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Latent infection can be established with drastically restricted transcription and replication of the HSV-1 genome.

Abstract：

:Viral functions essential for the establishment of latent infection in murine sensory neurons in vivo were investigated by employing a herpes simplex virus type 1 (HSV-1) variant (KD6/B11) deleted for expression of the ICP4 gene and therefore unable to replicate. Since the viral DNA persisted in these cells, the latency-associated transcripts were expressed for prolonged periods of time, and the variant was biologically retrievable by superinfection with an ICP4-competent agent, we concluded that a latent infection had been established. In situ hybridization experiments designed to investigate gene expression during the acute phase of infection with the variant revealed a highly restricted pattern compared to that of the wild-type parent virus HSV-1 KOS(M). While latency-associated transcripts were detected in a large number of infected neurons, expression of other virus genes was limited to a subset of immediate-early and early genes (ICP0, ICP8, ICP27, and HSV-1 DNA polymerase genes). Expression was further limited to a small proportion of the infected neurons (approximately 1% of neurons expressing latency-associated transcripts). No hybridization was detected with probes specific for the viral TK gene and late genes VP5 and gC. Quantitative assays of viral DNA during the acute phase of infection indicated that the input viral DNA did not replicate. From these results we conclude that HSV-1 latent infection can be established in murine sensory neurons under conditions in which viral genetic expression and DNA replication are severely restricted.

journal_name

Virology

journal_title

Virology

authors

Sedarati F,Margolis TP,Stevens JG

doi

10.1006/viro.1993.1089

subject

Has Abstract

pub_date

1993-02-01 00:00:00

pages

687-91

issue

2

eissn

0042-6822

issn

1096-0341

pii

S0042-6822(83)71089-5

journal_volume

192

pub_type

杂志文章

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