Medline ® Abstract for Reference 49 of ‘Pathogenesis of herpes simplex virus type 1 infection’

Medline ® Abstract for Reference 49 of 'Pathogenesis of herpes simplex virus type 1 infection'

Medline ® Abstract for Reference 49 of 'Pathogenesis of herpes simplex virus type 1 infection'
Herpes simplex virus 1 (HSV-1) causes recurrent mucocutaneous ulcers and is the leading cause of infectious blindness and sporadic encephalitis in the United States. The lifelong aspect of infection results from latent viral infection of neurons, a reservoir from which the virus reactivates periodically. When low-virulent strains were inoculated separately, no vaginitis/vulvitis was produced despite replication in the vagina. That the inherent characteristics of the viral strain are a determinant in the outcome of the disease process was also clearly demonstrated. gen. Wagner and W. Nevertheless, inoculation of 5BlacZ or the double-mutant dl5-29 at distal sites reduced acute replication and latent infection of 186DeltaKpn following intranasal challenge.

In addition to the number of latent sites, the number of viral genome copies within the individual latently infected neurons has recently been demonstrated to be variable. Interestingly, neurons latently infected with KOS contained significantly fewer viral genome copies than those infected with either 17syn+ or McKrae. Thus, the HSV-1 genome copy number profile is viral strain specific and positively correlates with the ability to reactivate in vivo. To date, there has been no genome-wide analysis of recombination. These data provide insight into the extent and origin of genome-wide intrastrain HSV-1 variation and present useful methods for expansion to in vivo patient infection studies.

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