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English: Figure 1. Molecular targets and potential antiviral treatments against influenza virus infection. The above diagram shows the life cycle of influenza virus and the proposed action of each class of antiviral. After attachment to the host cell receptor containing sialic acid, the virus particle undergoes the processes of fusion, endocytosis, and uncoating, and subsequently replication by the RNA polymerase. Surface protein-coated envelope then forms around the genome to produce a complete virion, which can then be released to infect other cells. DAS 181, a sialidase fusion protein, acts on the first step of virus invasion by cleaving the sialic acid linkages on human epithelial cells. Adamantanes are M2 channel blockers which inhibit proton entry through the channel into the virion, thus preventing its disintegration. Favipiravir is a pyrazinecarboxamide derivative which inhibits the viral RNA-dependent RNA polymerase. Ribavirin’s antiviral actions are multiple, though it mainly interferes with RNA synthesis. Nitazoxanide may block haemagglutinin maturation (and act as an interferon-inducer). Neuraminidase inhibitors, by attaching to the viral neuraminidase, block the release of virus from host cells, thus halting the progression of infection. A combination of agents from different drug classes may produce synergistic effects (see text).