Herpesvirus ateles and herpesvirus saimiri transform marmoset T cells into continuously proliferating cell lines that can mediate natural killer cell-like cytotoxicity.

Johnson, Donald R.; Jondal, Mikael

doi:10.1073/pnas.78.10.6391

Cited by 20 publications

(5 citation statements)

References 31 publications

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“…Like the rhadinoviruses, the macaviruses A1HV-1 and OvHV-2 cause apathogenic infections in their natural hosts (wildebeest and sheep, respectively), but in related ruminants cause fatal T-lymphoproliferative disease called malignant catarrhal fever (Ensser and Fleckenstein, 2005; Russell et al, 2009). All four of these γ-herpesviruses (highlighted in red in Figure 7B) establish latency in host CD8 T cells, promoting constitutive activation of TCR signaling molecules, clonal expansion and expression of activation markers, including high levels of IFN-γ secretion (Dewals and Vanderplasschen, 2011; Johnson and Jondal, 1981; Kiyotaki et al, 1986; Nelson et al, 2010; Noraz et al, 1998). …”

Section: Resultsmentioning

confidence: 99%

“…HVS undergoes asymptomatic lytic replication in its natural host, the squirrel monkey ( Saimiri sciureus ), whereas latent infection progresses to acute T-cell lymphomas and leukemias in other New World primates, such as the common marmoset ( Callithrix jacchus ) (Ensser and Fleckenstein, 2005). HVS-transformed marmoset cells are predominantly activated CD8 cytotoxic T cells (Johnson and Jondal, 1981; Kiyotaki et al, 1986). HVS is also capable of transforming human T cells in vitro (Ensser and Fleckenstein, 2005).…”

Section: Introductionmentioning

confidence: 99%

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Alternative Capture of Noncoding RNAs or Protein-Coding Genes by Herpesviruses to Alter Host T Cell Function

et al. 2014

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SUMMARY In marmoset T cells transformed by Herpesvirus saimiri (HVS), a viral U-rich noncoding RNA, HSUR 1, specifically mediates degradation of host microRNA-27 (miR-27). High-throughput sequencing of RNA after crosslinking immunoprecipitation (HITS-CLIP) identified mRNAs targeted by miR-27 as enriched in the T-cell receptor (TCR) signaling pathway, including GRB2. Accordingly, transfection of miR-27 into human T cells attenuates TCR-induced activation of mitogen-activated protein kinases (MAPKs) and induction of CD69. MiR-27 also robustly regulates SEMA7A and IFN-γ, key modulators and effectors of T-cell function. Knockdown or ectopic expression of HSUR 1 alters levels of these proteins in virally-transformed cells. Two other T-lymphotropic γ-herpesviruses, AlHV-1 and OvHV-2, do not produce a noncoding RNA to downregulate miR-27, but instead encode homologs of miR-27 target genes. Thus, oncogenic γ-herpesviruses have evolved diverse strategies to converge on common targets in host T cells.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Alternative Capture of Noncoding RNAs or Protein-Coding Genes by Herpesviruses to Alter Host T Cell Function

et al. 2014

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“…In contrast to the rapid oncogenic transformation seen in vivo after inoculation of HVS, in vitro transformation by HVS has been difficult to demonstrate (27), although the closely related HVA readily transforms T lymphocytes in vitro (6,12).…”

Section: Discussionmentioning

confidence: 99%

Analysis of herpesvirus saimiri structural proteins with monoclonal antibodies

Dahlberg¹,

Zintz²,

Ablashi³

1985

J Virol

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Herpesvirus saimiri is a lymphotrophic virus isolated from squirrel monkeys that causes highly malignant lymphomas in owl monkeys, marmosets, and rabbits, but not in its natural host. We have been interested in exploring immunological and biological aspects of this phenomenon and describe in this report the isolation of 27 monoclonal antibodies (MCAs) to herpesvirus saimiri which were grouped into 11 distinct sets based on the proteins they immunoprecipitated. In total, these 11 groups of MCAs identify the majority of the proteins present in the virion. Immunofluorescence was used to study how the viral antigens are compartmentalized in infected cells. One antibody produced intense nuclear staining and immunoprecipitated both the largest protein seen in gels (150,000 daltons) and one of the smallest (13,000 daltons). All of the other groups of MCAs principally stained the cytoplasm of infected cells. One of the unexpected results of this study was the observation that a majority of the MCAs precipitated more than one protein (15 of 27 antibodies, 7 of 11 groups). Whereas one group of MCAs, which normally precipitated four proteins, identified only single polypeptides after dithiothreitol pretreatment, the other sets of antibodies continued to recognize two or more viral antigens under reducing conditions. Immunoprecipitation of viral proteins with polyvalent sera obtained from virus-infected rabbits and monkeys was carried out to verify and extend previously published reports on the proteins of herpesvirus saimiri.

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“…miR-142-3p is abundantly expressed in hematopoietic tissues and is essential for normal hematopoietic lineage development and differentiation [43][44][45] but it is mostly absent in non-hematopoietic tissues [46]. HVS establishes latency in predominantly CD8 + T-cells that express natural killer (NK) cell markers and show NK cell-like cytotoxicity [47][48][49], and in which this miRNA is abundantly expressed [50]. Since miR-142-3p activity is required for repression of all HSUR 2 targets [32], it is expected that HSUR 2 will not be able to modulate host gene expression in tissues where this miRNA is not expressed, curtailing the ability of HVS to successfully establish long-term latent infections in nonhematopoietic tissues.…”

Section: Why Does Hsur 2 Tether Specifically Mir-142-3p and Mir-16 Tomentioning

confidence: 99%

Novel roles for Sm-class RNAs in the regulation of gene expression

Cazalla

2018

RNA Biology

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Viruses masterfully regulate host gene expression during infection. Many do so, in part, by expressing non-coding RNAs. Recent work has shown that HSUR 2, a viral non-coding RNA expressed by the oncogenic Herpesvirus saimiri, regulates mRNA expression through a novel mechanism. HSUR 2 base pairs with both target mRNAs and host miRNAs in infected cells. This results in HSUR 2-dependent recruitment of host miRNAs and associated Ago proteins to target mRNAs, and the subsequent destabilization of target mRNAs. Using this mechanism, this virus regulates key cellular pathways during viral infection. Here I discuss the evolution of our thinking about HSUR function and explore the implications of recent findings in relation to the current views on the functions of interactions between miRNAs and other classes of non-coding RNAs, the potential advantages of this mechanism of regulation of gene expression, and the evolutionary origin of HSUR 2.

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Herpesvirus ateles and herpesvirus saimiri transform marmoset T cells into continuously proliferating cell lines that can mediate natural killer cell-like cytotoxicity.

Cited by 20 publications

References 31 publications

Alternative Capture of Noncoding RNAs or Protein-Coding Genes by Herpesviruses to Alter Host T Cell Function

Alternative Capture of Noncoding RNAs or Protein-Coding Genes by Herpesviruses to Alter Host T Cell Function

Analysis of herpesvirus saimiri structural proteins with monoclonal antibodies

Novel roles for Sm-class RNAs in the regulation of gene expression

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