The Pathogenicity of Ribonucleotide Reductase-Null Mutants of Herpes Simplex Virus Type 1 in Mice

The pathogenicity of ribonucleotide reductase (RR)-null mutants (hrR3 and ICP6Δ) of herpes simplex virus (HSV) type 1 was studied after intracerebral and corneal inoculation in newborn and adult ICR mice. ICP6Δ failed to replicate in brains of mice ⩾8 days old but exhibited significant virulence for...

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Bibliographic Details
Published in:The Journal of infectious diseases 1991-12, Vol.164 (6), p.1091-1097
Main Authors: Yamada, Yoshinari, Kimura, Hiroshi, Morishima, Tsuneo, Daikoku, Tohru, Maeno, Koichirou, Nishiyama, Yukihiro
Format: Article
Language:English
Subjects:
Animals
Animals, Newborn
Brain
Brain - microbiology
DNA, Viral - analysis
Eye - microbiology
herpes simplex virus 1
herpes simplex virus 2
Human herpesvirus 1
Human herpesvirus 2
Infections
Inoculation
Male
Mice
Mice, Inbred ICR
Mutation
Polymerase Chain Reaction
Ribonucleotide Reductases - genetics
Ribonucleotide Reductases - physiology
Ribonucleotides
Simplexvirus
Simplexvirus - enzymology
Simplexvirus - genetics
Simplexvirus - pathogenicity
Trigeminal ganglion
Trigeminal Ganglion - microbiology
Vero Cells
Virulence
Virus Replication
Viruses
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Summary:The pathogenicity of ribonucleotide reductase (RR)-null mutants (hrR3 and ICP6Δ) of herpes simplex virus (HSV) type 1 was studied after intracerebral and corneal inoculation in newborn and adult ICR mice. ICP6Δ failed to replicate in brains of mice ⩾8 days old but exhibited significant virulence for newborn mice as a result of viral replication in the brains. The RR- and a thymidine kinase (TK)-deficient mutant ofHSV-1 strain KOS could grow in eye tissues of adult ICR mice. Viral DNA of hrR3 was detected in brain tissues of intracerebrally infected mice or in the trigeminal ganglia of corneally infected mice ⩾50 days after infection, and infectious hrR3 could be recovered from these tissues by superinfection of the mice with wild-type HSV-2. These observations indicate that pathogenicity of RR− mutants in mice is highly dependent on the physiologic state of tissues infected and that RR− mutants have the ability to establish latency in nervous system tissues of mice by either the peripheral or intracerebral route. It was also demonstrated that the inability of the RR- mutants to invade the central nervous system was efficiently complemented by simultaneous infection with another defective virus, the TK− mutant of KOS.
ISSN:0022-1899
1537-6613
DOI:10.1093/infdis/164.6.1091