Detection by complementation of defective or uninducible (herpes simplex type 1) virus genomes latent in human ganglia.

Abstract

Reconstruction experiments showed that temperature-sensitive (ts) mutants of herpes simplex virus type 1 (HSV-1) (Glasgow strain 17) grow, complement and recombine with similar efficiency in human nerve ganglion cells, human brain cells, normal human fibroblasts (WI38) and baby hamster kidney (BHK) 21/C13 cells. Cultures of human trigeminal, superior cervical and vagus ganglia that failed to release HSV spontaneously were superinfected with a range of ts mutants of HSV-1 and incubated at permissive (31.degree. C) and nonpermissive (38.5.degree. C) temperatures to determine if complementation of or recombination with the input genomes occurred. The ganglia from 8 of 14 individuals, which were consistently negative for spontaneous release of virus, contained information that could be detected or rescued following superinfection with ts mutants of HSV. In 2 additional cases, positive results were obtained after the superinfection of negative ganglia explants, but in each of these HSV was previously spontaneously released from 1 of 6 ganglia explanted.