Homologous recombination between corresponding RNA segments of different influenza viruses has not been observed, in contrast to the high frequency of recombination observed among the genomes of positive-sense RNA viruses, like polioviruses, retroviruses. The virulence host range of influenza viruses relate to the surface glycoproteins, as well as to other viral proteins. Zoonotic influenza virus infections are also spread by these routes through direct indirect exposures perhaps rarely by gastrointestinal infection. Influenza virus RNA is readily detected on fomites, virus retains infectiousness longer on hard, nonporous surfaces, in low humidity, at cooler temperatures, but the importance of transmission via fomites is unclear. Pathogenicity cell tropism of influenza viruses relate in part to the hemagglutinin (HA) cleavability by particular host cell enzymes. Serine proteases, presumably derived from host epithelial cells, cleave the HA precursor molecule into HA1 HA2 to render human influenza viruses infectious. Currently, use of inactivated influenza vaccine is the most important measure for reducing influenza virus-related morbidity mortality. Drug recipients may experience subclinical infection, which usually confers protection against infection by the same strain. As antiviral chemoprophylaxis does not interfere with the immune response to inactivated vaccine, they can be administered concurrently. However, concurrent use of any anti-influenza antiviral drug might interfere with the immunogenicity of live attenuated influenza virus vaccines (LAIV).
- Antiviral chemoprophylaxis
- Influenza virus
- Live attenuated influenza virus vaccines (LAIV)