Upon invading the host, hemagglutinin binds to sialic acid sugars on the epithelial cell surface, where a protease then cleaves it, resulting in endocytosis of the virus1. Within the host cell, the virus begins to interact, causing a fusion between the envelope and hemagglutinin1. This fusion activates the M2 ion channel, which starts proton movement through the envelope and consequently acidifies the virus core. The acidic core then dissimulates so the viral RNA can be transported to the nucleus for replication where the host cell machinery and RNA-dependent RNA polymerase transcribes complementary viral RNA. Once the mature virus binds to the host cell via hemagglutinin, neuraminidase hydrolyzes sialic acid residues, allowing the virus to bud from the host cell and spread to the adjacent, non-infected cells to repeat the process again (Figure …show more content…
Not only does it give healthcare providers a fast-acting treatment option, it gives patients with unique situations another route of administration—intravenously. Peramivir’s increased selectivity and unique structure allows for resistance to the emergence of strains that resist its pharmacologic class members. Additionally, peramivir can serve as a template for future development of antiviral drugs to continue to solve the issue of drug resistance. It follows the action of neuraminidase inhibitors with slight differences that make it much more effective. Although it is limited to the first two days of symptoms, healthcare providers can still actively utilize peramivir throughout future flu seasons and pandemics. Overall, the development of peramivir functions as a solid foundation for the future of antiviral therapies and for the fight against the influenza