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Marburg and Ebola Virus Infections
Published in James H. S. Gear, CRC Handbook of Viral and Rickettsial Hemorrhagic Fevers, 2019
The Sudanese outbreak involved 284 cases with 151 deaths (53%), and in the Zaire outbreak there were 318 cases with 280 deaths (88%). The significantly higher case-fatality rate in Zaire is attributable to the greater virulence of the Zaire Ebola virus than of the Sudanese isolate, as suggested by clinical and epidemiologic differences during the 1976 epidemics. Bo wen et al. confirmed these observations experimentally; other investigators, by polypeptide structural analyses, demonstrated that the Zairean and Sudanese Ebola virus isolates are two distinct biotypes.14,15 They were found to be relatively stable, and Buchmeier et al. concluded that the occurrence of two almost simultaneous and identical epidemics in the same region represents a remarkable coincidence and was not due to transport of the hitherto unknown etiologic agent from Sudan to Zaire as originally believed.16Figure 4 shows the geographic areas involved.
African Cities and Ebola
Published in Igor Vojnovic, Amber L. Pearson, Gershim Asiki, Geoffrey DeVerteuil, Adriana Allen, Handbook of Global Urban Health, 2019
Zacchaeus Anywaine, Ggayi Abubaker Mustapher
The 2014–2016 Ebola outbreak in West Africa started as a small localized outbreak from one village in Guinea, where an 18-month-old boy is believed to have been infected by bats in December 2013 (CDC 2018). The occurrence of this index case was followed in January 2014 by five reports of death from diarrhea in the same locality. In March 2014 the Guinea Ministry of Health issued a public alert for morbidity and mortality following an undiagnosed disease. Tests at the Pasteur Institute in France confirmed it to be EVD caused by the Zaire ebolavirus species. By the end of March 2014 over 49 cases and 29 deaths had been confirmed to be due to EVD. An unknown large number of people had come in contact with the cases or asymptomatic contacts. In July 2014, the outbreak had progressed to a full-blown epidemic affecting both the rural populations and the metropolitan cities of Conakry, Freetown and Monrovia.
Viruses
Published in Loretta A. Cormier, Pauline E. Jolly, The Primate Zoonoses, 2017
Loretta A. Cormier, Pauline E. Jolly
Zaire ebolavirus is the most virulent and has been responsible for outbreaks in central and western Africa, documented since 1976 with mortality rates ranging from 36% to 90% (Tseng and Chan 2015). The 1976 outbreak was worsened by the inadvertent spread of the disease through the reuse of unsterilized needles and syringes, as well as causes of nosocomial transmission through the health care system (Geisbert 2015). The most recent epidemic occurred between 2014 and 2016 with 28,000 cases and 11,000 deaths, primarily in Guinea, Liberia, and Sierra Leone (Shagari et al. 2016). In addition, the disease was exported by travelers to the U.S., U.K., Spain, and Sardinia. The virus is extremely contagious and if strict body fluid precautions are not taken, it can spread to health care workers and other patients and as a community infection (Geisbert 2015).
The role of sialic acid-binding immunoglobulin-like-lectin-1 (siglec-1) in immunology and infectious disease
Published in International Reviews of Immunology, 2023
Shane Prenzler, Santosh Rudrawar, Mario Waespy, Sørge Kelm, Shailendra Anoopkumar-Dukie, Thomas Haselhorst
Ebola viruses belong to the Filoviridae family and consist of many strains which are capable of causing hemorrhagic fever [27]. Ebola viruses also utilize dendritic cells and macrophages to disseminate to the lymph nodes, liver and spleen [88]. Ebola virus dendritic cell entry involves several steps requiring multitude of receptors. DC-SIGN mediates attachment of the Ebola virus to dendritic cells by glycoprotein recognition, meanwhile TIM/TAM receptors bind phosphatidylserine on the membrane of virus facilitating viral cell entry by means of apoptotic mimicry [89–91]. From here Ebola viruses enters the cell after macropinocytosis and the viral glycoprotein is cleaved using cellular proteases like cathepsin B [27, 92]. The cleavage allows for glycoprotein recognition by endosome receptor Niemann-Pick C1, which allows the virus to enter the cytoplasm [93, 94]. It was recently discovered that in a similar way to HIV-1, ebola virus buds from host cells and incorporates GM1 gangliosides which bind Siglec-1 [27]. The role of Siglec-1 in attachment and entry of Ebola virus is poorly understood, but it has been shown that anti-Siglec-1 antibodies are able to hinder viral entry and that Siglec-1 is more prominent to the entry of the virus than other well-known receptors like DC-SIGN [27]. Currently, there are studies underway to create vaccines for Zaire ebolavirus (ZEBOV), which is the species responsible for a recent outbreak in West Africa. However, there are other species which will not be covered by vaccine efforts and Siglec-1 may represent an important therapeutic target [27].
Ebola vaccine trials: progress in vaccine safety and immunogenicity
Published in Expert Review of Vaccines, 2019
Keesha M. Matz, Andrea Marzi, Heinz Feldmann
Ebolaviruses, in the Filoviridae family, were first recognized in 1976 during simultaneous outbreaks in what is now known as the Democratic Republic of Congo (DRC) and South Sudan [1,2]. Ebola virus (EBOV), Sudan virus (SUDV), and Bundibugyo virus (BDBV), representing the Zaire ebolavirus, Sudan ebolavirus, and Bundibugyo ebolavirus species of the genus Ebolavirus, respectively, have been implicated as the cause of human disease outbreaks in Africa with case fatality rates ranging from 25% to 90% [3]. Ebola virus disease (EVD) initially starts with rather unspecific symptoms such as fever, headache, myalgia, and arthralgia, quickly developing into severe diarrhea, systemic inflammatory responses, vascular permeability and coagulopathies leading to multi-organ failure followed by shock and death [4]. Ebolaviruses are zoonotic in nature and animal-to-human transmission has occurred during spillover events with bats (tentative reservoir) as well as nonhuman primates (intermediate/amplifying as well as end host) [5,6]. Human-to-human transmission can occur within a population through close contact with blood and bodily fluids from infected individuals [7,8]. There are no ebolavirus-specific vaccines or antivirals licensed by the U.S. Food and Drug Administration (FDA); however, the Chinese, Russian and European regulatory agencies have approved three EBOV vaccines.
From bench to almost bedside: the long road to a licensed Ebola virus vaccine
Published in Expert Opinion on Biological Therapy, 2018
Gary Wong, Emelissa J. Mendoza, Francis A. Plummer, George F. Gao, Gary P. Kobinger, Xiangguo Qiu
The Zaire ebolavirus species contain one member virus: Ebola virus (EBOV), which causes a severe, acute, and often-fatal hemorrhagic fever in humans and non-human primates (NHPs). The virus has an incubation period of 2–21 days [1], and patients initially present non-specific, flu-like symptoms such as sudden onset of high fever (39–40°C), headaches, muscle and joint pain in addition to general fatigue and malaise, lasting typically between 2 and 4 days [2]. The disease then progresses to more severe symptoms and manifestations including gastrointestinal, respiratory, vascular, and neurological distress [1]. A maculopapular rash accompanied by erythema, petechiae, or ecchymoses appears between 5 and 7 days, and uncontrolled bleeding may be observed from puncture sites and the mucosa [1]. Up to 90% of cases progress to terminal disease, which is characterized by severe metabolic imbalances, anuria, convulsions, and hypovolemic shock. Death occurs approximately 2–3 days afterwards due to multi-organ failure from massive tissue injury, as well as capillary extravasation from vascular permeability and diffuse coagulopathy [2]. Survivors undergo a prolonged convalescent phase including intense fatigue, loss of appetite, weight and memory loss, and migratory joint pains [2]. Sequelae from the disease are both physical and psychological in nature, and may include orchitis, myelitis, recurrent hepatitis, uveitis, as well as psychosis [1]. Shedding of live EBOV in bodily fluids, such as semen, is detectable for up to three months, and perhaps longer, after the onset of disease [3,4].