Prevalence of herpes B virus genome in the trigeminal ganglia of seropositive cynomolgus macaques.

Herpes B virus infection is almost asymptomatic in macaques (Macaca spp.), which are the natural hosts of this pathogen, but is the cause of high mortality in humans. Reactivation of the latent virus in the trigeminal ganglia (TG) results in the shedding of infectious particles into the oral mucosal membrane. Saliva contaminated with the reactivated virus from the ganglia of the natural host is considered to be important for viral transmission to humans and other monkeys. In the present study, we investigated the prevalence of the herpes B virus genome in the left and right TG of seropositive asymptomatic cynomolgus macaques. The latent virus genome was detected using a polymerase chain reaction and microplate hybridization assay. We found that the virus DNA was present in one or both TG of 12 of the 30 macaques (40%) tested, with the virus being detected from both TG in five of the 12 macaques and from a single TG in the remaining seven.

Distribution of varicella-zoster virus strains carrying a PstI-site-less mutation in Japan and DNA change responsible for the mutation.

We have analyzed 53 varicella-zoster virus (VZV) strains isolated in Japan for the presence of a PstI cleavage site in a middle portion of the long unique region of VZV genome. About 25% of the strains examined did not have this PstI cleavage site, although the majority of strains retained this site. For several VZV strains lacking this PstI cleavage site, we sequenced a recombinant DNA-derived short segment containing the mutation. In all strains analyzed, we identified a base replacement from A to G within the PstI recognition sequence. Because no wild-type VZV strain carrying this mutation has been found so far in other countries, it is very likely that the mutation once occurred in the past and has been conserved in some strains in Japan. We have concluded that the PstI-site-less mutation is reliable marker for discrimination of VZV strains in Japan.

Titration of human cytomegalovirus (HCMV) DNA in urine by combined use of PCR and microplate hybridization in a renal transplant patient with HCMV pneumonitis.

We titrated human cytomegalovirus (HCMV) DNA in urine specimens obtained from 14 healthy individuals and a renal transplant patient with HCMV pneumonitis by modifying the method for titration of varicella-zoster virus DNA previously described (1,2). Of 14 HCMV seropositive healthy individuals, 13 had HCMV DNA under the detection limit of 10(2.0) copies/ml, whereas one person had 10(2.0) copies/ml. The viral DNA in urine samples was at a low level in healthy individuals with latent infection. In a case with HCMV pneumonitis after renal transplantation, the amount of HCMV DNA in urine gradually increased from the level under 10(2.0) copies/ml and reached a peak of 10(4.7) copies/ml one month prior to the manifestation of pneumonitis. It, thereafter, decreased with the course of clinical remission, and finally settled at under 10(2.0) copies/ml. Serial titrations of HCMV DNA in urine specimens proved to be useful in identifying recipients at risk of developing active HCMV infection after renal transplantation and as a guide for treatment of patients.