One of the deadliest of epidemic viral diseases, Ebola virus disease (EVD) has, since its 1976 emergence, challenged our attempts to understand its ecology and epidemiology, its pathophysiology and pathogenesis, and its optimal treatment and prevention.EBOV is a nonsegmented negative-strand RNA virus with a genome size of approximately 19 kb, EBOV particles have a uniform diameter of about 80 nm but vary greatly in length (up to 14,000 nm) and form, with the filamentous form being the most characteristic. EBOV proteins have distinct functions in the replication cycle of ebolaviruses. EBOV infects cells by attaching to a variety of cellular attachment molecules, including lectintype molecules.
The surface GP undergoes proteolytic processing (i.e., by cathepsins) in the endosome, allowing it to interact with the cellular receptor cholesterol transporter NiemannPick C1 (NPC1) protein, to fuse with the endosomal membrane, and to release the RNP into the cytoplasm, where primary transcription is initiated.EBOV VP35 and VP24 are, respectively, strong inhibitors of interferon production and of interferon signaling. VP35 has multiple additional functions that interfere with the early innate host response. The functions of sGP and ssGP remain unknown. sGP has been thought to act as a decoy for antibodies that otherwise would bind to GP.

References

1.Laura Baseler,et al. Annu. Rev. Pathol. Mech. Dis. 2017. 12:15.1–15.32.