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People infected with the cold sore–causing herpes simplex virus 1 (HSV-1) often complain of abnormal sensations around the site of initial infection, a symptom apparently caused by the virus's ability to reduce the excitability of infected neurons. On page 1251, Storey et al. describe the molecular mechanism responsible for this phenomenon. Their findings may also be relevant to the normal rearrangements of voltage-dependent sodium channels that occur during neuronal development.
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The authors found that neurons from the rat dorsal root ganglion show a profound and rapid loss of voltage-dependent sodium currents 24 h after infection with HSV-1. Loss of excitability in these neurons correlates with the loss of sodium channels from the cell surface. Blocking endocytosis or preventing the production of HSV-1 late proteins prevents the loss of excitability, and a mutant virus lacking the neuro-virulence factor ICP 34.5 does not cause the loss of sodium channels seen in wild-type viral infections.Previous work has shown that HSV-1 modifies the ubiquitin–proteasome pathway, leading to the destruction of many cellular proteins, and this may also explain the internalization of sodium channels. If the virus is tapping into a normal cellular pathway, then the same ubiquitin–proteasome pathway may also explain the rapid disappearance of sodium channels at nodes of Ranvier during development.(HSV-1 infection (bottom) prompts a loss ) |
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发表于 2009-3-6 00:22
发表于 2015-5-30 18:16
