Diagnosis is confirmed by testing blood samples for the presence of viral RNA, viral antibodies or the virus itself.Control of outbreaks requires coordinated medical services and community engagement, including rapid detection, contact tracing of those exposed, quick access to laboratory services, care for those infected, and proper disposal of the dead through cremation or burial. Samples of body fluids and tissues from people with the disease should be handled with extreme caution. Prevention measures include wearing proper protective clothing and washing hands when around a person with the disease, and limiting the spread of the disease from infected animals to humans – by wearing protective clothing while handling potentially infected bushmeat, and by cooking bushmeat thoroughly before eating it. An Ebola vaccine was approved in the United States in December 2019. While there is no approved treatment for Ebola as of 2019, two treatments (atoltivimab/maftivimab/odesivimab and ansuvimab) are associated with improved outcomes. Supportive efforts also improve outcomes. These include oral rehydration therapy (drinking slightly sweetened and salty water) or giving intravenous fluids, and treating symptoms. In October 2020, Atoltivimab/maftivimab/odesivimab (Inmazeb) was approved for medical use in the United States to treat the disease caused by Zaire ebolavirus.The disease was first identified in 1976, in two simultaneous outbreaks: one in Nzara (a town in South Sudan) and the other in Yambuku (the Democratic Republic of the Congo), a village near the Ebola River, from which the disease takes its name. Ebola outbreaks occur intermittently in tropical regions of sub-Saharan Africa.
EBOV proteins blunt the human immune systems response to viral infections by interfering with the cells ability to produce and respond to interferon proteins such as interferon-alpha, interferon-beta, and interferon gamma.The VP24 and VP35 structural proteins of EBOV play a key role in this interference. When a cell is infected with EBOV, receptors located in the cells cytosol (such as RIG-I and MDA5) or outside of the cytosol (such as Toll-like receptor 3 (TLR3), TLR7, TLR8 and TLR9) recognise infectious molecules associated with the virus. On TLR activation, proteins including interferon regulatory factor 3 and interferon regulatory factor 7 trigger a signalling cascade that leads to the expression of type 1 interferons. The type 1 interferons are then released and bind to the IFNAR1 and IFNAR2 receptors expressed on the surface of a neighbouring cell. Once interferon has bound to its receptors on the neighbouring cell, the signalling proteins STAT1 and STAT2 are activated and move to the cells nucleus. This triggers the expression of interferon-stimulated genes, which code for proteins with antiviral properties. EBOVs V24 protein blocks the production of these antiviral proteins by preventing the STAT1 signalling protein in the neighbouring cell from entering the nucleus. The VP35 protein directly inhibits the production of interferon-beta. By inhibiting these immune responses, EBOV may quickly spread throughout the body. Diagnosis
When EVD is suspected, travel, work history, and exposure to wildlife are important factors with respect to further diagnostic efforts.