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16. Ebola Virus Disease anja.boehme.pdf

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immunoglobulin raised against EBOV has been used in Russia to treat a laboratory worker who
accidentally infected herself with EBOV—but the patient died anyway. Experimentally,
recombinant vesicular stomatitis Indiana virus (VSIV) expressing the glycoprotein of EBOV or SUDV
has been used successfully in nonhuman primate models as post-exposure prophylaxis. Such a
recombinant post-exposure vaccine was also used to treat a German researcher who accidentally
pricked herself with a possibly EBOV-contaminated needle. Treatment might have been successful as
she survived. However, actual EBOV infection could never be demonstrated without a doubt. Novel,
very promising, experimental therapeutic regimens rely on antisense technology. Both small
interfering RNAs (siRNAs) and phosphorodiamidate morpholino oligomers (PMOs) targeting the
EBOV genome could prevent disease in nonhuman primates.
Prognosis is generally poor (average case-fatality rate of all EVD outbreaks to date = 68%). If a
patient survives, recovery may be prompt and complete, or protracted with sequelae, such
as orchitis, arthralgia, myalgia, desquamation or alopecia. Ocular manifestations, such
as photophobia, hyperlacrimation, iritis, iridocyclitis, choroiditis and blindness have also been
described. Importantly, EBOV and SUDV are known to be able to persist in the sperm of some
survivors, which could give rise to secondary infections and disease via sexual intercourse.
Distribution of Ebola and Marburg virus in Africa (note that integrated genes from filoviruses have
been detected in mammals from the New World as well). (A) Known points of filovirus disease.
Projected distribution of ecological niche of: (B) all filoviruses, (C) ebolaviruses, (D) marburgviruses.
For more about specific outbreaks and their descriptions, see List of Ebola outbreaks.
Outbreaks of EVD have mainly been restricted to Africa. The virus often consumes the population.
Governments and individuals quickly respond to quarantine the area while the lack of roads and
transportation helps to contain the outbreak. EVD was first described after almost simultaneous viral
hemorrhagic fever outbreaks occurred in Zaire and Sudan in 1976. EVD is believed to occur after an
ebolavirus is transmitted to a human index case via contact with an infected animal host. Human-tohuman transmission occurs via direct contact with blood or bodily fluids from an infected person
(including embalming of a deceased victim) or by contact with contaminated medical equipment such
as needles. In the past, explosive nosocomial transmission has occurred in underequipped African
hospitals due to the reuse of needles and/or absence of proper barrier nursing. Aerosol transmission
has not been observed during natural EVD outbreaks. The potential for widespread EVD epidemics is
considered low due to the high case-fatality rate, the rapidity of demise of patients, and the often
remote areas where infections occur.
Ebola Virus Disease (EVD) Outbreaks:
Year-Virus-Geographic Location-Human Cases/Deaths (Case-Fatality Rate)
1. 1976: SUDV: Juba, Maridi, Nzara, and Tembura, Sudan: 284/151 (53%)
2. 1976: EBOV: Yambuku, Zaire: 318/280 (88%)
3. 1977: EBOV: Bonduni, Zaire: 1/1 (100%)
4. 1979: SUDV: Nzara, Sudan: 34/22 (65%)
5. 1988: EBOV: Porton Down, United Kingdom 1/0 (0%) [laboratory accident]
6. 1994: TAFV: Taï National Park, Côte d'Ivoire; Switzerland: 1/0 (0%)
7. 1994–1995: EBOV Woleu-Ntem and Ogooué-Ivindo Provinces, Gabon: 52/32 (62%)
8. 1995: EBOV: Kikwit, Zaire: 317/245 (77%)