Birds Belonging to the Family Paridae as Another Potential Reservoir of Murine Gammaherpesvirus 68

AbstractMurine gammaherpesvirus 68 (MHV-68) is a natural pathogen of free-living murid rodents, isolated from a bank vole (Clethrionomys glareolus) in Slovakia. It belongs to the family Herpesviridae, the genus Rhadinovirus, the species Murid herpesvirus 4. Neutralizing serum MHV-68 antibodies were found in animals of other species living with infected rodents in the same biotope (fallow deer, wild boars, deer, sheep, foxes, and mouflons) as well as in humans (laboratory personnel working with MHV-68 or wild rodents, hunters, general population). In this study, the shedding of MHV-68 in the nature was investigated on the model of laboratory mice experimentally infected with the virus. The virus was first detected in breast milk and lactic glands at day 4, in urine and salivary glands at day 9, and in saliva and tear glands at day 14 p.i. Out of intranasal, peroral, intramuscular, intraperitoneal, and subcutaneous routes of infection the first two proved most effective.

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Faculty Opinions recommendation of RTA promoter demethylation and histone acetylation regulation of murine gammaherpesvirus 68 reactivation.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1157092.617190 ◽

2009 ◽

Author(s):

Marcia Blackman

Keyword(s):

Histone Acetylation ◽

Murine Gammaherpesvirus ◽

Gammaherpesvirus 68 ◽

Murine Gammaherpesvirus 68

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Faculty Opinions recommendation of Murine gammaherpesvirus 68 infection protects lupus-prone mice from the development of autoimmunity.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.717952727.793458204 ◽

2012 ◽

Author(s):

Howard Young

Keyword(s):

Murine Gammaherpesvirus ◽

Gammaherpesvirus 68 ◽

Murine Gammaherpesvirus 68

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Alpha beta-crystallin expression and presentation following infection with murine gammaherpesvirus 68

Autoimmunity ◽

10.3109/08916934.2013.785535 ◽

2013 ◽

Vol 46 (6) ◽

pp. 399-408 ◽

Cited By ~ 5

Author(s):

Vinita S. Chauhan ◽

Daniel A. Nelson ◽

Ian Marriott ◽

Kenneth L. Bost

Keyword(s):

Murine Gammaherpesvirus ◽

Alpha Beta ◽

Gammaherpesvirus 68 ◽

Murine Gammaherpesvirus 68

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Two Kinetic Patterns of Epitope-Specific CD8 T-Cell Responses following Murine Gammaherpesvirus 68 Infection

Journal of Virology ◽

10.1128/jvi.02229-09 ◽

2010 ◽

Vol 84 (6) ◽

pp. 2881-2892 ◽

Cited By ~ 37

Author(s):

Michael L. Freeman ◽

Kathleen G. Lanzer ◽

Tres Cookenham ◽

Bjoern Peters ◽

John Sidney ◽

...

Keyword(s):

T Cell ◽

Expression Patterns ◽

T Cell Responses ◽

Cd8 T Cell ◽

T Cell Response ◽

Immune Control ◽

Murine Gammaherpesvirus ◽

Cell Responses ◽

Gammaherpesvirus 68 ◽

Murine Gammaherpesvirus 68

ABSTRACT Murine gammaherpesvirus 68 (γHV68) provides an important experimental model for understanding mechanisms of immune control of the latent human gammaherpesviruses. Antiviral CD8 T cells play a key role throughout three separate phases of the infection: clearance of lytic virus, control of the latency amplification stage, and prevention of reactivation of latently infected cells. Previous analyses have shown that T-cell responses to two well-characterized epitopes derived from ORF6 and ORF61 progress with distinct kinetics. ORF6487-specific cells predominate early in infection and then decline rapidly, whereas ORF61524-specific cells continue to expand through early latency, due to sustained epitope expression. However, the paucity of identified epitopes to this virus has limited our understanding of the overall complexities of CD8 T-cell immune control throughout infection. Here we screened 1,383 predicted H-2b-restricted peptides and identified 33 responses, of which 21 have not previously been reported. Kinetic analysis revealed a spectrum of T-cell responses based on the rapidity of their decline after the peak acute response that generally corresponded to the expression patterns of the two previously characterized epitopes. The slowly declining responses that were maintained during latency amplification proliferated more rapidly and underwent maturation of functional avidity over time. Furthermore, the kinetics of decline was accelerated following infection with a latency-null mutant virus. Overall, the data show that γHV68 infection elicits a highly heterogeneous CD8 T-cell response that segregates into two distinctive kinetic patterns controlled by differential epitope expression during the lytic and latency amplification stages of infection.

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The Gammaherpesvirus Chemokine Binding Protein Binds to the N Terminus of CXCL8

Journal of Virology ◽

10.1128/jvi.77.15.8588-8592.2003 ◽

2003 ◽

Vol 77 (15) ◽

pp. 8588-8592 ◽

Cited By ~ 21

Author(s):

Louise M. C. Webb ◽

Ian Clark-Lewis ◽

Antonio Alcami

Keyword(s):

Receptor Binding ◽

Chemokine Receptor ◽

Chemokine Receptors ◽

Binding Protein ◽

Sequence Similarity ◽

Structural Requirements ◽

Murine Gammaherpesvirus ◽

N Terminus ◽

Gammaherpesvirus 68 ◽

Murine Gammaherpesvirus 68

ABSTRACT Viruses encode proteins that disrupt chemokine responses. The murine gammaherpesvirus 68 gene M3 encodes a chemokine binding protein (vCKBP-3) which has no sequence similarity to chemokine receptors but inhibits chemokine receptor binding and activity. We have used a panel of CXCL8 analogs to identify the structural requirements for CXCL8 to bind to vCKBP-3 in a scintillation proximity assay. Our data suggest that vCKBP-3 acts by mimicking the binding of chemokine receptors to CXCL8.

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