Pathogenicity of Glycoprotein C-Deficient Herpes Simplex Virus 1 Strain TN-1 Which Encodes Truncated Glycoprotein C

J-STAGE
  • Minagawa Hiroko
    Department of Virology, Faculty of Medicine, Kyushu University
  • Liu Ying
    Department of Virology, Faculty of Medicine, Kyushu University
  • Yoshida Tetsuhiko
    Department of Virology, Faculty of Medicine, Kyushu University
  • Hidaka Yasufumi
    Department of Virology, Faculty of Medicine, Kyushu University
  • Toh Yasushi
    Department of Virology, Faculty of Medicine, Kyushu University
  • Mori Ryoichi
    Department of Virology, Faculty of Medicine, Kyushu University

抄録

A clinical isolate of herpes simplex virus 1 (TN-1) from a stromal keratitis patient was found to be defective in the glycoprotein C (gC) gene (UL44), thus resulting in the production of truncated gC upon infection. To study the pathogenetic role of truncated gC, we prepared a recombinant LTN-8 derived from TN-1 with deletions of the 1.5 kilobase pairs of the gC gene including the initiation codon. A penetration assay revealed LTN-8 to be less efficient in its penetration ability than TN-1, the laboratory strain KOS and RTN-1-20-3, a recombinant derived from TN-1 with the KOS gC gene. The penetration of LTN-8 was facilitated by the addition of TN-1-infected culture medium. TN-1 virus preparations had no hemagglutinating activity. However, the animals infected with TN-1 did develop hemagglutination inhibition (HI) antibodies. The LTN-8-infected animals did not develop HI antibodies. The pathogenicity in BALB/c mice following either corneal, intraperitoneal or intracerebral inoculation did not significantly differ among TN-1, RTN-1-20-3 or LTN-8. Our results indicate that truncated gC was sufficient for the induction of HI antibodies and was also able to facilitate penetration in vitro. Although truncated gC might be a virulence factor acting as a decoy, both truncated gC and intact gC had little effect on the outcome following intracerebral, intraperitoneal or corneal inoculation.

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