OBJECTIVETo establish an animal model of Bell's palsy induced by the reactivation of latent herpes simplex virus type 1 (HSV-1), and observe the effect of interferon and IgG on the facial nerve paralysis induced by HSV-1 infection. METHODS Totally 64 four-week-old female Balb/c mice weighted 16-18 gram were selected. Using scratching the surface of bilateral auricles by a 26-gauge needle, 25 microl HSV-1 with a titer of 6.7 x 10(8) PFU/ml was inoculated into the left auricle and the same volume of PBS was placed in the right in order to develop a mouse model of latent HSV-1. In this study, interferon and IgG administration were performed before and after facial nerve paralysis and continued for 3 days. Controls were given normal sodium instead of interferon and IgG, and the incidence and duration of facial nerve paralysis were compared in the groups interferon and IgG and control. Ciclosporin was given to the mice eight weeks after recovery from facial nerve paralysis caused by inoculation with HSV-1. The HSV-1 DNA in bilateral facial nerve and bilateral trigeminal ganglion after the treatment were examined with polymerase chain reaction (PCR) analysis. RESULTS There were 10 mice of facial nerve paralysis in the first group. The incidence of facial nerve paralysis was 50% and the duration of facial nerve paralysis was (7.2 +/- 2.2) days. There were 6 mice of facial nerve paralysis in the second group. The incidence of facial nerve paralysis was 30% and the duration of facial nerve paralysis was (4.5 +/- 1.8) days. There were 16 mice of facial nerve paralysis in the control group. The incidence of facial nerve paralysis was 67% and the duration of facial nerve paralysis was (8.9 +/-2.6) days. IgG didn't reduce the incidence and duration of facial nerve paralysis by statistics analysis (P > 0.05), but interferon reduced the incidence and duration of facial nerve paralysis (P < 0.05). After administration of ciclosporin, 3/28 of mice developed facial nerve paralysis. The HSV-1 DNA was detected from facial nerve of all the mice of facial palsy. No facial palsy was observed in mice in which no HSV-1 DNA was detected from facial nerve.

CONCLUSIONSFacial nerve paralysis might be caused by reactivation of latent HSV-1, and the reactivation might be related with immunosuppression. Administration of interferon reduces the incidence and duration of facial nerve paralysis. Administration of IgG can't reduced the incidence and duration of facial nerve paralysis.