Ebola virus pathogenesis and immune evasion mechanism

Identification: Pei, Jingjing


Ebola virus pathogenesis and immune evasion mechanism
Jingjing Pei
Washington University School of Medicine, Saint Louis, MO, USA
Ebola virus (EBOV) is an enveloped virus with non-segmented negative-sense genomic RNA and is classified as a member of the filovirus family, which causes sporadic outbreaks with high case fatality rates in people. Such severity of this disease caused by EBOV is due to uncontrolled virus replication and the activation of host antiviral response. Host strategies to counter viral infections, including immune response and induction of cell death, however, no approved specific therapy is available and the precise infection machinery is not yet confirmed. Thus, it is essential to clarify the characterization of the different stages of EBOV life cycle to develop novel therapeutic approaches for effectively controlling infection.
In the course of virus infection with host cells, viral RNA synthesis and virus assembly need to be completed under the protection and regulation of EBOV nucleocapsids, including eNP, eVP24, eVP35, eVP30 and eL, following by redistribution from the perinuclear region to the plasma membrane where eVP40 and eGP contribute to progeny virus release. Understanding which viral protein plays key role in the different steps of EBOV life cycle is very critical for controlling disease transmission. Our lab has done a lot of work on virus pathogenesis, particularly the RNA synthesis and innate immune escape mechanisms depending on the structural basis and biochemical methods, which can provide deeper insight into probability for controlling viral infection. Our recent results point to a significant role of the host cytoskeleton. Using a combination of microscopy, structural and biochemical studies, we will describe how the virus usurps the host cytoskeleton to promote virus replication that leads to pathogenesis. These new observations not only provide insights into new biology, but also identify novel therapeutic targets.


Credits: None available.

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