[2] Four of the six known ebolaviruses, including EBOV, cause a severe and often fatal hemorrhagic fever in humans and other mammals, known as Ebola virus disease (EVD).

[citation needed] EBOV carries a negative-sense RNA genome in virions that are cylindrical/tubular, and contain viral envelope, matrix, and nucleocapsid components.

The outer viral envelope of the virion is derived by budding from domains of host cell membrane into which the GP spikes have been inserted during their biosynthesis.

[16][17][18] The overall shape of the virions after purification and visualization (e.g., by ultracentrifugation and electron microscopy, respectively) varies considerably; simple cylinders are far less prevalent than structures showing reversed direction, branches, and loops (e.g., U-, shepherd's crook-, 9-, or eye bolt-shapes, or other or circular/coiled appearances), the origin of which may be in the laboratory techniques applied.

Sections of the NP, VP35 and the L genes from filoviruses have been identified as endogenous in the genomes of several groups of small mammals.

The first is a cholesterol transporter protein, the host-encoded Niemann–Pick C1 (NPC1), which appears to be essential for entry of Ebola virions into the host cell and for its ultimate replication.

[29] In another study, small molecules were shown to inhibit Ebola virus infection by preventing viral envelope glycoprotein (GP) from binding to NPC1.

Together, these studies suggest NPC1 and TIM-1 may be potential therapeutic targets for an Ebola anti-viral drug and as a basis for a rapid field diagnostic assay.

Encapsidated, negative-sense genomic ssRNA is used as a template for the synthesis (3'–5') of polyadenylated, monocistronic mRNAs and, using the host cell's ribosomes, tRNA molecules, etc., the mRNA is translated into individual viral proteins.

[36][37][38] These viral proteins are processed: a glycoprotein precursor (GP0) is cleaved to GP1 and GP2, which are then heavily glycosylated using cellular enzymes and substrates.

[39] Ebola virus outbreaks tend to occur when temperatures are lower and humidity is higher than usual for Africa.

[40] Even after a person recovers from the acute phase of the disease, Ebola virus survives for months in certain organs such as the eyes and testes.

During the 1976 Ebola outbreak in Zaire, Ngoy Mushola travelled from Bumba to Yambuku, where he recorded the first clinical description of the disease in his daily log: The illness is characterized with a high temperature of about 39°C, hematemesis, diarrhea with blood, retrosternal abdominal pain, prostration with "heavy" articulations, and rapid evolution death after a mean of three days.

[43]Since the first recorded clinical description of the disease during 1976 in Zaire, the recent Ebola outbreak that started in March 2014, in addition, reached epidemic proportions and has killed more than 8000 people as of January 2015.

A few cases were also reported in countries outside of West Africa, all related to international travelers who were exposed in the most affected regions and later showed symptoms of Ebola fever after reaching their destinations.

[44] The severity of the disease in humans varies widely, from rapid fatality to mild illness or even asymptomatic response.

[45] Studies of outbreaks in the late twentieth century failed to find a correlation between the disease severity and the genetic nature of the virus.

Consequently, in 2010, a group of researchers recommended that the name "Ebola virus" be adopted for a subclassification within the species Zaire ebolavirus, with the corresponding abbreviation EBOV.

[56] At present, ICTV does not officially recognize "Ebola virus" as a taxonomic rank, but rather continues to use and recommend only the species designation Zaire ebolavirus.

[60][61] Then, around the 1960s, most likely due to climate change or human activities, the genetic diversity of the virus dropped rapidly and most lineages became extinct.

This genetic bottleneck effect has implications for the species' ability to cause Ebola virus disease in human hosts.