Genetic Makeup of the COVID-19 Virus
A global pandemic, caused by a novel coronavirus (SARS-CoV-2, previously known as 2019-nCoV), the coronavirus disease 2019 (COVID-19) originated in China few months back costing millions of people suffering physically, emotionally and financially. According to the World Health Organization, the number of confirmed cases globally reached 2.9 million in 212 countries and number of deaths 180,000 by 22 April 2020.
Human coronaviruses (CoV), first characterized in the 1960s, are a large family of viruses, causing respiratory illnesses ranging from the common cold to more severe diseases responsible for significant morbidity and mortality. (Kahn & McIntosh, 2005) The highly pathogenic SARS-CoV-2 belongs to β-coronavirus, the same virus family which were responsible for the severe acute respiratory syndrome coronavirus (SARS-CoV) epidemic in 2002 and Middle East respiratory syndrome coronavirus epidemic (MERS-CoV) in 2012.(Guo et al., 2020).
SARS-CoV-2’s ability to infect at speeds quicker than the original virus has led to great interest in the new virus’s ability to spread and virulence. SARS-CoV-2 is an RNA virus that has a specific spike protein that allows it to bind itself to the host cell 10x faster than the original virus. The Furin enzyme in the human body allows the virus to attack pivotal organs in the body including the liver, lungs, and small intestines. The last time the world responded to a global emerging disease epidemic of the scale of the current COVID-19 pandemic with no access to vaccines was the 1918-19 H1N1 influenza pandemic killed at least 50 million people. (Kash et al., 2006)
Next-generation sequencing (NGS) provides an effective, novel way to screen samples and detect viruses. The gene sequencing of SARS-CoV-2 is crucial in order to see precisely what makes it so contagious. Our study will help in learning more about this rapidly spreading virus and will inform whether or not the virus is mutating away from the original sequence, when the virus was first sequenced in China. The diverse structure of the virus in our positive patients will help us understand where the new cases came to Texas. This information allows us to track the spread and evolution of the virus. Recent research is suggesting that SARS-CoV-2, appears to be mutating slowly. The ability to see how quickly the virus mutates is vital information for developing an effective vaccine.
The aim of the study is to sequence the genome of the SARs-CoV-2 in patient’s samples that tested positive for COVID-19 in Texas in order to identify unique variants that may contribute to disease virulence and genetic diversity.
This study will present an overview of the virus and some viral proteins in terms of genetic structure by conducting the whole genome sequence to determine the alteration of nucleotides and amino acids sequences in our sample population.
Nasopharyngeal swab samples were collected from patients with symptoms of COVID-19 at the Ayass Bioscience in Texas. Fourteen SARS-CoV-2 positive samples by real-time reverse transcriptase PCR(rRT-PCR), have been sequenced for quality control and will be included in the sequencing study along with other patients who will be referred for diagnosis of COVID-19. We have collected sociodemographic information (name, age, gender, ethnicity), address and history of travel during their visit for COVID-19 test.
There was no apparent risk for collection of nasopharyngeal swab except discomfort or irritation during the process of sample collection.
For research participants, there is no additional anticipated benefits as we will not be contacting them but this genetic information will add knowledge about the behavior of virus in terms of origin, spread and virulence for COVID-19.
Guo, Y. R., Cao, Q. D., Hong, Z. S., Tan, Y. Y., Chen, S. D., Jin, H. J., . . . Yan, Y. (2020). The origin, transmission and clinical therapies on coronavirus disease 2019 (COVID-19) outbreak – an update on the status. Mil Med Res, 7(1), 11. doi:10.1186/s40779-020-00240-0
Kahn, J. S., & McIntosh, K. (2005). History and recent advances in coronavirus discovery. Pediatr Infect Dis J, 24(11 Suppl), S223-227, discussion S226. doi:10.1097/01.inf.0000188166.17324.60
Kash, J. C., Tumpey, T. M., Proll, S. C., Carter, V., Perwitasari, O., Thomas, M. J., . . . Katze, M. G. (2006). Genomic analysis of increased host immune and cell death responses induced by 1918 influenza virus. Nature, 443(7111), 578-581. doi:10.1038/nature05181
Shanks, G. D., Waller, M., Mackenzie, A., & Brundage, J. F. (2011). Determinants of mortality in naval units during the 1918-19 influenza pandemic. Lancet Infect Dis, 11(10), 793-799. doi:10.1016/s1473-3099(11)70151-7
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