The ability of an HSV strain to initiate zosteriform spread correlates with its neuroinvasive disease potential

N. Goel, H. Mao, Q. Rong, J. J. Docherty, D. Zimmerman, K. S. Rosenthal

Research output: Contribution to journalArticle

16 Scopus citations


The requirements for disease development in the mouse epidermal scarification-zosteriform model of HSV infection are likely to parallel those required for primary HSV disease of humans. HSV-1 strains, which are neuroinvasive in the mouse footpad model of HSV encephalitis, caused local site lesions within 3 days and secondary zosteriform lesions along the dermatome within approximately 5 days. HSV-1 strains, which are not neuroinvasive, failed to progress to zosteriform lesion development and local site lesions were mild or absent. Relative differences in the rate and extent of zosteriform lesion development paralleled the behavior of the viruses in the mouse footpad model of neuroinvasion. In conclusion, the viral properties which are important for neuroinvasiveness appear to also determine the ability of an HSV strain to cause zosteriform disease.

Original languageEnglish (US)
Pages (from-to)763-773
Number of pages11
JournalArchives of Virology
Issue number4
StatePublished - Apr 22 2002
Externally publishedYes


ASJC Scopus subject areas

  • Virology

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