Murine Gammaherpesvirus 68 (MHV-68), a Newly Discovered Tick Borne Virus

Kúdelová, M; Štibrániová, Iveta

doi:10.5772/intechopen.81025

Cited by 5 publications

(4 citation statements)

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“…In rodent populations, the virus is transmitted directly, mainly through the intranasal route. However, during the last decade, the presence of MHV-68 has repeatedly been detected by molecular methods in ticks of different species and developmental stages in Slovakia (Table 1) and the question has been raised if ticks can serve as vectors of the virus (Kúdelová and Štibrániová 2019). The first report dates back to 2011, when the presence of viral DNA was detected for the first time in I. ricinus subadults collected from green lizards (Ficová et al 2011) and subsequently in questing D. reticulatus (Kúdelová (Vrbová et al 2016), and I. ricinus adults (Kúdelová et al 2018).…”

Section: Other Viruses Detected In Ticksmentioning

confidence: 99%

Ticks and their epidemiological role in Slovakia: from the past till present

et al. 2021

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In Slovakia, 22 tick species have been found to occur to date. Among them, Ixodes ricinus, Dermacentor reticulatus, D. marginatus and marginally Haemaphysalis concinna, H. inermis and H. punctata have been identified as the species of public health relevance. Ticks in Slovakia were found to harbour and transmit zoonotic and/or potentially zoonotic agents such as tickborne encephalitis virus (TBEV), spirochaetes of the Borrelia burgdorferi sensu lato (s.l.) complex, the relapsing fever sprirochaete Borrelia miyamotoi, bacteria belonging to the orders Rickettsiales (Rickettsia spp., Anaplasma phagocytophilum, Neoehrlichia mikurensis), Legionellales (Coxiella burnetii), and Thiotrichales (Francisella tularensis), and Babesia spp. parasites (order Piroplasmida). Ixodes ricinus is the principal vector of the largest variety of microorganisms including viruses, bacteria and piroplasms. TBEV, B. burgdorferi s.l., rickettsiae of the spotted fever group, C. burnetii and F. tularensis have been found to cause serious diseases in humans, whereas B. miyamotoi, A. phagocytophilum, N. mikurensis, Babesia microti, and B. venatorum pose lower or potential risk to humans. Distribution of TBEV has a focal character. During the last few decades, new tick-borne encephalitis (TBE) foci and their spread to new areas have been registered and TBE incidence rates have increased. Moreover, Slovakia reports the highest rates of alimentary TBE infections among the European countries. Lyme borreliosis (LB) spirochaetes are spread throughout the distribution range of I. ricinus. Incidence rates of LB have shown a slightly increasing trend since 2010. Only a few sporadic cases of human rickettsiosis, anaplasmosis and babesiosis have been confirmed thus far in Slovakia. The latest large outbreaks of Q fever and tularaemia were recorded in 1993 and 1967, respectively. Since then, a few human cases of Q fever have been reported almost each year. Changes in the epidemiological characteristics and clinical forms of tularaemia have been observed during the last few decades. Global changes and development of modern molecular tools led to the discovery and identification of emerging or new tick-borne microorganisms and symbionts with unknown zoonotic potential. In this review, we provide a historical overview of research on ticks and tick-borne pathogens in Slovakia with the most important milestones and recent findings, and outline future directions in the investigation of ticks as ectoparasites and vectors of zoonotic agents and in the study of tick-borne diseases.Keywords Tick-borne pathogens . Tick-borne encephalitis virus . Borrelia . Anaplasma . Rickettsia . Coxiella burnetii . Francisella tularensis . Babesia

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Section: Other Viruses Detected In Ticksmentioning

confidence: 99%

Ticks and their epidemiological role in Slovakia: from the past till present

et al. 2021

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“…Recently, experimental transmission of MHV-68 between I. ricinus ticks and mouse and vice versa proved that MHV-68 could be vertically and horizontally transmitted from F0 to F1 tick generation, and thus, MHV-68 is suggested to be a tick-borne virus. (Hajnická et al, 2017;Kúdelová and Štibrániová, 2019). The recently characterized RHVP was found to be related to MHV-68 and KSHV; it was isolated from a lung homogenate of a pygmy rice rat (oligoryzomys microtis) trapped in Peru (Loh et al, 2011).…”

Section: Chemokine-binding Proteins Encoded By γ-Herpesvirusesmentioning

confidence: 99%

Chemokine-binding proteins encoded by herpesviruses

Benko¹,

Lenhartová²,

Kempová³

et al. 2020

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To establish infection, a wide variety of pathogens, including viruses, have evolved a number of strategies to avoid immune elimination. Viruses have acquired and optimized molecules that interact with the host chemokine network in order to disrupt immune surveillance and defense of vertebrates, helping to promote cell entry, facilitating dissemination of infected cells, and evasion the immune response. Viral immunomodulators include ligands, chemokine receptors and chemokinebinding proteins (vCKBPs) functioning as either cell surface receptor mimics, ligand mimics, or secreted chemokine-binding proteins. vCKBPs specifically modulate chemokine gradient formation and ligandreceptor recognition when they have a potential to even completely block chemokine-mediated responses to viral infection. Members of only two virus families (Herpesviridae and Poxviridae) encode vCKBPs capable of sequestering host chemokines through either the chemokine receptor, GAG-binding pocket, or both, which may result in the inhibition of chemotaxis in vivo. Here, we focused on vCKBPs encoded by α-, β-, and γ-herpesviruses, of which several have been experimentally used as anti-inflammatory or anti-immune reagents in animal models. Current results suggest that vCKBPs could be used to regulate the activity of both chemokines and chemokine receptors for the treatment of infections such as AIDS, diseases such as arthritis, neurotrauma, inflammatory CNS disorders, atherosclerosis, transplant rejection, and metastatic spread and angiogenesis. Better understanding of vCKBPs biology will help evaluate, which human diseases related to chemokine network dysregulation might be effectively treated with these novel promising immunomodulatory drugs to enable the manipulation of chemokine functions and leukocyte trafficking.

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“…In addition to MHV-68, closely related MHV-72 and MHV-4556 strains have also been thoroughly studied with respect to their pathogenicity and molecular properties [14]. Recently, MHV-68 pathogenesis was also shown in ticks, thereby making MHV-68 an arthropod-borne virus (arbovirus) [15,16]. Most recent studies, however, have focused on the immunomodulatory M3 (44 kDa) encoded by MHV-68, which has an exceptional ability among viral immunomodulators to bind a wide range of chemokines [17].…”

Section: Introductionmentioning

confidence: 99%

Residue Mutations in Murine Herpesvirus 68 Immunomodulatory Protein M3 Reveal Specific Modulation of Chemokine Binding

Šebová¹,

Bauerová-Hlinková²,

Beck³

et al. 2020

Prime Archives in Microbiology

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The M3 protein (M3) encoded by murine gammaherpesvirus 68 (MHV-68) is a unique viral immunomodulator with a highaffinity for a broad spectrum of chemokines, key mediators responsible for the migration of immune cells to sites of inflammation. M3 is currently being studied as a very attractive and desirable tool for blocking the chemokine signaling involved in some inflammatory diseases and cancers. In this study, we elucidated the role of M3 residues E70 and T272 in binding to chemokines by examining the effects of the E70A and T272G mutations on the ability of recombinant M3, prepared in Escherichia coli cells, to bind the human chemokines CCL5 and CXCL8. We found that the E70A mutation enhanced binding of M3 to CCL5 two-fold but had little effect on its binding to Prime Archives in Microbiology 3 www.videleaf.com CXCL8. In contrast, the T272G mutation was found to be important for thermal stability of M3 and significantly decreased M3's binding to both CCL5 (by about 4×) and CXCL8 (by about 5×). We also constructed in silico models of the wild-type M3-CCL5 and M3-CCL8 complexes and found substantial differences in their physical and chemical properties. Models of the E70A and T272G M3 mutants suggested the roles of these two residues in chemokine binding. In sum, we have confirmed that site-directed mutagenesis could be an effective tool for modulating the blockade of particular chemokines by M3, as desired in therapeutic treatments for severe inflammatory illnesses arising from chemokine network dysregulation.

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Murine Gammaherpesvirus 68 (MHV-68), a Newly Discovered Tick Borne Virus

Cited by 5 publications

References 74 publications

Ticks and their epidemiological role in Slovakia: from the past till present

Ticks and their epidemiological role in Slovakia: from the past till present

Chemokine-binding proteins encoded by herpesviruses

Residue Mutations in Murine Herpesvirus 68 Immunomodulatory Protein M3 Reveal Specific Modulation of Chemokine Binding

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