Glycoprotein G isoforms from some alphaherpesviruses function as broad-spectrum chemokine binding proteins

Bryant, Neil

doi:10.1093/emboj/cdg092

Cited by 123 publications

(166 citation statements)

References 48 publications

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“…Secreted virally-encoded glycoprotein Gs from several alpha herpesviruses are potent chemokine binding proteins capable of blocking neutrophil recruitment (117,118). Oddly, HSV-1 gG is an exception; no chemokine binding capability is observed despite homology with other gGs assayed by Bryant et al (117). Alternatively, HSV-1 gG may specifically bind a chemokine(s) not assayed for in this study or use other mechanisms to block chemokine signaling.…”

Section: Perspectivementioning

confidence: 81%

“…Members of the alpha herpesvirus family, of which HSV-1 is a member, also subvert chemokine responses. Secreted virally-encoded glycoprotein Gs from several alpha herpesviruses are potent chemokine binding proteins capable of blocking neutrophil recruitment (117,118). Oddly, HSV-1 gG is an exception; no chemokine binding capability is observed despite homology with other gGs assayed by Bryant et al (117).…”

Section: Perspectivementioning

confidence: 99%

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The role of chemokines during herpes simplex virus-1 infection

Todd¹

2008

Front Biosci

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Herpes simplex virus-type 1 is among the most prevalent and successful humans pathogens. Although infection is largely uncomplicated in the immunocompetent human host, HSV-1 infection can cause blinding corneal disease, and individuals with defects in innate or adaptive immunity are susceptible to herpes simplex encephalitis. Chemokines regulate leukocyte trafficking to inflamed tissues and play a crucial role in orchestrating the immune response to HSV-1 infection. In this review we will focus on the pathways that induce chemokine expression during HSV-1 infection and the implications of chemokine signaling on control of viral replication.

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Section: Perspectivementioning

confidence: 81%

Section: Perspectivementioning

confidence: 99%

The role of chemokines during herpes simplex virus-1 infection

Todd¹

2008

Front Biosci

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“…BHV-1 infects cells of the respiratory and reproductive tracts and causes clinical diseases, namely infectious bovine rhino-tracheitis and infectious pustular vulvo-vaginitis [14], which result in significant production losses in affected herds, including the death of some animals. BHV-1-encoding proteins have a number of immunomodulatory activities, including downregulation of type I interferon responses [15] and expression of class I MHC proteins [16], and interference with chemokine activities [17], which collectively are associated with suppressed cellular immune responses during infection. This immunosuppression is implicated in predisposition to secondary infections with other respiratory pathogens, both viral and bacterial, which cause severe disease and mortality in intensive cattle-rearing units (reviewed in [18]).…”

Section: Introductionmentioning

confidence: 99%

Identification of immediate early gene products of bovine herpes virus 1 (BHV-1) as dominant antigens recognized by CD8 T cells in immune cattle

Hart

MacHugh

Sheldrake

et al. 2017

Journal of General Virology

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In common with other herpes viruses, bovine herpes virus 1 (BHV-1) induces strong virus-specific CD8 T-cell responses. However, there is a paucity of information on the antigenic specificity of the responding T-cells. The development of a system to generate virus-specific CD8 T-cell lines from BHV-1-immune cattle, employing Theileria-transformed cell lines for antigen presentation, has enabled us to address this issue. Use of this system allowed the study to screen for CD8 T-cell antigens that are efficiently presented on the surface of virus-infected cells. Screening of a panel of 16 candidate viral gene products with CD8 T-cell lines from 3 BHV-1-immune cattle of defined MHC genotypes identified 4 antigens, including 3 immediate early (IE) gene products (ICP4, ICP22 and Circ) and a tegument protein (UL49). Identification of the MHC restriction specificities revealed that the antigens were presented by two or three class I MHC alleles in each animal. Six CD8 T-cell epitopes were identified in the three IE proteins by screening of synthetic peptides. Use of an algorithm (NetMHCpan) that predicts the peptide-binding characteristics of restricting MHC alleles confirmed and, in some cases refined, the identity of the epitopes. Analyses of the epitope specificity of the CD8 T-cell lines showed that a large component of the response is directed against these IE epitopes. The results indicate that these IE gene products are dominant targets of the CD8 T-cell response in BHV-I-immune cattle and hence are prime-candidate antigens for the generation of a subunit vaccine.

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“…Viral TNF receptors (vTNFRs) encoded by poxviruses block the activity of this proinflammatory cytokine and are examples of viral decoy receptors with sequence similarity to the extracellular cytokine-binding domain of their cellular counterparts. Some poxviruses and herpesviruses encode secreted chemokine-binding proteins belonging to a second class of viral decoy receptors with unique structures unrelated to host receptors (6, 7) that bind with high affinity a broad range of chemokines, which are mediators of cell migration (5,(8)(9)(10)(11)(12)(13)(14). The secreted 35-kDa protein that binds CC chemokines is the only viral chemokine-binding protein identified in VaV and the vaccinia virus (VV) smallpox vaccine strains Lister and DryVax (Wyeth) (8)(9)(10).…”

mentioning

confidence: 99%

A chemokine-binding domain in the tumor necrosis factor receptor from variola (smallpox) virus

Alejo

Ruiz-Argüello

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

134

162

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Variola virus (VaV) is the causative agent of smallpox, one of the most devastating diseases encountered by man, that was eradicated in 1980. The deliberate release of VaV would have catastrophic consequences on global public health. However, the mechanisms that contribute to smallpox pathogenesis are poorly understood at the molecular level. The ability of viruses to evade the host defense mechanisms is an important determinant of viral pathogenesis. Here we show that the tumor necrosis factor receptor (TNFR) homologue CrmB encoded by VaV functions not only as a soluble decoy TNFR but also as a highly specific binding protein for several chemokines that mediate recruitment of immune cells to mucosal surfaces and the skin, sites of virus entry and viral replication at late stages of smallpox. CrmB binds chemokines through its C-terminal domain, which is unrelated to TNFRs, was named smallpox virus-encoded chemokine receptor (SECRET) domain and uncovers a family of poxvirus chemokine inhibitors. An active SECRET domain was found in another viral TNFR (CrmD) and three secreted proteins encoded by orthopoxviruses. These findings identify a previously undescribed chemokine-binding and inhibitory domain unrelated to host chemokine receptors and a mechanism of immune modulation in VaV that may influence smallpox pathogenesis.immune evasion ͉ viral pathogenesis ͉ cytokine receptor ͉ poxvirus ͉ inflammation

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Glycoprotein G isoforms from some alphaherpesviruses function as broad-spectrum chemokine binding proteins

Cited by 123 publications

References 48 publications

The role of chemokines during herpes simplex virus-1 infection

The role of chemokines during herpes simplex virus-1 infection

Identification of immediate early gene products of bovine herpes virus 1 (BHV-1) as dominant antigens recognized by CD8 T cells in immune cattle

A chemokine-binding domain in the tumor necrosis factor receptor from variola (smallpox) virus

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