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Ebola Virus Immuno-Evasion and Cellular Dysfunctional Mechanics: A Bio-Terrorizing Agent of Zoonotic Origin

Author

Listed:
  • Iquo A. Archibong

    (Department of Biochemistry, College of Medicine, University of Ibadan, Nigeria.)

  • Mfonabasi U. Inyang

    (Department of Biochemistry, College of Medicine, University of Ibadan, Nigeria.)

  • Emmanuel Okon

    (Department of Biochemistry, College of Medicine, University of Ibadan, Nigeria.)

  • Idongesit A. Victor

    (Department of Biochemistry, College of Medicine, University of Ibadan, Nigeria.)

Abstract

Ebola virus disease remains one of the most deadly epidemic viral disease in humans, characterized by severe hemorrhagic fever, caused by Ebola viruses – an aggressive viral pathogen of a zoonotic origin. A robust immune response against pathogens requires a coordinated-synergistic activities of both innate and adaptive immunological response. However, Ebola virus attacks immune cells to compromise both innate and adaptive immunological responses against their cytopathic induction by adopting myriads of biochemical mechanisms. Ebola virus infection is mediated following viral attachment, receptor-mediated (co-receptor binding) endocytosis and macropinocytosis fusion mechanisms to invade its host cells and subsequently attacking the innate immune response cells (monocyte, macrophages, natural killer cells, dendritic cells, neurophiles, basophils and eosinophils) and the adaptive immune response cells (CD8 T-cells, CD4 T-cells, B-cells, regulatory T-cells, natural killer T-cells) to evade the immunological response of the host cell. Immuno-evasion and cellular disruption of both immune cells and non-immune cells/tissues remain one of the major hallmarks of Ebola virus infection. The biochemical mechanisms of Ebola virus disease involves rapid viral genomic integration/expression and viremic dissemination of the viral pathogen to other distant cells/tissues; induction of apoptotic signals in both healthy bystander immune cells and non-immune cells/tissues; deregulation in inflammatory response and intravascular coagulation leading to multi-cells/tissue/organs toxicities and eventually death if supportive measures are not adequate to repair and rejuvenate the Ebola virus induced disarray to its host. This review work elucidates the mechanisms of Ebola virus immuno-evasion and cellular dysfunction, geared towards providing an insightful paradigm that can be utilized to combat Ebola virus bio-terrorizing nature.

Suggested Citation

  • Iquo A. Archibong & Mfonabasi U. Inyang & Emmanuel Okon & Idongesit A. Victor, 2020. "Ebola Virus Immuno-Evasion and Cellular Dysfunctional Mechanics: A Bio-Terrorizing Agent of Zoonotic Origin," International Journal of Research and Scientific Innovation, International Journal of Research and Scientific Innovation (IJRSI), vol. 7(9), pages 324-338, September.
    • Handle: RePEc:bjc:journl:v:7:y:2020:i:9:p:324-338
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    References listed on IDEAS

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    1. Jan E. Carette & Matthijs Raaben & Anthony C. Wong & Andrew S. Herbert & Gregor Obernosterer & Nirupama Mulherkar & Ana I. Kuehne & Philip J. Kranzusch & April M. Griffin & Gordon Ruthel & Paola Dal C, 2011. "Ebola virus entry requires the cholesterol transporter Niemann–Pick C1," Nature, Nature, vol. 477(7364), pages 340-343, September.
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