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Fluorescence-based Neuraminidase Inhibition Assay to Assess the Susceptibility of Influenza Viruses to The Neuraminidase Inhibitor Class of Antivirals
09:31

Fluorescence-based Neuraminidase Inhibition Assay to Assess the Susceptibility of Influenza Viruses to The Neuraminidase Inhibitor Class of Antivirals

Published on: April 15, 2017

Role of neuraminidase in influenza virus-induced apoptosis

S J Morris, G E Price, J M Barnett

    The Journal of General Virology
    |February 6, 1999
    PubMed

    Insights

    Influenza virus neuraminidase contributes to apoptosis in host cells, particularly during viral entry. Inhibiting neuraminidase or viral entry partially blocks this process, suggesting its role in early infection stages.

    Area of Science:

    • Virology
    • Cell Biology
    • Biochemistry

    Background:

    • Influenza virus infection can induce apoptosis in host cells.
    • Neuraminidase is a key viral enzyme involved in influenza virus replication and release.
    • The precise role of neuraminidase in apoptosis induction remains unclear.

    Purpose of the Study:

    • To investigate the role of influenza virus neuraminidase in the induction of apoptosis in MDCK cells.
    • To determine the stage of the viral life cycle at which neuraminidase influences apoptosis.
    • To compare the neuraminidase activity and apoptosis-inducing potential of virulent and attenuated influenza strains.

    Main Methods:

    • Comparing apoptosis levels induced by virulent clone 7a and attenuated A/Fiji influenza strains in MDCK cells.
    • Treating cells with anti-neuraminidase compounds (GR121158A, Zanamivir, DANA) at different stages of viral infection.
    • Assessing neuraminidase activity using fetuin and sialyl lactose substrates.
    • Using UV-inactivated virus, ammonium chloride, and amantadine to investigate specific viral processes.

    Main Results:

    • Virulent clone 7a induced higher apoptosis than A/Fiji. Anti-neuraminidase compounds blocked apoptosis when added during viral entry but not later.
    • GG167 inhibited viral yields late in infection but did not affect infected cell numbers.
    • Neuraminidase activity differed between strains, with clone 7a showing higher activity; no active site sequence differences were found.
    • UV-inactivated virus and ammonium chloride reduced apoptosis, while amantadine inhibited apoptosis in a strain-dependent manner.

    Conclusions:

    • Influenza virus neuraminidase plays a role in apoptosis induction, acting early in the infection cycle, likely during or before viral entry.
    • Intracellular processes are also involved in influenza virus-induced apoptosis.
    • Differences in neuraminidase activity may be due to residues outside the enzyme's active site.

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