Failure to complement infectivity of EBV and HSV-1 glycoprotein B (gB) deletion mutants with gBs from different human herpesvirus subfamilies

Suk Kyeong Lee, Teresa Compton, Richard Longnecker*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

16 Scopus citations

Abstract

Glycoprotein B (gB) is conserved among the herpesvirus family which infects a broad range of species. To investigate the functional homology of human α-herpesviruses, β-herpesviruses, and γ-herpesviruses gB proteins, complementation studies were performed with gB genes from each subfamily member using EBV gp110 (EBV gB homologue) and HSV-1 gB null mutants. Neither the α-herpesvirus HSV-1 gB gene nor the β-herpesvirus HCMV gB gene were able to complement the gp110 null mutant. Conversely, neither the β-herpesvirus HCMV gB or the γ-herpesvirus EBV gp110 gene were able to complement HSV-1 gB null mutants. To further investigate functional domains of EBV gp110 and HSV-1 gB, gB-gp110 chimeric proteins were constructed. Surprisingly, none of the chimeric proteins were able to complement either HSV-1 gB null mutants or EBV gp110 null mutants. These results demonstrate that there is not sufficient functional homology between the different gas to allow complementation in other subfamily members of the herpesvirus family.

Original languageEnglish (US)
Pages (from-to)170-181
Number of pages12
JournalVirology
Volume237
Issue number1
DOIs
StatePublished - Oct 13 1997

ASJC Scopus subject areas

  • Virology

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