Saliva of Ixodes ricinus enhances TBE virus replication in dendritic cells by modulation of pro-survival Akt pathway
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
29156399
DOI
10.1016/j.virol.2017.11.008
PII: S0042-6822(17)30379-3
Knihovny.cz E-resources
- Keywords
- Dendritic cells, Signaling, TBEV, Tick saliva,
- MeSH
- Apoptosis MeSH
- Arachnid Vectors virology MeSH
- Dendritic Cells cytology metabolism virology MeSH
- Ixodes virology MeSH
- Encephalitis, Tick-Borne metabolism physiopathology transmission virology MeSH
- Humans MeSH
- Guinea Pigs MeSH
- Mice, Inbred C57BL MeSH
- Mice MeSH
- Proto-Oncogene Proteins c-akt genetics metabolism MeSH
- Virus Replication MeSH
- Saliva virology MeSH
- STAT1 Transcription Factor genetics metabolism MeSH
- Encephalitis Viruses, Tick-Borne genetics physiology MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Guinea Pigs MeSH
- Mice MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Proto-Oncogene Proteins c-akt MeSH
- STAT1 Transcription Factor MeSH
It has been suggested that tick saliva facilitates transmission of tick-borne encephalitis virus (TBEV) to vertebrates. The mechanism of this facilitation has not been elucidated yet. Since dendritic cells (DCs) are among first cells attacked by the virus, we examined the amount of virus and changes induced by saliva in TBEV-infected DCs. We found that virus replication was significantly increased by saliva of Ixodes ricinus tick. Next, saliva-induced enhancement of Akt pathway activation was observed in TBEV-infected DCs. Akt mediated pathway is known for its anti-apoptotic and pro-survival effects. Accordingly, apoptosis of TBEV-infected DCs was declined and cellular viability increased in the presence of tick saliva. Saliva-induced enhancement of STAT1 and NF-κB was also observed in TBEV-infected DCs. In conclusion, we suggest that tick saliva provides pro-survival and anti-apoptotic signals to infected DCs via upregulation of Akt, which may have positive consequences for TBEV replication and transmission.
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