Molecular basis of host responses through herpes simplex virus US3 protein kinase

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1 We have investigated the molecular basis of herpes simplex virus US3, an accessory gene, in terms of its functions such as regulation of apoptosis, immunity and neumvirulence.2 We used a highly neumvirulent strain (186), US3-deficient mutants (L1BR1 and LB101) and US3-rescued virus (L1B-11) in order to analyze the functions of US3 comprehensively.3 With refarence to the molecular basis of US3 for regulation of apoptosis in peripheral neurons and neurovirulence, 186 and L1B-11 did not induce apoptosis (i.e., TUNEL negative) in olfactory neurons, while L1BR1 induced apoptosis in these peripheral neurons (TUNEL positive).4 These results suggest that L1BI1 can promote viral entry and spread via the natural mute of infretion through negatively regulating virus-induced apoptosis and augment neurovirulence.5 A newly developed mutant, LB101, did not infect olfactory neurons, the reason remaining unknown.6 The molecular mechanisms of L1BR1 to induce apoptosis remain unknown. JNK, a protein kinase, may be involved in a process of apoptosis induction.7 Ibal-immunopositive microglia can not be detected in olfactory neurons.