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Related Experiment Videos

Early interaction between mouse hepatitis virus 3 and cells.

K Krzystyniak, J M Dupuy

    The Journal of General Virology
    |November 1, 1981
    PubMed
    Summary
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    Mouse hepatitis virus 3 (MHV3) uptake by cells is similar across different mouse strains, regardless of genetic sensitivity. Early infection events, like virus uptake, do not explain varying MHV3 replication rates in vivo.

    Area of Science:

    • Virology
    • Immunology
    • Genetics

    Background:

    • Mouse hepatitis virus 3 (MHV3) exhibits differential replication in mice with varying genetic sensitivities.
    • Understanding early viral interactions with host cells is crucial for explaining these differences.

    Purpose of the Study:

    • To investigate if early cellular events, specifically virus uptake, contribute to differential MHV3 replication observed in genetically distinct mouse strains.
    • To determine if cellular uptake mechanisms vary between resistant and susceptible mouse populations.

    Main Methods:

    • Studied MHV3 uptake kinetics in macrophages and L cells using radiolabeled virus.
    • Assessed the impact of cytochalasin B and prostaglandin E1 on virus uptake and phagocytosis.
    • Compared MHV3 uptake in various immune cells (spleen cells, T lymphocytes, thymocytes) and macrophages from mice of differing MHV3 sensitivities (A/J, (C57Bl/6 x A/J)F1, susceptible).

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    Main Results:

    • MHV3 uptake by macrophages and L cells was time- and temperature-dependent.
    • Inhibition of phagocytosis by cytochalasin B or prostaglandin E1 did not affect MHV3 uptake.
    • No significant differences in radiolabeled MHV3 uptake were observed across various cell types or between macrophages from MHV3-resistant, semi-susceptible, and susceptible mouse strains.

    Conclusions:

    • Genetically determined in vivo sensitivity to MHV3 infection is not attributable to differential virus uptake by host cells.
    • Early cellular interaction, specifically virus entry, is unlikely to be the primary factor driving variations in MHV3 replication across different mouse strains.