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A Primary Neuron Culture System for the Study of Herpes Simplex Virus Latency and Reactivation
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Published on: April 2, 2012

Multiplicity reactivation of alkylating agent damaged herpes simplex virus (type I) in human cells

S K Das

    Mutation Research
    |August 1, 1982
    PubMed

    Insights

    Herpes simplex virus type 1 (HSV-1) DNA can be repaired by infected human cells through multiplicity reactivation when treated with MMS and MNNG. This repair mechanism was not observed with HN2-treated HSV-1.

    Area of Science:

    • Virology
    • Molecular Biology
    • Cellular Biology

    Background:

    • Herpes simplex virus type 1 (HSV-1) causes various human infections.
    • Chemical mutagens can induce lesions in viral DNA.
    • Understanding viral DNA repair mechanisms is crucial for antiviral strategies.

    Purpose of the Study:

    • To investigate the potential for multiplicity reactivation in HSV-1 treated with chemical agents.
    • To determine if infected human cells can repair chemically induced DNA lesions in HSV-1.

    Main Methods:

    • HSV-1 (Strain KOS) was treated with methyl methanesulfonate (MMS), N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), and N-methyl-bis(2-chloroethyl)amine (HN2).
    • Viral infectivity was assessed using plaque assays on Vero cells and infectious center assays with FS2 cells.
    • Viral survival rates were compared at different multiplicities of infection (MOI).

    Main Results:

    • MMS and MNNG inactivated HSV-1, but viral survival was higher at MOI of 1.0 PFU/cell compared to 0.01 PFU/cell.
    • This suggests multiplicity reactivation, where infected cells repair chemically induced lesions.
    • No evidence of multiplicity reactivation was observed for HN2-treated HSV-1.

    Conclusions:

    • Human cells infected with HSV-1 possess a DNA repair mechanism (multiplicity reactivation) effective against MMS and MNNG induced lesions.
    • The efficacy of multiplicity reactivation may depend on the type of chemical mutagen and viral MOI.
    • HN2-treated HSV-1 did not exhibit multiplicity reactivation under the tested conditions.

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