Ebola Virus: An Updated Review on Immunity and Vaccine

Abstract

Ebola virus (EBOV) is one of the most dangerous viruses in the world which causes fatal hemorrhagic fever syndrome both in humans and nonhuman primates. Major innate immunity mechanisms against EBOV are associated with the production of interferon's that are inhibited by viral proteins. Activation of host NK cells was recognized as a leading immune function responsible for recovery of EBOV infected people. Uncontrolled cell infection by EBOV leads to an impairment of immunity. EBOV proteins interaction with host cellular proteins disrupt type I and type II interferon responses, RNAi antiviral responses, antigen presentation, T-cell-dependent B cell responses, humoral immunity, and cell-mediated immunity. These multifaceted approaches to evasion and suppression of innate and adaptive immune responses in their target hosts lead to the severe immune deregulation and "cytokine storm" that is characteristic of fatal EBOV infection. Long-term control of viral outbreaks requires the use of vaccines to impart acquired resistance and ensuing protection. Development of a safe and efficacious vaccine against EBOV has proven elusive so far, but various inventive strategies are now being employed to counteract the threat of outbreaks caused by EBOV and related filoviruses. This review highlights the host immune responses to EBOV infection, its ability to subvert host immunity and discuss recent advances in prevention of EBOV infection by vaccination.

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“…Injected VLPs recruited nearly twice the number of NK cells in both the mediastinal lymph node and spleen compared to animals receiving PBS alone. 58 This finding indicates that administration of VLP induces NK cell proliferation in mice lymphoid tissues with VLP-pretreatment lacking functional NK cells 63,64 while, using antiasialoGM1 antibodies in mice with depleted NK cells did not protect from EBOV infection, unlike VLP injected wild-type C57Bl/6mice. Moreover, native mice against EBOV infection protected by the adoptive transfer of NK cells which are stimulated in association with VLPs.…”

“…Entry pathway of Ebola Virus into host cell. 64 Upon binding to cell-surface receptors, Ebola gets internalized in endosome. Within endosome, endosomal proteases: cathepsin B and cathepsin L, slash the viral GP1 protein into N-terminal fragment and then cathepsin B digests it further into only GP2.…”