Novel Variant of Tickborne Encephalitis Virus, Russia

Терновой, В. А.; Протопопова, Е. В.; Чаусов, Е. В.; Новиков, Д. В.; Леонова, Г Н; Netesov, Sergey V.; Локтев, В Б

doi:10.3201/eid1310.070158

Cited by 22 publications

(10 citation statements)

References 8 publications

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“…These results confirm the results of the authors' previous studies (20,26) as well as other studies that showed replication of highly virulent strains of TBEV starting from 12 h pi by using different cell cultures (31,35,45,52).…”

Section: Dynamics Of Infection Of Donors' Blood Cells By Tbev Strainssupporting

confidence: 95%

Molecular Mechanisms of Interaction Between Human Immune Cells and Far Eastern Tick-Borne Encephalitis Virus Strains

2015

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Although studies have established that immune mechanisms are important in controlling tick-borne encephalitis virus (TBEV) infection, the interactions of different TBEV strains with cells of innate and adaptive immunity are not well understood. In this study, the ability of two Far Eastern subtype TBEV strains (Dal'negorsk and Primorye-183) with various degrees of pathogenicity for humans to modulate the expression of membrane molecules differently on human immune cells were investigated using a whole-blood flow cytometry-based assay. The whole-blood samples (from 10 healthy donors) were infected with TBEV strains and analyzed for the virus binding to the blood cells, as well as expression of adhesion (CD11b and ICAM-1) and activation (CD69, CD25, CD95) molecules on the surfaces of monocytes, granulocytes, natural killer (NK) cells, and T-lymphocytes (CD4+, CD8+) at selected times (3, 6, and 24 h post-infection). It was found that the highly pathogenic Dal'negorsk strain penetrated rapidly and was actively replicated in the blood cells, inducing downregulation of CD11b, ICAM-1, and CD69 on monocytes and a significant decrease of NK cells expressing CD69, CD25, CD95, and CD8 T-lymphocytes expressing CD69 compared with the mock-infected cells. The nonpathogenic Primorye-183 strain penetrated slowly and was replicated in the blood cells, but caused a significant increase in the adhesion and activation of molecule expression to trigger innate defense mechanisms and enable the rapid elimination of the virus from the organism. Thus, TBEV-induced activation or suppression of adhesion and activation receptors expression form an essential part of fundamental virus properties, that is, virulence and pathogenicity.

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Section: Dynamics Of Infection Of Donors' Blood Cells By Tbev Strainssupporting

confidence: 95%

Molecular Mechanisms of Interaction Between Human Immune Cells and Far Eastern Tick-Borne Encephalitis Virus Strains

2015

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“…However, to investigate more detailed and improved phylogeny of TBEV, a complete genome-based phylogenetic analysis is indispensable. Here, we performed a larger phylogenetic analysis than a previous study [37], using 31 fully sequenced TBEV strains and two complete polyprotein sequences. The complete genome-based phylogenetic tree showed that viruses were obviously divided three distinct subtypes and revealed that the two TBEV Korean strains are more closely related to the Salem and Czech 263 strains of the Western subtype than to other TBEV strains.…”

Section: Discussionmentioning

confidence: 99%

First complete genomic characterization of two tick-borne encephalitis virus isolates obtained from wild rodents in South Korea

Yun

Kim

et al. 2011

Virus Genes

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We determined for the first time the complete genome sequences of two Korean strains of the tick-borne encephalitis virus (TBEV), designated KrM 93 and KrM 213, isolated from the lung tissues of wild rodents in 2006. The genomes are 11,097 nucleotides (nt) in length and consist of a 132 nt 5'-noncoding region (NCR), a 10,245 nt open reading frame (ORF) containing 10 viral protein-coding regions (3,415 amino acids), and a 720 nt 3'-NCR. Compared with the 31 fully sequenced TBEV strains currently available, KrM 93 and KrM 213 show genomic nucleotide (and deduced amino acid) sequence divergences ranging from 1.8 (0.7) to 19.2 (26.6)% and 1.9 (0.8) to 19.3 (26.7)%, respectively. Phylogenetic and recombination analyses based on the complete genome sequence were performed to identify genetic variations and relationships between the TBEV strains. These showed that the Korean TBEV strains clustered with the Western subtype rather than with Far-Eastern or Siberian subtypes, and phylogenetic trees derived from capsid (C), envelope (E), nonstructural (NS) 4B and NS5 regions represented the same branching pattern shown by the complete genome-based tree. Although no recombination events were identified in these two Korean strains, 11 putative recombination events were identified within the NS5 regions or in the 3'-NCRs of TBEV strains in general. The results provide insight into the genetics of TBEV strains to understand the molecular epidemiology, genetic diversity, and evolution of TBEV.

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“…TBEV antigens were detected via enzyme immunoassay analysis as described previously (Ternovoi et al 2007). Briefly, the viral antigen was captured on the surface of 96-well polystyrene plates from 100 µl of the homogenates of ticks and internal organs (spleen, liver and brain from individual bird) using monoclonal antibodies 10H10 against protein E of TBEV that was preliminarily immobilised on the plates.…”

Section: Enzyme Immunoassaymentioning

confidence: 99%

Detection of tick-borne pathogens in wild birds and their ticks in Western Siberia and high level of their mismatch

et al. 2021

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Novel Variant of Tickborne Encephalitis Virus, Russia

Cited by 22 publications

References 8 publications

Molecular Mechanisms of Interaction Between Human Immune Cells and Far Eastern Tick-Borne Encephalitis Virus Strains

Molecular Mechanisms of Interaction Between Human Immune Cells and Far Eastern Tick-Borne Encephalitis Virus Strains

First complete genomic characterization of two tick-borne encephalitis virus isolates obtained from wild rodents in South Korea

Detection of tick-borne pathogens in wild birds and their ticks in Western Siberia and high level of their mismatch

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