Herpes spoils excitement

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.

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...