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--- group_2_presentation_3_-_ebola [2017/11/30 11:56]
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 ===== 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 |}}
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 ====== 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|}}
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 **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 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. 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**
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 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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