Chemokine Subversion by Human Herpesviruses

Pontejo, Sergio M.; Murphy, Philip M.; Pease, James E.

doi:10.1159/000492161

Cited by 25 publications

(28 citation statements)

References 131 publications

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“…116 The β-subfamily and γ-subfamily of the herpes viruses encode for own viral chemokines and even viral chemokine receptors known to bind and interfere with the functions of the host cell chemokines. 117 The CMV UL21.5 mRNA is also packed within the virion, and its protein binds and blocks the function of CCL5 (Rantes), 118 whereas the CMV-encoded protein US28 blocks CCL5 function. 119 KSHV expresses the viral chemokine vCCL2, which is a broad-spectrum chemokine receptor antagonist, which might impair the recruitment of antiviral immune cells to the site of infection.…”

Section: Open Accessmentioning

confidence: 99%

Molecular mechanisms of human herpes viruses inferring with host immune surveillance

Jasinski‐Bergner

Mandelboim

Seliger

2020

J Immunother Cancer

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Several human herpes viruses (HHVs) exert oncogenic potential leading to malignant transformation of infected cells and/or tissues. The molecular processes induced by viral-encoded molecules including microRNAs, peptides, and proteins contributing to immune evasion of the infected host cells are equal to the molecular processes of immune evasion mediated by tumor cells independently of viral infections. Such major immune evasion strategies include (1) the downregulation of proinflammatory cytokines/chemokines as well as the induction of anti-inflammatory cytokines/chemokines, (2) the downregulation of major histocompatibility complex (MHC) class Ia directly as well as indirectly by downregulation of the components involved in the antigen processing, and (3) the downregulation of stress-induced ligands for activating receptors on immune effector cells with NKG2D leading the way. Furthermore, (4) immune modulatory molecules like MHC class Ib molecules and programmed cell death1 ligand 1 can be upregulated on infections with certain herpes viruses. This review article focuses on the known molecular mechanisms of HHVs modulating the above-mentioned possibilities for immune surveillance and even postulates a temporal order linking regular tumor immunology with basic virology and offering putatively novel insights for targeting HHVs.

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Section: Open Accessmentioning

confidence: 99%

Molecular mechanisms of human herpes viruses inferring with host immune surveillance

Jasinski‐Bergner

Mandelboim

Seliger

2020

J Immunother Cancer

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“…Consequently, viral-induced chemotaxis contributes to the epidemiology and persistence of herpes viruses [394]. The high prevalence of herpes viruses in humans is principally due to their ability to establish life-long latency and their exceptional capacity to modulate the host immune responses [395]. Functions of the chemokine components of herpes viruses include: attraction of target cells, blockade of leukocyte migration, and modi ication of gene expression and cell entry by the viruses [395].…”

Section: Role Of Cytokines In Vzv Infectionsmentioning

confidence: 99%

“…Studies have shown that: (1) the transcription factor NFκβ is a key factor in inducing the expression of IFN and other proin lammatory cytokines that are involved in antiviral response, and (2) effector proteins are involved in: inhibition of protein synthesis, degradation of RNA, modulation of viral genome, activation of the innate immune system, and development of the adaptive immune response [396]. Human herpes viruses deploy viral chemokines and viral chemokine receptors as well as chemokines and chemokine receptors pirated from the host to exploit and evade the host immune response [395]. Cells respond to a variety of cytokines and chemokines that allow them to migrate in different body locations depending on where they are required [394].…”

Section: Role Of Cytokines In Vzv Infectionsmentioning

confidence: 99%

The beneficial effects of varicella zoster virus

Al-Anazi¹,

Wk²,

Al-Jasser³

2019

J Hematol Clin Res

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Varicella zoster virus behaves differently from other herpes viruses as it differs from them in many aspects. Recently, there has been growing evidence on the benefi cial effects of the virus in immune compromised hosts and these effects are translated into prolongation of survival. The reported benefi cial effects of the virus include: (1) stimulation of bone marrow activity in patients with hematologic malignancies and bone marrow failure syndromes, (2) antitumor effects in various hematologic malignancies and solid tumors, and (3) association with graft versus host disease which has anticancer effects. Additionally, there are several reports on the safety of the live-attenuated even in severely immune suppressed individuals and on the emerging role of the virus in cancer immunotherapy. In this review, the following aspects of the virus will be thoroughly discussed: (1) new data on the genetic background, pathogenesis, vaccination, and new therapeutic modalities; (2) bone marrow microenvironment and hematopoiesis; (3) cells involved in the pathogenesis of the virus such as: mesenchymal stem cells, dendritic cells, natural killer cells, T-cells and mononuclear cells; (4) cellular proteins such as open reading frames, glycoproteins, promyelocytic leukemia protein, chaperons, and SUMOs; (5) extracellular vesicles, exosomes, and micro-RNAs; and (6) signaling pathways, cytokines, and interferons.

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“…These include the ability to alter the repertoire of molecules expressed on cell surfaces and chemokine and cytokine expression and secretion [8]. Another immunomodulation strategy utilized by herpesviruses, including HHV-6, is the ability to encode viral chemokines and chemokine receptors [9]. HHV-6 encodes two viral chemokine receptors U12 and U51, which are structurally similar to cellular G protein-coupled receptors (GPCR) [10], but the role of these genes is not well understood.…”

Section: Introductionmentioning

confidence: 99%

Immunological Investigations of HHV-6 U12 and U51 Encoded Proteins Involvement in Autoimmune Thyroiditis Development

Sultanova

Cistjakovs

Sokolovska

et al. 2020

Preprint

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Human herpesvirus 6 (HHV-6) is a human pathogen with a wide cell tropism and many immunomodulating properties. HHV-6 has been linked to the development of multiple diseases, among them – autoimmune. Conflicting evidence implicates HHV-6 in autoimmune thyroiditis (AIT). HHV- 6 contains two genes (U12 and U51) that encode putative homologues of human G-protein-coupled receptors (GPCR) like CCR1, CCR3 and CCR5. It has been shown that proteins encoded by HHV-6 U12 and U51 genes can be expressed on the surface of epithelial and some peripheral blood mononuclear cells populations, which makes them a potential cause for evoking autoimmunity.

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Chemokine Subversion by Human Herpesviruses

Cited by 25 publications

References 131 publications

Molecular mechanisms of human herpes viruses inferring with host immune surveillance

Molecular mechanisms of human herpes viruses inferring with host immune surveillance

The beneficial effects of varicella zoster virus

Immunological Investigations of HHV-6 U12 and U51 Encoded Proteins Involvement in Autoimmune Thyroiditis Development

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