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Pathogenicity of Glycoprotein C‐Deficient Herpes Simplex Virus 1 Strain TN‐1 Which Encodes Truncated Glycoprotein C
Author(s) -
Minagawa Hiroko,
Yoshida Ying Liu Tetsuhiko,
Hidaka Yasufumi,
Toh Yasushi,
Mori Ryoichi
Publication year - 1997
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.1997.tb01890.x
Subject(s) - biology , herpes simplex virus , virology , recombinant dna , virus , antibody , virulence , microbiology and biotechnology , vero cell , glycoprotein , gene , immunology , genetics
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.