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Early interactions between human cytomegalovirus and cells.

B Wahren, L Einhorn, H Gadler

    Archives of Virology
    |January 1, 1984
    PubMed
    Summary

    Cytomegalovirus (CMV) adsorption to human cells is not blocked by other herpes viruses. CMV efficiently transports to the nucleus and expresses early antigens, suggesting late antigen defectiveness may relate to viral dose.

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    Area of Science:

    • Virology
    • Cell Biology
    • Molecular Biology

    Background:

    • Cytomegalovirus (CMV) is a significant human pathogen.
    • Understanding CMV entry and replication is crucial for therapeutic development.
    • Herpes virus interactions at the cellular level warrant further investigation.

    Purpose of the Study:

    • To investigate the initial steps of human cytomegalovirus (CMV) infection in human fibroblasts.
    • To determine the role of other herpes viruses in inhibiting CMV adsorption.
    • To analyze the transport kinetics and gene expression of CMV within host cells.

    Main Methods:

    • Studying the adsorption of CMV to human fibroblasts.
    • Assessing inhibition by preincubation with herpes simplex virus type 1 (HSV-1), herpes simplex virus type 2 (HSV-2), and varicella-zoster virus (VZV).
    • Tracking viral transport to the nucleus using 3H-thymidine labeled CMV.
    • Quantifying the synthesis of early (EA) and late (LA) viral antigens in permissive human lung fibroblasts.

    Main Results:

    • CMV adsorption was not inhibited by preincubation with HSV-1, HSV-2, or VZV.
    • Radioactivity, indicating viral presence, was detected in the nucleus within 20 minutes of virus addition.
    • Plaque-purified CMV predominantly induced early antigen (EA) synthesis over both early and late antigen (EA and LA) synthesis.
    • This ratio of EA to LA induction was consistent across virions of varying densities, suggesting a dose-dependent effect or inherent virion property.

    Conclusions:

    • CMV entry into human fibroblasts is independent of other common herpes viruses.
    • CMV efficiently enters the host cell nucleus, initiating viral genome expression.
    • The observed defect in late antigen production may be linked to the viral dose or an intrinsic characteristic of the virion, rather than virion density.

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