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Hypotheses for herpes neurolatency
Dynamic state
-- persistence of low levels of infectious virus in sensory ganglia, neurons are not killed. This leads to retrograde vs anterograde transport of virus through peripheral sensory nerve endingsStatic state -- DNA of virus is maintained in a non-replicating state at some extrachromosomal site in neuron or is integrated into cellular DNA
a. Virus in skin or mucous membrane enters peripheral nerve ending and travels to dorsal root ganglia.
b. Neural cells in dorsal root ganglia are sites for latent HSV infection.
c. Stimuli such as neurectomy, stress, menstration or infection can activate latent virus
d. Progeny virions produced in ganglia travel down peripheral nerves, presumably inside axons to reach the skin. This leads to initiation of replication in epidermal cells and result in a skin lesion