Only the IL10 promoter rs1800872 SNP was associated with predisposition to chronic hepatitis C. This SNP seems to be a common genetic marker of predisposition to two diseases caused by hepatitis C and tick-borne encephalitis viruses in Russian population.
Using HSP70 in the content of the chimeric protein represents an efficient means for presenting the main antigenic domain of the TBEV envelope protein to the immune system, whereas the incorporation of this chimeric protein into the TI-complex further contributes to the development of a stronger immune response against the TBEV infection.
Furthermore, in the SIT group cellular parameters reflected the induction of immunomodulation due to increased Tregs, elevated baseline IL10 and lack of TBE-specific IL5.
The fusion peptides are derived from the influenza virus hemagglutinin fusion protein (HA2-FP) and from the tick-borne encephalitis virus envelope glycoprotein E (TBEV-FP).
A comparative analysis on the physicochemical properties of tick-borne encephalitis virus envelope protein residues that affect its antigenic properties.
Among nine genes associated with severe forms of TBEV infection, three genes/proteins (CCR5, IL10, ARID1B) were found to have protein-protein interactions within the network, and two genes/proteins (IFNL3 and the IL10, that was just mentioned) were up- or down-regulated in response to TBEV infection.
In this study we aimed to search for the relationship between single nucleotide polymorphism in the promoter region of the CD209, IL-10, IL-28 and 32 base pair deletion in CCR5 coding region (Δ 32) with the human predisposition to development of various clinical presentations of TBE.
Recombinant domains III of Tick-Borne Encephalitis Virus envelope protein in combination with dextran and CpGs induce immune response and partial protectiveness against TBE virus infection in mice.
The results obtained suggest that both studied IL28B gene SNPs, as well as the IL10 gene rs1800872 SNP are associated with predisposition to TBE in Russian population.
Tick-borne encephalitis (TBE) and hepatitis B nonresponders feature different immunologic mechanisms in response to TBE and influenza vaccination with involvement of regulatory T and B cells and IL-10.
Sequencing of the full-length genome of this virus strain (AS33) revealed 2 unique amino acid substitutions in the envelope protein known to play a role in the pathogenicity of TBE virus.
The baculovirus expression system that utilizes Autographa californica nuclear polyhedrosis virus was used to express the highly antigenic envelope protein E of a tick-borne encephalitis (TBE) complex virus, as well as a C-terminally truncated form of protein E (Etr).
Of note, it has been described that polymorphisms in CD209, GSTM1, IL-10, IL-28B, MMP9, OAS2, OAS3, and TLR3 have a statistically significant impact on TBEV infection.
Using HSP70 in the content of the chimeric protein represents an efficient means for presenting the main antigenic domain of the TBEV envelope protein to the immune system, whereas the incorporation of this chimeric protein into the TI-complex further contributes to the development of a stronger immune response against the TBEV infection.
A comparative analysis on the physicochemical properties of tick-borne encephalitis virus envelope protein residues that affect its antigenic properties.
The serum concentration of TNFα was increased in TBE patients bearing a high-expression TLR3rs5743305 TT genotype, which also associated with the increased risk of TBE.
Recombinant domains III of Tick-Borne Encephalitis Virus envelope protein in combination with dextran and CpGs induce immune response and partial protectiveness against TBE virus infection in mice.
Previously, we reported an association between seven single nucleotide polymorphisms (SNPs) in four innate immunity genes (OAS2, OAS3, CD209, and TLR3) and human predisposition to tick-borne encephalitis, caused by a virus from the same Flaviviridae family, in a Russian population.
These results indicate that the G allele (within the G/G homozygous genotype) of the TLR3rs3775291 SNP is associated with predisposition to TBE in the Russian population.
Sequencing of the full-length genome of this virus strain (AS33) revealed 2 unique amino acid substitutions in the envelope protein known to play a role in the pathogenicity of TBE virus.
The baculovirus expression system that utilizes Autographa californica nuclear polyhedrosis virus was used to express the highly antigenic envelope protein E of a tick-borne encephalitis (TBE) complex virus, as well as a C-terminally truncated form of protein E (Etr).