QUANTITATION OF HERPES-SIMPLEX VIRUS TYPE-1 DNA AND LATENCY-ASSOCIATED TRANSCRIPTS IN RABBIT TRIGEMINAL GANGLIA DEMONSTRATES A STABLE RESERVOIR OF VIRAL NUCLEIC-ACIDS DURING LATENCY

Citation
Jm. Hill et al., QUANTITATION OF HERPES-SIMPLEX VIRUS TYPE-1 DNA AND LATENCY-ASSOCIATED TRANSCRIPTS IN RABBIT TRIGEMINAL GANGLIA DEMONSTRATES A STABLE RESERVOIR OF VIRAL NUCLEIC-ACIDS DURING LATENCY, Journal of virology, 70(5), 1996, pp. 3137-3141
Citations number
46
Categorie Soggetti
Virology
Journal title
ISSN journal
0022538X
Volume
70
Issue
5
Year of publication
1996
Pages
3137 - 3141
Database
ISI
SICI code
0022-538X(1996)70:5<3137:QOHVTD>2.0.ZU;2-9
Abstract
In this investigation we determined the dynamics of herpes simplex vir us type 1 (HSV-1) DNA and latency associated transcripts (LAT) in the latently infected rabbit trigeminal ganglion. Rabbit eyes were infecte d with either the McKrae strain or the 17Syn(+) strain of HSV-1. Rabbi ts were sacrificed between 5 and 360 days after infection and their tr igeminal ganglia were analyzed for the number of HSV DNA genomes and t he number of neuronal cells expressing LAT. There was no statistically significant change in the number of HSV genomes or the number of neur onal cells expressing LAT in these ganglia between 20 and 360 days aft er infection. For both strains, the amount of HSV DNA averaged 16.8 ge nomes per 100 cells, and 9.2% of the neurons expressed LAT. There were 17 to 34 HSV genomes per LAT-expressing neuronal cell, The number of LAT-expressing neurons did not change over the 360 days. Spontaneous r eactivation (HSV-1 recovery in tear film) and recurrence (HSV-l-specif ic epithelial lesions) occurred during the period of this study; howev er,these events did not alter the quantity of HSV-1 DNA or the number of LAT-expressing cells. These results suggest that after the latent i nfection is established, the viral DNA in the ganglia does not replica te to any measurable extent over long periods of latency, since no sig nificant change in the number of HSV genomes occurs. The results also suggest that only a very small number of latently infected neuronal ce lls are needed to produce infectious HSV-1 during reactivation.