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Related Experiment Videos

Latency in vitro using irradiated herpes simplex virus.

Y Nishiyama, F Rapp

    The Journal of General Virology
    |January 1, 1981
    PubMed
    Summary
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    UV-irradiated herpes simplex virus type 2 (HSV-2) can establish latency in human embryonic fibroblasts. Reactivation was enhanced by human cytomegalovirus (HCMV) or UV light, suggesting damaged HSV-2 genomes persist without significant repair.

    Area of Science:

    • Virology
    • Cell Biology
    • Molecular Biology

    Background:

    • Herpes simplex virus type 2 (HSV-2) can establish latent infections.
    • Viral latency is a complex process influenced by various factors, including host cell conditions and co-infections.
    • Understanding the mechanisms of HSV-2 latency and reactivation is crucial for developing antiviral strategies.

    Purpose of the Study:

    • To investigate the establishment and reactivation of UV-irradiated HSV-2 in a human embryonic fibroblast latency model.
    • To determine the effect of human cytomegalovirus (HCMV) and UV irradiation on HSV-2 reactivation from latency.
    • To explore the fate of UV-damaged HSV-2 genomes during latency.

    Main Methods:

    • Infection of human embryonic fibroblasts with UV-irradiated HSV-2 and incubation at 40.5°C to prevent replication.

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  • Induction of virus synthesis via temperature shift-down to 36.5°C.
  • Superinfection with HCMV or additional UV irradiation at the time of temperature shift-down to study reactivation enhancement.

    • Main Results:

    • UV-irradiated HSV-2 did not yield detectable virus at 40.5°C but could be induced by temperature shift-down.
    • Induced virus showed poor growth and rapid inactivation at 40.5°C.
    • Enhanced reactivation of HSV-2 was observed upon superinfection with HCMV or UV irradiation during temperature shift-down.
    • HCMV enhanced the synthesis of UV-irradiated HSV-2 but not normally growing HSV-2.

    Conclusions:

    • UV irradiation damages HSV-2 genomes, allowing them to enter a non-replicating latent state in vitro.
    • Reactivation from this latent state can be enhanced by co-infection with HCMV or further UV treatment.
    • These findings suggest that damaged HSV-2 genomes can persist in a non-replicating state without complete destruction or repair in this latency model.