Alphaherpesvirus Saimiri in Rabbits: A Model For Human Encephalitis?

Leib, David A.; McCarthy, K.

doi:10.1099/0022-1317-69-7-1609

Cited by 6 publications

(2 citation statements)

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“…Owl monkeys, tamarins, and marmosets all succumb rapidly to HVS1 infection, and lesions are histologically indistinguishable from those produced by HSV-1 (Holmes et al, 1964). Rabbits infected with HVS1 by intradermal inoculation develop latent infections in dorsal root ganglia serving the site of inoculation as does HSV-1 (Leib et al, 1988; McCarthy and Tosolini, 1975). HVS1 also displays aggressive invasion and destruction of the central nervous system in mice after inoculation by skin scarification (Breshears et al, 2001, 2005).…”

Section: Introductionmentioning

confidence: 99%

Structure and sequence of the saimiriine herpesvirus 1 genome

Tyler¹,

Severini²,

Black³

et al. 2011

Virology

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We report here the complete genome sequence of the squirrel monkey α-herpesvirus saimiriine herpesvirus 1 (HVS1). Unlike the simplexviruses of other primate species, only the unique short region of the HVS1 genome is bounded by inverted repeats. While all Old World simian simplexviruses characterized to date lack the herpes simplex virus RL1 (γ34.5) gene, HVS1 has an RL1 gene. HVS1 lacks several genes that are present in other primate simplexviruses (US8.5, US10–12, UL43/43.5 and UL49A). Although the overall genome structure appears more like that of varicelloviruses, the encoded HVS1 proteins are most closely related to homologous proteins of the primate simplexviruses. Phylogenetic analyses confirm that HVS1 is a simplexvirus. Limited comparison of two HVS1 strains revealed a very low degree of sequence variation more typical of varicelloviruses. HVS1 is thus unique among the primate α-herpesviruses in that its genome has properties of both simplexviruses and varicelloviruses.

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Section: Introductionmentioning

confidence: 99%

Structure and sequence of the saimiriine herpesvirus 1 genome

Tyler¹,

Severini²,

Black³

et al. 2011

Virology

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“…12-O-Tetradecanoylphorbol 13-acetate (a protein kinase C activator) and sodium n-butyrate both had a stimulating action on replication in Vero cells but did not affect the release of ctHVS from latently infected rabbit dorsal root ganglia.Two isolates of alphaherpesvirus saimiri (c~HVS) (formerly herpesvirus tamarinus) have been shown to produce fatal encephalitis (KM91) (Leib et al, 1988) or to establish latency (KM322) in dorsal root ganglia (DRGs) (Tosolini et al, 1982) when injected intradermally into rabbits. These isolates are very closely related in terms of restriction endonuclease digest patterns, polypeptide immunoprecipitation and growth characteristics (Leib et al, 1987).…”

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confidence: 99%

The Effects of 5-Azacytidine, 12-O-Tetradecanoylphorbol 13-acetate and Sodium n-butyrate on Reactivation of Alphaherpesvirus Saimiri from Explant Cultures of Latently Infected Rabbit Dorsal Root Ganglia

Mossman

Leib²,

McCarthy

1989

Journal of General Virology

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SUMMARYThe DNA hypomethylating agent 5-azacytidine greatly increased the reactivation of alphaherpesvirus saimiri-1 (~tHVS) from latently infected rabbit dorsal root ganglia, although it inhibited the virus yield and plaque formation efficiency of ~HVS in Veto cells. 12-O-Tetradecanoylphorbol 13-acetate (a protein kinase C activator) and sodium n-butyrate both had a stimulating action on replication in Vero cells but did not affect the release of ctHVS from latently infected rabbit dorsal root ganglia.Two isolates of alphaherpesvirus saimiri (c~HVS) (formerly herpesvirus tamarinus) have been shown to produce fatal encephalitis (KM91) (Leib et al., 1988) or to establish latency (KM322) in dorsal root ganglia (DRGs) (Tosolini et al., 1982) when injected intradermally into rabbits. These isolates are very closely related in terms of restriction endonuclease digest patterns, polypeptide immunoprecipitation and growth characteristics (Leib et al., 1987). Intradermal inoculation of rabbits in the flank with ~HVS KM322 produces an initial skin lesion followed by ganglionitis as manifested by areas of hypoaesthesia (Tosolini et al., 1982). This is followed by a period of prolonged latency during which spontaneous reactivation has never been observed (Tosolini et al., 1981) although virus can be recovered by cocultivation of DRGs with a monolayer of permissive cells. However a very low proportion of ganglia serving the inoculated dermatomes yield reactivating virus by cocultivation (< 20 %), thus necessitating the sacrifice of a high number of rabbits to produce statistically significant results. In order to improve the sensitivity of detection of latent virus a number of agents known to stimulate other virus systems were incorporated into explant culture media. Since the molecular mechanisms involved in maintaining the latent state and in triggering reactivation are ill understood the agents used were selected for their different modes of action.5-Azacytidine (5-AzaC) is a DNA hypomethylating agent. The level of methylation of cytosine in CpG dinucleotides in DNA has been implicated as a means of cellular and viral gene control in a number of systems (reviewed by Doerfler, 1983). Generally a high degree of DNA methylation correlates with gene inactivation whereas low levels of methylation are associated with active parts of the genome. Inverse correlations between DNA methylation and gene expression have been observed in a number of virus replication systems including those of herpesviruses. In an in vitro latency system Youssoufian et al. (1982) showed latent herpes simplex virus type 1 (HSV-1) DNA to be extensively methylated, but this was not the case in actively replicating virus. In gammaherpesvirus saimiri (a virus not closely related to ~HVS) DNA is methylated in non-producing lymphoid cell lines but not in producing lines (Desrosiers et al., 1979). Also, the experimental induction of a previously inactive thymidine kinase gene in HSV-I is associated with concurrent demethylation of the gene promoter (Clough et ...

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Alphaherpesvirus saimiri infection in rabbits

1990

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A light and electron microscopic study was undertaken to determine pathological changes in cutaneous spinal nerves of rabbits following intradermal inoculation with alphaherpesvirus saimiri (alpha HVS) isolate KM 322. Infected rabbits were killed at 3, 10, 17, 45 days and 2 years after infection. No abnormalities were seen at 3 days postinoculation. In the nerves of the rabbits killed at 10, 17 and 45 days after infection, axonal (Wallerian-type) degeneration was the main pathological feature. Regeneration, manifested by axonal sprouting, was observed in the nerves of the rabbits killed at 45 days post-inoculation. Neural fibrosis and paucity of unmyelinated axons was the final outcome. The severity of the neural damage not only varied according to the progression of the disease but between nerves taken from the same rabbit. This was probably associated with variation in the numbers of virus particles that had reached the dorsal root ganglion of the dermatome served by a particular nerve. Since alpha HVS (isolate KM 322) provides a model system for the study of virus latency in dorsal root ganglia, and consequently for the study of varicellazoster infection in man, these findings give further insight into the pathology of herpetic neuropathy.

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Alphaherpesvirus Saimiri in Rabbits: A Model For Human Encephalitis?

Cited by 6 publications

References 10 publications

Structure and sequence of the saimiriine herpesvirus 1 genome

Structure and sequence of the saimiriine herpesvirus 1 genome

The Effects of 5-Azacytidine, 12-O-Tetradecanoylphorbol 13-acetate and Sodium n-butyrate on Reactivation of Alphaherpesvirus Saimiri from Explant Cultures of Latently Infected Rabbit Dorsal Root Ganglia

Alphaherpesvirus saimiri infection in rabbits

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