Viral Immunol. 2014 Nov 14. [Epub ahead of print]
Immune Evasion in Ebolavirus Infections.
Abstract
Abstract
Ebola virus (EBOV) infects humans as well as several animal species. It can lead to a highly lethal disease, with mortality rates approaching 90% in primates. Recent advances have deepened our understanding of how this virus is able to prevent the development of protective immune responses.
The EBOV genome encodes eight proteins, four of which were shown to interact with the host in ways that counteract the immune response.
The viral protein 35 (VP35) is capable of capping dsRNA and interacts with IRF7 to prevent detection of the virus by immune cells.
The main role of the soluble glycoprotein (sGP) is still unclear, but it is capable of subverting the anti-GP1,2 antibody response.
The GP1,2 protein has shown anti-tetherin activity and the ability to hide cell-surface proteins.
Finally, VP24 interferes with the production of interferons (IFNs) and with IFN signaling in infected cells.
Taken together, these data point to extensive adaptation of EBOV to evade the immune system of dead end hosts.
While our understanding of the interactions between the human and viral proteins increases, details of those interactions in other hosts remain largely unclear and represent a gap in our knowledge.
Ebola virus (EBOV) infects humans as well as several animal species. It can lead to a highly lethal disease, with mortality rates approaching 90% in primates. Recent advances have deepened our understanding of how this virus is able to prevent the development of protective immune responses.
The EBOV genome encodes eight proteins, four of which were shown to interact with the host in ways that counteract the immune response.
The viral protein 35 (VP35) is capable of capping dsRNA and interacts with IRF7 to prevent detection of the virus by immune cells.
The main role of the soluble glycoprotein (sGP) is still unclear, but it is capable of subverting the anti-GP1,2 antibody response.
The GP1,2 protein has shown anti-tetherin activity and the ability to hide cell-surface proteins.
Finally, VP24 interferes with the production of interferons (IFNs) and with IFN signaling in infected cells.
Taken together, these data point to extensive adaptation of EBOV to evade the immune system of dead end hosts.
While our understanding of the interactions between the human and viral proteins increases, details of those interactions in other hosts remain largely unclear and represent a gap in our knowledge.
- PMID:
- 25396298
- [PubMed - as supplied by publisher]
- Kommentti: Herää kysymys: Onko EBOLA jo nyt myöhäisessä kehityksessään pandemisessa vaiheessa, jossa on suuri aukko alkuvaiheissa, koska se tapahtuu eläimissä jotka eivät koske ihmisten karjataloutta.
- Siis kuka EI sairastuisi ebolaviruksesta nykyihmiskunnassa? Ja miksi?
- Tässä muistui mieleen lähetyssaaranajien kertomus Ugandassa, missä lapset pyydystivät rottia koulumatkalle evääkseen, ja menivät raaka kuollut rota olkapäillä kouluun. Jyrsijät olivat siis tavallaan kuin karjaeläimiä. Tästä ei ole montaa vuosikymmentä. Tapa voi vieläkin olla olemassa.Lieneekö Ugandan alueella ebolavasta-aineita ihmisissä?
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