The biggest hazard to public health is posed by RNA viruses, which have the capacity to trigger catastrophic biological processes on a global scale. There have been several viral epidemics that put susceptible people at high risk, but they vary in the modes of transmission, mortality rates, and invasiveness. While certain infections, including COVID-19 and the Ebola viral disease, travel rapidly from person to person, many viruses need an intermediary host for their dissemination. The global community has used the lessons learned during the Ebola epidemic in West Africa to help develop the first and most rapid management methods for SARS-CoV-2. Hence, it seems reasonable to compare the essentials of these two viruses.
The Ebola virus is a helical-symmetric negative-sense RNA virus that is a member of the Filoviridae class. The Ebola virus has a number of subgroups, each of which is named for the location in Africa where it was first discovered. These viruses now go by the name Ebola virus disease, which results in an abrupt and severe illness that is frequently fatal (up to 90% of victims die) (Feldmann et al., 2020). Close communication, contact with bodily fluids (such as blood, excrement, or vomit), or contact with objects polluted by bodily fluids are the three main ways that the Ebola virus is spread.
This implies that the mentioned virus cannot spread as quickly as many other viral infections since it cannot be disseminated by conventional airborne channels (wheezing, coughing, etc.). People neither serve as the Ebola virus’ original host nor its reservoir. It is thought that fruit bats act as the virus’ host species and that diseased bats excrete the pathogen, which subsequently spreads to monkeys, antelope, rats, and other species. When people capture and kill these creatures, they subsequently come into touch with the virus. As a result, it is a pandemic illness that affects both people and animals.
The SARS CoV-2 new coronavirus belongs to the virus group Coronaviridae. It should be noted that the SARS virus and MERS virus are members of this category (MERS-CoV). This pathogen has a helical shape and is positive-sense RNA. The coronavirus is so named because it contains many protrusions from the membrane of the virus particles that give it the look of a corona or a tiara.
One strategy employed by RNA viruses – to which both SARS-CoV-2 – is to pack their genetic material into a compact genome, which is promptly converted into the proteins required for viral multiplication upon viral entrance. One linear negative sense RNA, measuring 19 kilobases, is present in EBOV and encodes for the proteins nucleoprotein, polymerase component VP35, structural protein VP40, glycoprotein, transcriptional initiator VP30, and the RNA-dependent RNA polymerase (Takamatsu et al., 2018). In turn, the SARS-CoV-2 virus is among the biggest RNA viral genomes, measuring about 30 kilobases (which equals the doubled size of the EBOV genome). The translation of the ORF results in the formation of the two big family proteins pp1a, as well as pp1ab, which in fact, culminates in the creation of functioning viral RNA transcription (Li & Qin, 2021). It should also be noted that SARS-CoV-2 and EBOV enter the recipient cell by a membrane glycoprotein that binds to a particular host cell receptor and causes endocytic integration of the virus. However, for viral entrance, EBOV uses glycoprotein, while SARS-CoV-2 uses the “S” protein.
SARS-CoV-2 is believed to originate mostly from bats, similar to how Ebola does. This is due to an 88% similarity between the genomic sequences of two bat-originating coronaviruses and the SARS CoV-2 (Rettner, 2020). Nevertheless, in the instance of COVID-19, it is now unclear which animal acted as a bridge between the bat and people. According to reports, bat excrement contaminated an animal that was later utilized for food or other reasons and, when slaughtered, afflicted humans. Therefore, it seems likely that the SARS-CoV-2 virus and the Ebola both started in bats before moving on to people via an intermediary species. The majority of instances of the new coronavirus, in contrast to Ebola, have been moderate.
Some of the deadliest pathogens known to mankind include the Ebola virus. It was initially found in many epidemics in Africa in 1976 (Furuyama et al., 2021). This virus penetrates through skin breaches or touch with a mucus layer and is spread by body fluids. Typically, the incubation period lasts 8 to 10 days. When the virus multiplies in monocyte, macrophage, or dendritic cells, the lymphatic system makes it easier for the virus to spread throughout the organism. The infection can then spread to other tissues. Significant cytokines and inflammation mediator release follow, creating a “cytokine thunderstorm” (Furuyama et al., 2021). Inflammatory and increased permeability result from this. Endothelial injury, heightened vascular leakage, lowered blood pressure, hypotension, and numerous blood arteries spilling blood and plasma are the other consequences of this. Diffuse intravenous coagulation may occur, which can cause bleeding and hemorrhaging from the mouth, urethra, eyeballs, ears, and/or nostrils.
In turn, SARS-CoV-2, a new coronavirus, is an airborne illness that spreads by respiratory droplets in a similar way to how flu viruses do. The virus and the classic SARS virus share about 85% of the same genomic elements (Tay et al., 2020). SARS-CoV-2, on the other hand, is more infectious than SARS-classic and the associated MERS-CoV. This is assumed to be because the SARS-CoV-2 spike proteins have a location that is triggered by the enzyme furin, which is present in various body cells. The upper lung and the lower airways are the major sites of assault for COVID-19, the illness that resulted from SARS-CoV-2. Symptoms may resemble those of an allergy, the flu, or a normal cold. However, in a few instances, it might result in serious pneumonia, necessitating ventilation for a person.
The initial barrier of resistance against a microbial onslaught is held by the innate immune system. The latter is made aware of the virus due to the presence of pathogen-associated molecular patterns that are formed from the infection and detected by pattern recognition receptors. Following this, cytokines are released, which subsequently cause the creation of pro-inflammatory chemicals, creating a pro-inflammatory feedback mechanism. This process has been postulated for SARS-CoV-2 and EBOV, which eventually stimulate Cytokine Storm Syndrome, a hyperinflammatory autoimmune reaction that must be treated with anti-cytokine treatment (Jain et al., 2020; Shang et al., 2020). Such treatments have been proposed for EBOV and SARS-CoV-2.
At this point, it should be stressed that the Ebola virus, SARS-original, and MERS CoV all originated in bats. SARS-CoV-2 is presently believed to have started in bats as well and, like the others, transmitted to humans through an intermediary species. At this moment, it is unknown what the intermediate animal for COVID-19 will be. There are also many similarities in terms of viral strategies presented above. However, the ways in which the Ebola virus and SARS-CoV-2 transmit and the symptoms they cause are very dissimilar. The typical mortality rate for Ebola virus disease (EVD) is 50%, but it has occasionally reached 90% in certain strains. One crucial aspect was how swiftly it ended. The illness is probably very mild in more than 80% of COVID-19 cases, with deaths typically occurring in elderly people or those with preexisting medical conditions.
References
Feldmann, H., Sprecher, A., & Geisbert, T. W. (2020). Ebola. The New England Journal of Medicine, 382(19), 1832–1842.
Furuyama, W., Shifflett, K., Feldmann, H., & Marzi, A. (2021). The Ebola virus soluble glycoprotein contributes to viral pathogenesis by activating the MAP kinase signaling pathway. PLoS pathogens, 17(9), e1009937. Web.
Jain, S., Khaiboullina, S. F., & Baranwal, M. (2020). Immunological perspective for Ebola virus infection and various treatment measures taken to fight the disease. Pathogens (Basel, Switzerland), 9(10), 850.
Li, R., & Qin, C. (2021). Expression pattern and function of SARS-CoV-2 receptor ACE2. Biosafety and health, 3(6), 312–318.
Rettner, R. (2020). New coronavirus may have started in bats. But how did it hop to humans? Live Science. Web.
Shang, J., Wan, Y., Luo, C., Ye, G., Geng, Q., Auerbach, A., & Li, F. (2020). Cell entry mechanisms of SARS-CoV-2. Proceedings of the National Academy of Sciences of the United States of America, 117(21), 11727–11734.
Takamatsu, Y., Kolesnikova, L., & Becker, S. (2018). Ebola virus proteins NP, VP35, and VP24 are essential and sufficient to mediate nucleocapsid transport. Proceedings of the National Academy of Sciences of the United States of America, 115(5), 1075–1080.
Tay, M. Z., Poh, C. M., Rénia, L., MacAry, P. A., & Ng, L. F. P. (2020). The trinity of COVID-19: immunity, inflammation and intervention. Nature Reviews. Immunology, 20(6), 363–374.