID: 30184455; McClellan & Perry, 2001; PMID: 11218071). Due to the high mutation rate of the virus, monitoring for resistance and developing broad-spectrum inhibitors of the replication machinery remain critical public health priorities (Hayden et al., 2018; PMID: 30184455).

Other names

Influenza viral replication cycleInfluenza gene expressionInfluenza virus life cycle

Inhibition of neuraminidase, inhibition of cap-dependent endonuclease, inhibition of M2 ion channel, and inhibition of RNA-dependent RNA polymerase.