Journal of Dental Research, Vol 75, 974-979, Copyright © 1996 by International & American Associations for Dental Research Online Journals
Highly virulent strains of herpes simplex virus fail to kill mice following infection via gingival route
Y. Monma, Z. J. Chen, H. Mayama, K. Kamiyama and F. Shimizu
Department of Pediatric Dentistry, Tohoku University School of Dentistry, Sendai, Japan.
Virulence of herpes simplex virus (HSV) in mice has been demonstrated to be
dependent on the site of infection. In this experiment, pathogenesis of HSV
was studied in 2 different routes of infection in a mouse model system.
When BALB/c mice were infected with 5 x 10(3) plaque-forming units (PFU) of
virulent HSV type 1 Miyama GC+ strain (HSV-1-GC+) intraperitoneally, all
mice were dead in 6 to 9 days. HSV-1-GC+ was recovered from organs such as
the cerebrum, cerebellum, brainstem, and spleen 2 to 5 days after
infection, but not from other organs such as trigeminal ganglia. However,
if mice were infected in the maxillary gingiva with 1.0 x 10(7) PFU of
HSV-1-GC+, all mice survived. HSV-1-GC+ was recovered from the trigeminal
ganglia and brainstem 2 to 5 days after infection, but not from other
organs tested. When mice were infected in maxillary gingiva with HSV-1-GC+,
followed by the intraperitoneal injection of 6 mg of cyclophosphamide 72
hrs after virus infection, all mice were dead within days.
Immunofluorescent and hematoxylin-eosin staining of gingival tissue
sections revealed that when mice were infected in maxillary gingiva with
HSV-1-GC+, 3 times as many gamma delta T-cells and 5 times as many
polymorphonuclear cells can be detected in sections of maxillary gingiva
when compared with non-infected mice. These data show that the gingiva of
mice is considerably more resistant to infection with HSV, compared with
the peritoneal cavity, and suggest the possible presence of an oral defense
mechanism which might be different from that in the peritoneal cavity.
