Primary structure of the herpesvirus saimiri genome

Albrecht, Jens; Nicholas, John; Biller, D.; Cameron, K. R.; Biesinger, Brigitte; Newman, C.E.; Wittmann, Sabine; Craxton, Molly; Coleman, Heather M.; Fleckenstein, Bernhard

doi:10.1128/jvi.66.8.5047-5058.1992

Cited by 416 publications

(164 citation statements)

References 117 publications

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“…Like other Rhadinoviruses, HVS is an enveloped, doublestranded DNA virus with a 155-kb genome having approximately 75 open reading frames (Albrecht et al, 1992;Ensser et al, 2003). The genes encoding the "saimiri transformation-associated protein" (STP) and the "tyrosine kinase interacting protein" (Tip) have been extensively studied due to their roles in oncogenicity and cell transformation (Jung and Desrosiers, 1992;Jung et al, 1999).…”

Section: Etiologymentioning

confidence: 99%

Viral Diseases of Nonhuman Primates

Wachtman

Mansfield

2012

Nonhuman Primates in Biomedical Research

103

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Section: Etiologymentioning

confidence: 99%

Viral Diseases of Nonhuman Primates

Wachtman

Mansfield

2012

Nonhuman Primates in Biomedical Research

103

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“…Several ORF of HVS that lack homologues in EBV have sequence homology with known cellular proteins. 51 In particular, the product of ORF ECRF-3 has 30% amino acid identity with the chemokine receptors. Expression of ECRF-3 in Xenopus oocytes results in mobilization of calcium in response to the binding of several CXC chemokines, such as IL-8, GRO/melanoma growth stimulatory activity (MGSA) and neutrophil activating peptide (NAP)-2, but not in response to binding of CC chemokines.…”

Section: Chemokine-binding Proteins Encoded By Virusesmentioning

confidence: 99%

Chemokines and chemokine receptors in infectious diseases

1999

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Summary Today, 10 years after the discovery of IL-8, chemokines (chemotactic cytokines) are seen as the stimuli that largely control leucocyte migration. Chemokines are low molecular weight chemoattractant cytokines secreted by a variety of cells, including leucocytes, epithelial cells, endothelial cells, fibroblasts and numerous other cell types. They are produced in response to exogenous stimuli, such as viruses and bacterial LPS, and endogenous stimuli, such as IL-1, TNF and IFN. These factors mediate chemotaxis and leucocyte activation. They also regulate leucocyte extravasation from the blood and/or lymph vessel luminal surface to the tissue space, the site of inflammation. There is no doubt that chemokines and chemokine receptors are critical for defence against infectious pathogens. It is also clear that these pathogens have evolved to accommodate the workings of the host immune system. Survival of these infectious agents appears dependent upon strategies that can evade, suppress, counteract or otherwise confound the constellation of host responses to invading pathogens. In this regard, the chemokines and their receptors are a major target. Reviewed in the present paper are several examples in which microbial pathogens have usurped the mammalian chemokine system to subvert the host immune response.

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“…Consistent with a role for regulation of cell cycle progression in ␥ -herpesvirus infection and disease, KSHV, HVS, and ␥ HV68 encode a v-cyclin, and EBV regulates the expression of host cyclin molecules (5,(18)(19)(20)(21)(22)(23)(24)(25). To determine the in vivo role for v-cyclin we characterized ␥ HV68 v-cyclin mutants.…”

Section: Introductionmentioning

confidence: 99%

Identification of the In Vivo Role of a Viral bcl-2

Gangappa

Dyk

Jewett

et al. 2002

The Journal of Experimental Medicine

119

159

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Many γ-herpesviruses encode candidate oncogenes including homologues of host bcl-2 and cyclin proteins (v-bcl-2, v-cyclin), but the physiologic roles of these genes during infection are not known. We show for the first time in any virus system the physiologic role of v-bcl-2. A γ-herpesvirus v-bcl-2 was essential for efficient ex vivo reactivation from latent infection, and for both persistent replication and virulence during chronic infection of immunocompromised (interferon [IFN]-γ−/−) mice. The v-cyclin was also critical for the same stages in pathogenesis. Strikingly, while the v-bcl-2 and v-cyclin were important for chronic infection, these genes were not essential for viral replication in cell culture, viral replication during acute infection in vivo, establishment of latent infection, or virulence during acute infection. We conclude that v-bcl-2 and v-cyclin have important roles during latent and persistent γ-herpesvirus infection and that herpesviruses encode genes with specific roles during chronic infection and disease, but not acute infection and disease. As γ-herpesviruses primarily cause human disease during chronic infection, these chronic disease genes may be important targets for therapeutic intervention.

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Primary structure of the herpesvirus saimiri genome

Cited by 416 publications

References 117 publications

Viral Diseases of Nonhuman Primates

Viral Diseases of Nonhuman Primates

Chemokines and chemokine receptors in infectious diseases

Identification of the In Vivo Role of a Viral bcl-2

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