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

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

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

Archives of virology

2002

2002-04

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.

Animal; Animals; Disease Models; Ganglia; Herpes Simplex/*physiopathology/virology; Herpesvirus 1; Human/*pathogenicity; Inbred BALB C; Mice; Skin Diseases/*physiopathology/virology; Spinal/*virology; Time Factors; Virulence

Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).

763–773

4

147