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Related Experiment Videos

Interaction between cyclic nucleotides and herpes simplex viruses: productive infection.

T L Stanwick, R W Anderson, A J Nahmias

    Infection and Immunity
    |November 1, 1977
    PubMed
    Summary

    Herpes simplex virus type 1 (HSV-1) infection alters cellular cyclic nucleotide levels. Enhancing cyclic adenosine monophosphate (cAMP) reduced HSV-1 yield in fibroblasts, while cGMP enhancement increased it.

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    Area of Science:

    • Virology
    • Cell Biology
    • Molecular Biology

    Background:

    • Herpes simplex virus type 1 (HSV-1) is a common human pathogen.
    • Cellular cyclic nucleotides, including cyclic adenosine 5'-monophosphate (cAMP) and cyclic guanosine 5'-monophosphate (cGMP), play crucial roles in cellular processes.
    • The interplay between viral infections and cellular cyclic nucleotide metabolism is not fully understood.

    Purpose of the Study:

    • To investigate the impact of HSV-1 infection on intracellular cAMP and cGMP levels in human fibroblasts and HEp-2 cells.
    • To determine the effect of modulating cyclic nucleotide levels on HSV-1 replication.

    Main Methods:

    • Infection of human fibroblasts and HEp-2 cells with HSV-1.
    • Measurement of intracellular cAMP and cGMP levels at various time points post-infection.

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  • Treatment of infected cells with compounds that enhance cAMP or cGMP levels.
  • Quantification of viral yield in treated and untreated infected cells.

    • Main Results:

    • HSV-1 infection led to decreased intracellular cAMP and increased cGMP levels in both cell types, with changes observed at 6 hours and maximal at 12 hours post-infection.
    • In human fibroblasts, cAMP-enhancing compounds (theophylline, dibutyryl cAMP, papaverine) significantly reduced HSV-1 yield, while cGMP-enhancing compounds (insulin, dibutyryl cGMP) increased it.
    • In HEp-2 cells, only theophylline reduced HSV-1 yield; cGMP-enhancing compounds had no significant effect.
    • The effects of cyclic nucleotide-enhancing compounds were observed only when added within 3 hours post-inoculation.

    Conclusions:

    • HSV-1 infection significantly alters cellular cyclic nucleotide homeostasis.
    • Modulation of intracellular cAMP levels can impact HSV-1 replication, particularly in human fibroblasts.
    • The timing of intervention with cyclic nucleotide-modulating agents is critical for affecting viral yield.