A sequence in HpaI-P fragment of herpes simplex virus-1 DNA determines intraperitoneal virulence in mice

Becker, Yechiel; Hadar, Julia; Tabor, Eynat; Ben‐Hur, Tamir; Raibstein, Israel; Rösen, Angela; Darai, Gholamreza

doi:10.1016/0042-6822(86)90128-5

Cited by 70 publications

(37 citation statements)

References 18 publications

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“…Centifanto-Fitzgerald et al [21] re ported that the region of the HSV genome defined by map units 0.70-0.83 was involved in the production of stromal disease in the eyes of rabbits, while Thompson et al [22,23] and Thompson and Stevens [24] have re ported that this region is involved in viral replication in neural tissues in the mouse. A subset of this region defined by map units 0.761-0.796 has also been reported to be in volved in intraperitoneal virulence in mice [25], Day et al [26] have reported that the 0.40-0.44 region of the viral genome is in volved in the spread of virus from corneas to the central nervous system, while Meignier et al [27] have shown that the deletion of several genes from the unique short region of the HSV genome results in a marked decrease in neurovirulence and latency. From these reports, it is obvious that HSV pathogenicity in animals is not due to a single HSV gene product, but is affected by several viral gene functions.…”

Section: Discussionmentioning

confidence: 99%

Role of the Herpes Simplex Virus 1 Internal Repeat Sequences in Pathogenicity

Jenkins

Martin²

1990

Intervirology

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Three independently isolated herpes simplex virus type 1 recombinant viruses containing a deletion of approximately 14 kilobase pairs, representing greater than 95% of the internal repeat DNA sequences, were analyzed for their pathogenicity in mice. The recombinant viruses were found to be avirulent, exhibiting drastically increased LD₅₀ values over wild-type herpes simplex virus 1(F) by intracerebral injection, nonneuroinvasive, unable to spread from the cornea to sensory ganglion, and unable to establish a reactivable latent infection in trigeminal ganglion following either intracerebral inoculation or inoculation of scarified corneas. The potential role of diploid genes in herpes simplex virus pathogenesis in the mouse is discussed.

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Section: Discussionmentioning

confidence: 99%

Role of the Herpes Simplex Virus 1 Internal Repeat Sequences in Pathogenicity

Jenkins

Martin²

1990

Intervirology

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“…Strains F and HFEM have been reported to be apathogenic in animal models tested (Centifanto-Fitzgerald et al, 1982;Dix et al, 1983;Rosen et aL, 1985;Becker et al, 1986) and strain HF (Flexner & Amoss, 1925) is the agent from which the strain HFEM was originally derived (Burnet & Lush, 1939;Watson et al, 1966). We also included the HSV-1 strain KOS (Dix et al, 1983;Thompson et al, 1986) which, although fully virulent when inoculated intracranially, is completely avirulent in mice when inoculated by a peripheral route.…”

Section: Introductionmentioning

confidence: 99%

Biological Basis for Virulence of Three Strains of Herpes Simplex Virus Type 1

Sedarati¹,

Stevens²

1987

Journal of General Virology

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SUMMARYHerpes simplex virus type 1 (HSV-1) strains F, HF and HFEM were studied with respect to pathogenicity in mice and growth characteristics in vivo and in vitro compared to the neurovirulent HSV-I strains 17 syn + and KOS. All three viruses demonstrated reduced virulence in mouse brains and were completely avirulent after footpad inoculation. They were shown to express high levels of thymidine kinase activity. Investigations concerning the virulence phenotype indicated that the defect(s) in strains F, HF and HFEM related to general replication deficiency in mouse cells. It was also shown that although the replication restriction observed for strains F and HF was specific for murine cells, strain HFEM did not replicate well in any cell type tested. Additional studies indicated that the avirulence phenotype which followed peripheral inoculation was related to different genotypes, since strain F complemented HF and HFEM and, as expected, the latter two agents did not complement each other. All three agents were found to complement the non-neuroinvasive strain KOS. Finally, the data also show that two herpesviruses which are highly restricted in murine cells (e.g. strains F and HF) can still interact in the animal and produce a lethal infection.

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“…According to nucleotide sequences, the HSV type 2 (HSV-2) UL56 gene is predicted to encode a protein of 235 amino acids containing a C-terminal hydrophobic domain (20,29). Although the UL56 gene is not required for growth in vitro, lack of the UL56 gene product abrogates the pathogenicity of HSV-1 in vivo (2,3,32,36,37,39). It has also been shown that HSV-1 UL56 protein associates with virions (21) and that the C-terminal hydrophobic region of the UL56 protein is important for the pathogenicity of HSV-1 (19).…”

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confidence: 99%

Identification and Characterization of the UL56 Gene Product of Herpes Simplex Virus Type 2

Koshizuka

Goshima

Takakuwa

et al. 2002

J Virol

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The UL56 gene product of herpes simplex virus (HSV) has been shown to play an important role in viral pathogenicity. However, the properties and functions of the UL56 protein are little understood. We raised rabbit polyclonal antisera specific for the UL56 protein of HSV type 2 (HSV-2) and examined its expression and properties. The gene product was identified as three polypeptides with apparent molecular masses ranging from 32 to 35 kDa in HSV-2-infected cells, and at least one species was phosphorylated. Studies of their origins showed that the UL56 protein of HSV-2 is also translated from the upstream in-frame methionine codon that is not present in the HSV-1 genome. Synthesis was first detected at 6 h postinfection and was not abolished by the viral DNA synthesis inhibitor phosphonoacetic acid. Indirect immunofluorescence studies revealed that the UL56 protein localized to both the Golgi apparatus and cytoplasmic vesicles in HSV-2-infected and single UL56-expressing cells. Deletion mutant analysis showed that the C-terminal hydrophobic region of the protein was required for association with the cytoplasmic membrane and that the N-terminal proline-rich region was important for its translocation to the Golgi apparatus and cytoplasmic vesicles. Moreover, the results of protease digestion assays and sucrose gradient fractionation strongly suggested that UL56 is a tail-anchored type II membrane protein associated with lipid rafts. We thus hypothesized that the UL56 protein, as a tail-anchored type II membrane protein, may be involved in vesicular trafficking in HSV-2-infected cells.

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A sequence in HpaI-P fragment of herpes simplex virus-1 DNA determines intraperitoneal virulence in mice

Cited by 70 publications

References 18 publications

Role of the Herpes Simplex Virus 1 Internal Repeat Sequences in Pathogenicity

Role of the Herpes Simplex Virus 1 Internal Repeat Sequences in Pathogenicity

Biological Basis for Virulence of Three Strains of Herpes Simplex Virus Type 1

Identification and Characterization of the UL56 Gene Product of Herpes Simplex Virus Type 2

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