INTERACTION OF EBOLA VIRUS WITH INNATE AND ADAPTIVE IMMUNE SYSTEM: AN IN SILICO STUDY
Keywords:
Ebola Virus, Innate Immune system, Adaptive Immune systemAbstract
Objective: Ebola virus (EBOV) is an extremely pathogenic, that can cause severe hemorrhagic fever in human with case fatality rates of up to 90% for which no vaccine or treatment is currently available. The mechanism underlying this lethal outcome is still unclear. However, an alteration of the immune responses represents one of the most important pathogenic mechanisms of Ebola virus infection. EBOV encodes two different proteins (VP24 and VP35) that block the induction of immune responses. Thus, we explored the potential interaction of Ebola virus proteins (VP24 and VP35) with the Toll-like receptor and MHC-1 receptor.
Methods: The interaction of Ebola virus protein towards immune system has been checked by Cluspro 2.0.
Results: Our results indicated that the Ebola Virus proteins (VP 24 and VP 35) have good interaction towards the Toll-like receptor (TLR-3) and MHC-1 which are a crucial component of innate and adaptive immune system.
Conclusion: The findings of this study will be helpful for researchers to design drugs or vaccines for the treatment/prevention of EBOV infections.
Keywords: Ebola Virus, Innate Immune system, Adaptive Immune system
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References
Wang Y, Liu Z, Dai Q. A highly immunogenic fragment derived from Zaire Ebola virus glycoprotein elicits effective neutralizing antibody. Virus Res 2014;189:254–61.
Bowen ETW, Lloyd G, Harris WJ, Platt GS, Baskerville A, Vella EE. Viral haemorrhagic fever in southern Sudan and northern Zaire: preliminary studies on the aetiological agent. Lancet 1977;309:571-3.
Johnson KM, Lange JV, Webb PA, Murphy FA. Isolation and partial characterisation of a new virus causing acute haemorrhagic fever in Zaire. Lancet 1977;309:569-71.
Peters CJ, Khan AS. Filovirus diseases. Curr Top Microbiol Immunol 1999;235:85–95.
Kumar A. Ebola virus is altered innate and adaptive immune response signalling pathways: Implications for novel therapeutic approaches. Infect Disord-Drug Targets 2016. Doi:10.2174/1871526516666160108114644. [Article in Press]
Hoenen T, Groseth A, Falzarano D, Feldmann H. Ebola virus: unraveling pathogenesis to combat a deadly disease. Trends Mol Med 2006;12:206-15.
Aderem A, Underhill DM. Mechanisms of phagocytosis in macrophages. Annu Rev Immunol 1999;17:593-623.
Alexopoulou L, Holt AC, Medzhitov R, Flavell RA. Recognition of double-stranded RNA and activation of NF-kappaB by toll-like receptor 3. Nature 2001;413:732–8.
Kumar A, Sharma N, Singh S, Sasmal D, Dev A. Oral vaccine antigen-induced immune response signalling pathways: current and future perspectives. J Vac Vaccination 2014;5:2-6.
Xu W, Edwards MR, Borek DM, Feagins AR, Mittal A, Alinger JB, et al. Ebola virus VP24 targets a unique NLS binding site on karyopherin alpha 5 to selectively compete with nuclear import of phosphorylated STAT1. Cell Host Microbe 2014;16:187–200.