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Ebola Virus
Linda Kidd, DVM, PhD, DACVIM

College of Veterinary Medicine, Western University of Health Sciences, Pomona, CA, USA

Etiology/Pathophysiology Epidemiology

Ebola virus is an enveloped, negative‐sense RNA virus Ebola was first discovered in 1976 near the Ebola River in
belonging to the genus Ebolavirus in the family Filoviridae. what is now the Democratic Republic of Congo. Several
Filoviruses cause severe lethal hemorrhagic disease in epidemics have occurred in Africa. The largest outbreak
people. The Ebola viral genome encodes a nucleoprotein began in 2014 and involved several West African coun-
(NP), a glycoprotein (GP), an RNA polymerase (L), and tries. It was considered ended in 2016. Infection has been
four structural proteins (VP 24, VP30, VP 35, and VP 40). reported in healthcare workers returning from Africa in
A soluble form of GP thought to be important in evading a few countries, including the United States, Spain, and
humoral immunity is produced through receptor editing. the United Kingdom. Further spread in these countries
The primary target cells of Ebola virus are dendritic has not occurred.
cells (DC) and macrophages. Other cells, including Handling of dead infected animals or consumption of
hepatocytes, endothelial cells, fibroblasts, and cells of infected primates was thought to be the mechanism of
the adrenal gland, can be infected. entry into the human population. Human‐to‐human
Ebola virus can both inhibit and evade innate and adap- spread is the primary means of infection in people. Infection
tive immunity. For example, the virus inhibits interferon occurs by exposure to bodily fluids through mucous
(IFN)‐alpha, IFN‐beta, and IFN‐gamma production. membranes or broken skin, or inoculation via needle sticks.
Infection also inhibits DC expression of CD 40, CD 80/86, Importantly, fomites may also play a role in transmission.
and MHC II, co‐stimulatory molecules that are important The incubation period is thought to be 2–21 days.
in the induction of adaptive immunity. Examples of eva- Bats are believed to be the reservoir host in Africa but this
sion tactics include shielding of GP epitopes that may be has not been confirmed. A summary of surveillance studies
recognized by the immune system, and releasing soluble of naturally infected species in outbreak areas detected
GPs that act as “decoys” that bind protective antibodies. virus in nonhuman primates and bats and an ungulate.
Despite being able to avoid immune recognition, Recovered human patients can still shed the virus in semen
infection is associated with massive production of proin- and virus has been amplified from bodily fluids in patients
flammatory cytokines. Thus, additional cells are with uveitis and meningoencephalitis after recovery.
recruited and available for the virus to infect. The Antibodies have been detected in additional species,
systemic effects of cytokines cause systemic inflamma- including dogs; 27.2% of dogs had formed antibodies to
tory response syndrome (SIRS). Increased vascular per- the virus in a survey of a 2001–2002 outbreak of Ebola in
meability and endothelial cell activation associated with people in Gabon. Dogs in the study were not ill. The dogs
infection are in part mediated by GP. Disordered hemo- were thought to be exposed to Ebola virus by eating car-
stasis may arise from endothelial cell dysfunction and cases of dead infected wild animals (bush meat) and
damage. Tissue factor expression induced by virus or vomit of infected people. No virus was amplified from
cytokines appears to play a major role in activation of the blood samples. A recent in vitro study suggested that
coagulation and induction of disseminated intravascular both canine and feline cells are less susceptible to infec-
coagulation (DIC). tion than primate and human cells.

Clinical Small Animal Internal Medicine Volume II, First Edition. Edited by David S. Bruyette.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/bruyette/clinical