Detection of influenza A(H3N2) viruses with the I38T mutation in baloxavir-treated children highlights the emergence of reduced susceptibility to this novel antiviral.
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Emergence of baloxavir-resistant I38T mutants in treated children warrants surveillance; leaves open questions on transmission and impact.
The novel cap-dependent endonuclease inhibitor baloxavir marboxil was approved for the treatment of influenza virus infection in Japan in February 2018. Two influenza A(H3N2) viruses carrying an I38T substitution in the polymerase acidic subunit (PA) were detected in baloxavir-treated children in December 2018. This mutation is known to confer reduced susceptibility to baloxavir, and the two mutant viruses exhibited 76- and 120-fold reduced susceptibility to baloxavir.
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Takashita et al. (2019) studied this question.
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