Key result
Influenza polymerase inhibitors such as favipiravir, pimodivir, and baloxavir marboxil provide novel therapeutic options, though treatment-emergent resistance mutations have been identified.
Why the study?
Because the influenza virus RNA-dependent RNA polymerase is essential for viral replication and highly conserved, several inhibitors targeting each subunit have been developed.
This review summarizes the mechanisms, efficacy, and resistance profiles of emerging influenza polymerase inhibitors.
May expand influenza treatment options; leaves open resistance mitigation strategies pending prospective trials.
The influenza virus RNA-dependent RNA polymerase is highly conserved among influenza A, B, C, and D viruses. It comprises three subunits: polymerase basic protein 1 (PB1), polymerase basic protein 2 (PB2), and polymerase acidic protein (PA) in influenza A and B viruses or polymerase 3 protein (P3) in influenza C and D viruses. Because this polymerase is essential for influenza virus replication, it has been considered as a target for antiviral agents. Recently, several polymerase inhibitors that target each subunit have been developed. This review discusses the mechanism of action, antiviral activity, and emergence of resistance to three inhibitors approved for the treatment of influenza or in late-phase clinical trials: the PB1 inhibitor favipiravir, the PB2 inhibitor pimodivir, and the PA inhibitor baloxavir marboxil.
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Emi Takashita (2020) conducted a review in Influenza. Influenza polymerase inhibitors (favipiravir, pimodivir, baloxavir marboxil) was evaluated. Influenza polymerase inhibitors such as favipiravir, pimodivir, and baloxavir marboxil provide novel therapeutic options, though treatment-emergent resistance mutations have been identified.
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