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Published on: November 5, 2021
Unraveling the Epidemiology, Geographical Distribution, and Genomic Evolution of Potentially Lethal Coronaviruses
Nosheen Masood1, Saima Shakil Malik2, Muhammad Naqqi Raja3
1Department of Biotechnology, Fatima Jinnah Women University, Rawalpindi, Pakistan.
Abstract:
SARS CoV appeared in 2003 in China, transmitted from bats to humans via eating infected animals. It affected 8,096 humans with a death rate of 11% affecting 21 countries. The receptor binding domain (RBD) in S protein of this virus gets attached with the ACE2 receptors present on human cells. MERS CoV was first reported in 2012 in Middle East, originated from bat and transmitted to humans through camels. MERS CoV has a fatality rate of 35% and last case reported was in 2017 making a total of 1,879 cases worldwide. DPP4 expressed on human cells is the main attaching site for RBD in S protein of MERS CoV. Folding of RBD plays a crucial role in its pathogenesis. Virus causing COVID-19 was named as SARS CoV-2 due its homology with SARS CoV that emerged in 2003. It has become a pandemic affecting nearly 200 countries in just 3 months' time with a death rate of 2-3% currently. The new virus is fast spreading, but it utilizes the same RBD and ACE2 receptors along with furin present in human cells. The lessons learned from the SARS and MERS epidemics are the best social weapons to face and fight against this novel global threat.
Insights
Lessons from SARS and MERS epidemics, caused by coronaviruses, offer crucial insights for combating the COVID-19 pandemic. Understanding viral receptor binding domains (RBDs) and host cell interactions is key.
Area of Science:
- Virology
- Epidemiology
- Pathogenesis
Background:
- Severe Acute Respiratory Syndrome (SARS-CoV) emerged in 2003, originating from bats and spreading globally via infected animals, with an 11% fatality rate.
- Middle East Respiratory Syndrome Coronavirus (MERS-CoV) emerged in 2012, transmitted from bats to humans through camels, exhibiting a 35% fatality rate.
- The COVID-19 pandemic, caused by SARS-CoV-2, shares similarities with SARS-CoV, highlighting the importance of understanding viral evolution and transmission.
Purpose of the Study:
- To compare the origins, transmission, and host cell interactions of SARS-CoV, MERS-CoV, and SARS-CoV-2.
- To emphasize the critical role of the receptor binding domain (RBD) in viral pathogenesis and host cell entry.
- To underscore the value of historical epidemic data in managing current and future viral threats like COVID-19.
Main Methods:
- Comparative analysis of epidemiological data and viral characteristics of SARS-CoV, MERS-CoV, and SARS-CoV-2.
- Identification of key viral proteins and host cell receptors involved in viral entry, such as RBD, ACE2, DPP4, and furin.
- Review of pathogenesis mechanisms, including the role of protein folding in viral infectivity.
Main Results:
- SARS-CoV and SARS-CoV-2 utilize the ACE2 receptor for cell entry, while MERS-CoV uses DPP4.
- The receptor binding domain (RBD) of the spike (S) protein is crucial for viral attachment and pathogenesis in all three coronaviruses.
- SARS-CoV-2 exhibits rapid global spread, similar to SARS-CoV, but with a lower current fatality rate.
Conclusions:
- Understanding the molecular mechanisms of viral entry, particularly the RBD-receptor interactions, is vital for developing effective countermeasures against coronaviruses.
- Historical data from SARS and MERS provide valuable insights and strategies for managing the COVID-19 pandemic.
- The rapid spread and genomic homology of SARS-CoV-2 underscore the need for global preparedness and response to novel infectious diseases.
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