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 ====== Introduction ======
+{{youtube>xUBpoyKxArU?medium}}
 ===== Etiology =====
 The Ebola virus was first identified in 1976, localized near the Ebola river, primarily in the Democratic Republic of Congo and Sudan (CDC). The virus is known to affect both humans and non-human primates, including chimpanzees, gorillas, and orangutangs. Moreover, there are 5 known strains of the Ebola virus, with the most common among humans being the Zaire virus. In addition, the Reston virus has been found to propagate disease in nonhuman primates but not among human populations (CDC).
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 {{:ebola.jpg?400|}}
-**Figure 1:** Zaire ebolavirus depicted as a thread-like virus under fluorescent microscopy imaging
+**Figure 1:** Zaire ebolavirus depicted as a thread-like virus under fluorescent microscopy imaging.
 Ebola Strains/ Variants:
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      * //Reston ebolavirus//
-The first outbreak was recorded in 1976-1979. The first outbreak was called Ebola Sudan as it occurred in Sudan. It affected mainly towns of Nzara and Maridi and resulted in about a 53% mortality rate (150/284). The second outbreak also happened near the borders of Democratic Republic of the Congo (DRC) and it was called the E. Zaire. This was in Yambuku, about 800km from Nzara. The mortality rate for this one was 89%. Ebola reemerged after 15 years in 1994 for a period of 3 years. It was a new subtype called E. Ivory Coast and it evolved from the E. Zaire outbreaks. The next outbreak was in 1996 where the index case was a hunter who died from hemorrhagic fever. At the same time, cases of chimpanzees were reported in the surrounding forest. A second hunter was found with the virus and he transferred it to a healer and his assistant leading to the infection of several towns and villages in Gabon (DRC). The hunter was infected because he ate a gorilla carcass.  Again in 2000-2004, E. Zaire and E. Sudan reemerged and had a large impact on large animal species such as gorillas. The largest numerical outbreak recorded was between Oct. 2000 - Jan. 2001 as a result of two E. Sudan outbreaks. Most of the outbreaks that occurred after 2000 was due to people handled animal carcasses in the forest, termed epidemic chain. There is also a possibility that humans were infected by EBOV reservoir species. Bats were reported for the outbreaks of 1976-1979 in the cotton factories of the first people thought to be infected. It is also noteworthy that the Australian who was infected by Marburg virus had just returned from a trip to Zimbabwe, during which he had slept frequently in the open and once in an abandoned house, the loft of which was inhabited by numerous bats (Xavier, 2005).
+The first outbreak was recorded in 1976-1979 and was classified as Ebola Sudan, given that it occurred in Sudan. The Sudan Ebola virus primarily affected the towns of Nzara and Maridi, resulting in a 53% mortality rate (150/284). The second outbreak originated approximately 800 kilometers from Nzara in a town called Yambuku, and spread near the borders of Democratic Republic of the Congo (DRC), called the E. Zaire. The first Ebola Zaire outbreak exhibited a mortality rate of 89% and re-emerged in 1994 as the Ebola Ivory Coast strain that evolved from the Zaire strain, lasting for a period of 3 years. The next outbreak was in 1996, where the index case was a hunter who died from hemorrhagic fever. At the same time, cases of chimpanzees were reported in the surrounding forest. A second hunter was found with the virus and he transferred it to a healer and his assistant leading to the infection of several towns and villages in Gabon (DRC). The hunter contracted the virus due to ingestion of contaminated bushmeat of a gorilla carcass. Again in 2000-2004, E. Zaire and E. Sudan re-emerged and had a large impact on the mortality rate of large non-human primates including gorillas. According to statistics provided by the World Heath Organization, the largest recorded outbreak prior to the outbreak of 2014 in West Africa, was between October of 2000 to January of 2001 as a result of two simultaneous E. Sudan outbreaks. Most of the outbreaks that occurred following 2000 were due to contamination by improper handling of infected primate carcasses, leading to an epidemic chain.There is also a possibility that humans were infected by EBOV reservoir species including fruit bats, which may have led to the outbreak presented from 1976-1979 (Xavier, 2005).
-Fruit bats seem to act as a reservoir for the Ebola virus. Fruit bats also seem to have antibody serum for Ebola in their bodies. 88 bats were tested via PCR and ELISA assay and 33 of them were positive for the serum. This makes them the perfect reservoir for EBOV. They found antibodies and viral RNA fragments in three species of bats, including hammer-headed fruit bats (Kai, 2017). But they failed to isolate the virus itself, so other species might be more important in transmitting it. However, the virus usually spreads to primates when bat species holding the virus are eaten. From then on, it is easily transferred to humans as they handle dead animals or ingest them.
+Fruit bats seem to act as a natural reservoir for the Ebola virus, likely given their innate capacity to carry an antibody serum for the Ebola virus in their bodies. According to a study published by Hayman et al. in 2012, 88 non-migratory fruit bats resident to the region of Ghana, were tested for an antibody serum for the Ebola virus via PCR and ELISA assays, and 33 of them were positive for the serum and enabling them to share a commensalistic relationship with the virus. Specifically, researchers found antibodies for the virus, in addition to viral RNA fragments in three species of bats, including hammer-headed fruit bats (Kai, 2017), however, they failed to isolate the virus in culture, hence other species may play a more significant role in transmitting the virus. The virus usually spreads to primates when bat species holding the virus are eaten as bushmeat. From then on, it is easily transferred to humans as they handle dead animals or ingest them as part of their diet.
 ===== Epidemiology: Ebola Outbreak (2013-2016) =====
-Ebola first emerged in 1976 in southern Sudan and Democratic Republic of Congo. Previous to the West Africa outbreak in 2014, there was only around 100-200 cases, while the 2014 outbreak alone had greater than 25000 cases. The West Africa outbreak involved transmission between both rural and urban areas, and across borders. The densest areas include Liberia, Guinea and Sierra Leone (Kramer et al. 2016). Differences in the magnitude of outbreaks between the 2014 outbreak and previous ones are due to external factors and not the virulence of the Ebola virus. These external factors included late diagnosis and recognition that symptoms were associated with Ebola. Another factor was the lack of experience and preparation of an Ebola outbreak in West Africa. These factors lead to the significant differences in cases.
+Ebola first emerged in 1976 in southern Sudan and Democratic Republic of Congo. Previous to the West Africa outbreak in 2014, there was only around 100-200 cases, while the 2014 outbreak alone had greater than 25000 cases. The West Africa outbreak involved transmission between both rural and urban areas, and across borders. The densest areas include Liberia, Guinea and Sierra Leone (Kramer et al. 2016). Differences in the magnitude of outbreaks between the 2014 outbreak and previous ones are due to external factors and not the virulence of the Ebola virus. These external factors included late diagnosis and recognition that symptoms were associated with Ebola. Another factor was the lack of experience and preparation of an Ebola outbreak in West Africa. These factors lead to the significant differences in cases (Mack et al. 2016).
 {{ :ebola_map.png |}}
+**Figure 2:** Geographical mapping of EBOV Zaire strain localization and concentration in West Africa during the outbreak of 2014.
 ====== Symptoms and Stages of Ebola ======
 There are 4 distinguishable stages of the Ebola virus and symptoms tend to arise 2-21 days following exposure to the disease via contaminated bodily fluids in most cases. It is usual for symptoms to occur between 8-10 days after contraction of the virus.
@@ Line 37: / Line 40: @@
 {{ :stages_of_ebola.png?600 |}}
-**Figure 2:** Center for Disease Control outline of stages and corresponding symptoms of Ebola following incubation period
+**Figure 3:** Center for Disease Control outline of stages and corresponding symptoms of Ebola following incubation period.
 **Overview of Symptoms**
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 {{ :transmission.png?direct&600 |}}
+**Figure 4:** Centre of Disease Control and Prevention guide to Ebola Virus transmission from reservior hosts (fruit bats) to secondary hosts that can pass virus in epidemic stages.
 ====== Diagnosis ======
@@ Line 69: / Line 73: @@
 {{ :diagnosis.png?direct&700 |}}
+**Figure 5:** World Health Organization guide to effective diagnostic laboratory testing of the Ebola virus.
 ====== Baltimore Classification of Viruses ======
-Viruses can either be made up of RNA or DNA. In order to be translated by host proteins however the viral genome must be converted into a positive strand mRNA template. The Baltimore classification is made up of 5 classes of viruses and is based on how the viral genome transforms itself into the positive strand mRNA template.
+Viruses can either be made up of RNA or DNA. In order to be translated by host proteins however the viral genome must be converted into a positive strand mRNA template. The Baltimore classification is made up of 5 classes of viruses and is based on how the viral genome transforms itself into the positive strand mRNA template (Baltimore, 1971).
-Class I: are composed of viruses with double stranded DNA genomes. These viruses insert their genomes into the nucleus and are highly dependent on host machinery such as DNA dependent DNA polymerase (DdDp) and RNA dependent RNA polymerase (RdRp) for replication and transcription of the positive mRNA strand respectively.
+Class I: are composed of viruses with double stranded DNA genomes. These viruses insert their genomes into the nucleus and are highly dependent on host machinery such as DNA dependent DNA polymerase (DdDp) and RNA dependent RNA polymerase (RdRp) for replication and transcription of the positive mRNA strand respectively (Dimmock, 2007).
-Class II: are composed of viruses with single stranded DNA genomes. Once inside the cell, either through virus or host machinery a double stranded DNA intermediate will be produced. This double stranded DNA intermediate will then be able to serve as a template for replication, which will construct a single stranded genome and transcription, which will produce a positive mRNA strand that can be translated.
+Class II: are composed of viruses with single stranded DNA genomes. Once inside the cell, either through virus or host machinery a double stranded DNA intermediate will be produced. This double stranded DNA intermediate will then be able to serve as a template for replication, which will construct a single stranded genome and transcription, which will produce a positive mRNA strand that can be translated (Dimmock, 2007).
-Class III: are composed of viruses with segmented double stranded RNA genomes. There are usually 11-12 segments that are transcribed to produce monocistronic mRNAs- each template codes for a separate protein. The virus uses host RdRp to replicate the segmented genome.
+Class III: are composed of viruses with segmented double stranded RNA genomes. There are usually 11-12 segments that are transcribed to produce monocistronic mRNAs- each template codes for a separate protein. The virus uses host RdRp to replicate the segmented genome (Dimmock, 2007).
-Class IV: are composed of viruses with segmented single stranded positive stranded RNA genomes. The mRNA genome can be replicated by host RdRp and can be directly transcribed by host machinery since it is already in positive sense formation. The genome is a polycistronic mRNA template which codes for one large protein that is then cleaved into individual components.
+Class IV: are composed of viruses with segmented single stranded positive stranded RNA genomes. The mRNA genome can be replicated by host RdRp and can be directly transcribed by host machinery since it is already in positive sense formation. The genome is a polycistronic mRNA template which codes for one large protein that is then cleaved into individual components (Dimmock, 2007).
-Class V: are composed of viruses with single stranded negative stranded RNA genomes. There are two main subclasses, segmented and non-segmented. The non-segmented mRNA genomes are transcribed into several monocistronic templates to form individual viral proteins. The genome is also transcribed into a positive stranded mRNA template via viral RdRp which can be then used to produce genome copies for viral progeny.
+Class V: are composed of viruses with single stranded negative stranded RNA genomes. There are two main subclasses, segmented and non-segmented. The non-segmented mRNA genomes are transcribed into several monocistronic templates to form individual viral proteins. The genome is also transcribed into a positive stranded mRNA template via viral RdRp which can be then used to produce genome copies for viral progeny (Dimmock, 2007).
 {{:baltimore_classification.png|}}
-Figure _: Baltimore classification is based upon how the viral genome is transformed into a positive stranded mRNA template to allow for vial protein translation.
+**Figure 6:** Baltimore classification is based upon how the viral genome is transformed into a positive stranded mRNA template to allow for vial protein translation.
@@ Line 93: / Line 99: @@
 **Transcription:** Transcription is also occurs in the host cytoplasm and is mediated by NP, L and Phosphoprotein (P) VP30. VP30 has dual function- it regulates nucleocapsid assembly by binding to NP as well as functions as a transcription activator via its zinc-binding domain. In vitro, loss of function of the zinc-binding domains led to a loss of transcription activation. Though the exact function of VP30 is unknown, it hypothesized to be involved in transcription initiation or early anti-termination. In order to be translated by host machinery, the virus mRNA template must have a 5' cap. It is inefficient to encode for components viruses can attain from the host, so they don't encode a 5' cap in their genome. Instead, an endonuclease cleaves 5' caps off of host mRNA and primes it to the viral mRNA species. The second component needed to ensure translation is the addition of a poly-A-tail. The termination codon is followed by a stretch of uridine residues that codes for the poly-A-tail and causes the polymerase to "fall off" the mRNA template (Mulberger, 2007).
 {{ :filovirus_virion2.png |}}
+**Figure 7:** Depiction of the structural features of the Ebola virus, including surface glycoprotein, nucelocapsid, and RNA-dependent RNA polymerase.
 {{::ebov_genome.png|}}
+**Figure 8:** Genes on monocistronic RNA genome of Ebola virus coding for key components of viral nucleocapsid (coded by NP gene on 3' end), glycoprotein epitope for viral endocytosis (coded by GP gene), and RNA-dependent RNA polymerase (coded by L gene).
 ===== Pathophysiology of Ebola =====
-Macrophages and dendritic cells are early targets of EBOV. Extensive infection of these cells leads to overproduction of inflammatory mediators and chemokines such as IL-1, IL-6, IL-8, TNF-a, and monocyte chemotactic protein-1 (MCP-1)(Marcinkiewicz et al., 2014). This “cytokine storm” is responsible for attracting neutrophils and eosinophils to the infected tissues, which subsequently induces coagulopathy (impaired coagulation) and increases endothelial permeability(Marcinkiewicz et al., 2014). Additionally, the infection of antigen presenting cells leads to extensive apoptosis of T cells and natural killers cells. Another key point of infection is the suppression of the type I interferon (IFN)  response, via the non structural proteins, VP24 and VP35. Type I IFNs are responsible for inducing transcription of a large group of genes which play a major role in host resistance to viral infection and activate key components of the innate and adaptive immune systems including; antigen presentation and the production of cytokines that activate T cells, B cells, and natural killer cells. Furthermore, VP35 inhibits maturation of dendritic cells by interfering with the RIG-I signaling pathway to prevent upregulation of MHC I and MHC II and the costimulatory molecules CD40, CD80, and CD86, thus impairing antigen presentation to CD8+ and CD4+ T cells and T-cell activation and thereby impeding linkage of the innate and adaptive immune responses (Ansari, 2014). The evasion of the immune system allows the virus to replicate unhindered and therefore permits subsequent dissemination of viral progeny. Infected antigen presenting cells (macrophages and dendritic cells) travel to the lymph nodes and to the spleen, where further replication takes place and dissemination to the rest of the body is made possible via the blood stream (Ansari, 2014). Viremia allows the virus to infect the liver, the adrenal gland and the gastro-intestinal tract (leading to diarrhea). Infection of the liver leads to the dysregulation of coagulation proteins and infection of the adrenal gland compromises the ability to make blood pressure regulating steroids, in tandem this dissemination leads to hemorrhagic fever, multi-organ failure, terminal shock and death (Ansari, 2014).
+Macrophages and dendritic cells are early targets of EBOV. Extensive infection of these cells leads to overproduction of inflammatory mediators and chemokines such as IL-1, IL-6, IL-8, TNF-a, and monocyte chemotactic protein-1 (MCP-1)(Marcinkiewicz et al., 2014). This “cytokine storm” is responsible for attracting neutrophils and eosinophils to the infected tissues, which subsequently induces coagulopathy (impaired coagulation) and increases endothelial permeability (Marcinkiewicz et al., 2014). Additionally, the infection of antigen presenting cells leads to extensive apoptosis of T cells and natural killers cells. Another key point of infection is the suppression of the type I interferon (IFN)  response, via the non structural proteins, VP24 and VP35. Type I IFNs are responsible for inducing transcription of a large group of genes which play a major role in host resistance to viral infection and activate key components of the innate and adaptive immune systems including; antigen presentation and the production of cytokines that activate T cells, B cells, and natural killer cells. Furthermore, VP35 inhibits maturation of dendritic cells by interfering with the RIG-I signaling pathway to prevent upregulation of MHC I and MHC II and the costimulatory molecules CD40, CD80, and CD86, thus impairing antigen presentation to CD8+ and CD4+ T cells and T-cell activation and thereby impeding linkage of the innate and adaptive immune responses (Ansari, 2014). The evasion of the immune system allows the virus to replicate unhindered and therefore permits subsequent dissemination of viral progeny. Infected antigen presenting cells (macrophages and dendritic cells) travel to the lymph nodes and to the spleen, where further replication takes place and dissemination to the rest of the body is made possible via the blood stream (Ansari, 2014). Viremia allows the virus to infect the liver, the adrenal gland and the gastro-intestinal tract (leading to diarrhea). Infection of the liver leads to the dysregulation of coagulation proteins and infection of the adrenal gland compromises the ability to make blood pressure regulating steroids, in tandem this dissemination leads to hemorrhagic fever, multi-organ failure, terminal shock and death (Ansari, 2014).
 {{ :ebola_patho.png |}}
-Figure_: The cascade of pathological events that results in the rapid severity of Ebolavirus infection.
+**Figure 9:** The cascade of pathological events that results in the rapid severity of Ebolavirus infection.
 ====== Treatments ======
@@ Line 110: / Line 122: @@
 **ZMapp**
-Developed by Mapp Biopharmaceutical, Inc., based in San Diego, is composed of three different laboratory-made proteins called monoclonal antibodies. The treatment is designed to prevent the progression of EVD within the body by targeting the main surface protein of the Ebola virus. Earlier studies in nonhuman primates demonstrated that ZMapp had strong antiviral activity and prevented death when administered as late as five days after experimental infection with Zaire ebolavirus. It is tested on animals and results indicate it helps alleviate the fever, viraemia and abnormalities of blood count. It also reverses elevated liver enzymes and mucosal haemorrhages. ELISA and neutralizing antibody assays indicate that ZMapp is cross-reactive with the Guinean variant of Ebola.
+Developed by Mapp Biopharmaceutical, Inc., based in San Diego, is composed of three different laboratory-made proteins called monoclonal antibodies. The treatment is designed to prevent the progression of EVD within the body by targeting the main surface glycoprotein of the Ebola virus that is essential in facilitating viral endocytosis of the host cell. The monoclonal antibodies work to bind complementarily to the viral glycoprotein epitope and inhibit binding to host cell receptors, thus preventing endocytosis and viral infection of the host cell. Earlier studies in nonhuman primates demonstrated that ZMapp had strong antiviral activity and prevented death when administered as late as five days after experimental infection with Zaire ebolavirus. It is tested on animals and results indicate it helps alleviate the fever, viraemia and abnormalities of blood count. It also reverses elevated liver enzymes and mucosal haemorrhages (Marcinkiewicz et al., 2014).
 **rVSV-ZEBOV**
-NewLink Genetics of Ames from Iowa collaborating with Canadian National Institute of Public Health genetically engineered the vesicular stomatitis virus (VSV), that has a natural tropism for livestock (Marcinkiewicz et al., 2014). VSV was attenuated, engineered to be replication-competent and to express the glycoprotein from a Zaire strain of Ebola virus (ZEBOV) in replacement of its own glycoprotein (rVSV-ZEBOV). Vaccination induces replication of these genetically engineered viral particles (rVSV-ZEBOV)(Regules et al., 2017). The ZEBOV glycoprotein is responsible for binding and fusion to host target cells, and is the viral epitope that is targeted by host cytotoxic T-cells and neutralizing antibodies. Therefore, exposing patients to the ZEBOV glycoprotein in the form of an attenuated and genetically engineered vesicular stomatitis virus, allows for the activation of adaptive immunity against ZEBOV without the risk of infection(Regules et al., 2017). In fact, the rVSV-ZEBOV vaccine has been shown to be attenuated in normal and immunocompromised nonhuman primates in safety and immunogenicity studies. In addition, multiple studies in cynomolgus macaques have shown that a single administration of the vaccine confers a high level of protection. There are various methods of vaccine delivery (oral, intranasal, or intramuscular) and all variants have shown protective efficacy in animal models (Regules et al., 2017).
+NewLink Genetics of Ames from Iowa collaborating with Canadian National Institute of Public Health genetically engineered the vesicular stomatitis virus (VSV), that has a natural tropism for livestock (Marcinkiewicz et al., 2014). VSV was attenuated, engineered to be replication-competent and to express the glycoprotein from a Zaire strain of Ebola virus (ZEBOV) in replacement of its own glycoprotein (rVSV-ZEBOV). Vaccination induces replication of these genetically engineered viral particles (rVSV-ZEBOV)(Regules et al., 2017). The ZEBOV glycoprotein is responsible for binding and fusion to host target cells, and is the viral epitope that is targeted by host cytotoxic T-cells and neutralizing antibodies. Therefore, exposing patients to the ZEBOV glycoprotein in the form of an attenuated and genetically engineered vesicular stomatitis virus, allows for the activation of adaptive immunity against ZEBOV without the risk of infection (Regules et al., 2017). In fact, the rVSV-ZEBOV vaccine has been shown to be attenuated in normal and immunocompromised nonhuman primates in safety and immunogenicity studies. In addition, multiple studies in cynomolgus macaques have shown that a single administration of the vaccine confers a high level of protection. There are various methods of vaccine delivery (oral, intranasal, or intramuscular) and all variants have shown protective efficacy in animal models (Regules et al., 2017).
 ====== Persistence of Ebola ======
@@ Line 123: / Line 135: @@
 {{ :24099019_10155946707362803_1905168344_n.png?direct&300 |}}
+**Figure 10:** Ebola virus can persist in organs such as eye, namely in the vitreous or aqueous humour, leading to high ophthalmic pressure, uveitis, and diminished visual accuity.
 ====== Lesson Learned From the Ebola Outbreak ======
@@ Line 129: / Line 142: @@
 Other ways to further prevent another viral outbreak includes minimization of unsafe handling of bush meat, to decrease spread of zoonotic diseases into human populations. Additionally, promotion of biosafety by providing health care workers with education on infection control, and increased supplies. There can also be a reduction in transmission by practicing safe burial methods, and educating the community about the disease. The transmission can be also reduced by creating adequate isolation and treatment centres, and provide health care workies with efficient protective materials and essential supplies. Furthermore, there needs to be an improved method for quick diagnosis and transport for samples.  Lastly, a data system in which disease cases and information can be reported for disease surveillance on a global level (Kaushik et al. 2016).
 {{ :lessons_ebola.png |}}
+**Figure 11:** Guide to preventative and disease controlling measures to manage or prevent viral epidemics.
+====== Presentation ======
+https://docs.google.com/a/mcmaster.ca/presentation/d/1t7wWL4e8zEutJfhT_hHH6Xs0af8PrTGIUMnaGdFHl30/edit?usp=sharing
 ====== References ======
@@ Line 144: / Line 162: @@
 Centers for Disease Control and Prevention (CDC). Ebola (Ebola Virus Disease). CDC. [accessed 2017 Nov 18]. https://www.cdc.gov/vhf/ebola/about.html
+Dimmock, N. (2007). Introduction to Modern Virology. Victoria, Australia. Blackwell Publishing.
 Falasca, L., Agrati, C., Petrosillo, N., Di Caro, A., Capobianchi, M. R., Ippolito, G., & Piacentini, M. (2015). Molecular mechanisms of Ebola virus pathogenesis: focus on cell death. Cell Death and Differentiation, 22(8), 1250–1259. http://doi.org/10.1038/cdd.2015.67
+Gates, B. The next epidemic—lessons from Ebola. N Engl J Med. 2015; 372: 1381–1384
+Hayman, D. T. S., Yu, M., Crameri, G., Wang, L.-F., Suu-Ire, R., Wood, J. L. N., & Cunningham, A. A. (2012). Ebola Virus Antibodies in Fruit Bats, Ghana, West Africa. Emerging Infectious Diseases, 18(7), 1207–1209. http://doi.org/10.3201/eid1807.111654
 Kai KupferschmidtJun. 1, 2017 , 1:00 PM, 20 2017 JKN, 20 2017 KKN, 20 2017 ESN, Marc Heller, E&E NewsNov. 20, 2017, 17 2017 MWN, 20 2017 N, 17 2017 N, 16 2017 N. Hunting for Ebola among the bats of the Congo. Science | AAAS. 2017 Jul 26 [accessed 2017 Nov 24]. http://www.sciencemag.org/news/2017/06/hunting-ebola-among-bats-congo
+Kaushik, A., Tiwari, S., Jayant, R. D., Marty, A., & Nair, M. (2016). Towards Detection and Diagnosis of Ebola Virus Disease at Point-of-Care. Biosensors & Bioelectronics, 75, 254–272. http://doi.org/10.1016/j.bios.2015.08.040
 Marcinkiewicz, J., Bryniarski, K., & Katarzyna, N. (2014). Ebola Haemorrhagic Fever Virus: Pathogenesis, Immune Responses, Potential Prevention. Folia Medica Cracoviensia, 3, 39-48. Retrieved from http://www.fmc.cm-uj.krakow.pl/pdf/54_3_39.pdf
-Regules, J., Beigel, J., Paolino, M., Voel, J., Castellano, A., Hu, Z.,…Thomas, J. (2017). A Recombinant Vesicular Stomatitis Virus Ebola Vaccine. The New England Journal of Medicine, 376, 330-341.  Retrieved from http://www.nejm.org/doi/full/10.1056/NEJMoa1414216?af=R&rss=currentIssue#t=article
+Kramer, A. M., Pulliam, J. T., Alexander, L. W., Park, A. W., Rohani, P., & Drake, J. M. (2016). Spatial spread of the West Africa Ebola epidemic. Royal Society Open Science, 3(8), 160294. http://doi.org/10.1098/rsos.160294
+Mack, A., Snair, M. R., & Mundaca-Shah, C. (2016). The ebola epidemic in West Africa: proceedings of a workshop. Washington, DC: The National Academies Press.
+Muhlberger, E. (2007). Filovirus replication and transcription. Retrieved from https://www.futuremedicine.com/doi/abs/10.2217/17460794.2.2.205.
+Regules, J., Beigel, J., Paolino, M., Voel, J., Castellano, A., Hu, Z.,…Thomas, J. (2017). A Recombinant Vesicular Stomatitis Virus Ebola Vaccine. The New England Journal of Medicine, 376, 330-341.  Retrieved from http://www.nejm.org/doi/full/10.1056/NEJMoa1414216af=R&rss=currentIssue#t=article
+Varkey, J. B., Shantha, J. G., Crozier, I., Kraft, C. S., Lyon, G. M., Mehta, A. K., ... & Ströher, U. (2015). Persistence of Ebola virus in ocular fluid during convalescence. New England Journal of Medicine, 372(25), 2423-2427. Retrieved from http://www.nejm.org/doi/full/10.1056/NEJMoa1500306#t=article.
 World Health Organization (WHO). (2014). Laboratory diagnosis of Ebola virus disease. [accessed 2017 Nov 18]. http://www.who.int/csr/resources/publications/ebola/laboratory-guidance/en/

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