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Nevaeh | 2 years ago
"These mutations unexpectedly allowed the usually host-restricted avian influenza polymerase to use the shorter human ANP32A and B and thus partially adapted the viral polymerase for replication in mammals. Although unintended, this consequence clearly indicates the importance of a robust genome editing strategy and subsequent appraisal that includes challenge with multiple avian influenza genotypes at non-physiological exposure levels to rule out the opportunity for adaptive viral evolution."
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