27th October 2020

The History of CoronaVirus ( Taxonomy, Physiology and Mode of Infection)

Coronavirus was once not listed as highly pathogenic to humans. Since Coronavirus before 2002 and 2003 were responsible for mild infections in immunologically strong humans and was severe to a few immunocompromised humans, infants, younger children, and old age people. The severe acute respiratory syndrome (SARs) was an epidemic in the province of Guangdong, China and the culprit was astonishingly Coronavirus. There was complete silence for 10 years; Coronavirus was forgotten in these 10 years. Then suddenly Middle east respiratory syndrome coronavirus (MERS-CoV). Captive breeding of wildlife is legal in china and provides a license for commercially utilizing wildlife. According to WHO civets are intermediate hosts that carry coronavirus transmitted in civets by bats. Thus, coronavirus was presented as food in civets in the markets of Wuhan leading to the SARS epidemic.

Diverse CORONAVIRUS (According to the international committee of Taxonomy)


Subfamily- Coronavirinae

Order- Nidovirales



Virus physiology

The genomes of coronaviruses were identified and were being under research form 5 to 6 decades. The coronavirus genome is a single-stranded RNA nonsegmented molecules of positive-sense, similar sense as mRNA. It has 50 caps and 30 poly(A) tails resembling the eukaryotic mRNAs (Brian et al., 2005). Though being structurally similar, coronavirus genomes are extremely large than eukaryotic mRNAs.

Now the interesting fact is what these common cold viruses which mostly infected animals, headed and ended up infecting humans. And the second question is what made them severely pathogenic.

The basic questions are how it started infecting humans and what it did in the human body?

Let’s start with what made coronavirus infecting humans. The main reason seems to be mutations and recombinations in mRNA which increases their protein binding capacity. RNA recombination was frequently noticed within coronaviruses of different times (Lai et al., 1997).

The coronavirus obtained from civet which caused  SARS and was named SARS-CoV and the strain named SZ3 was found to be originated through the recombination of two previously existing bat strains known as  WIV16 and Rf4092 (HU et al., 2017). The most frequently recombining breakpoints or mutating regions are within the S gene, which encodes the spike (S) protein that contains the receptor-binding domain (RBD), and upstream of orf8, which encodes an accessory protein (Hom et al., 2008;  Wu et al.,  2013).



Mode of Infecting Human

Reports revealed that SARS-CoV binds to the angiotensin-converting enzyme 2 (ACE2) and employ ACE2 for entry into the cell (Ilona et al., 2020). SARS-CoV promotes lung injury when its spike protein (SARS-S) downregulates ACE2 expression, which is responsible for lung pathogenesis. ACE2 is an important component of the system of renin-angiotensin which is responsible for regulating blood pressure (Jia et al., 2009; Kuba et al., 2005).  In addition, Kuba and colleagues and Imai and colleagues showed that pulmonary ACE2 protects against lung injury which was induced experimentally as demonstrated in the study conducted by Kuba et al., and  Imai et al (Iwai et al., 2009; Lambert et al., 2008).  Thus, it proves a vital role of ACE2 in the maintenance of lung health. Coronavirus directly interrupts ACE2 expression and thus causes respiratory illness.

Interestingly, Coronavirus is very specific about whom they will infect, and that comes from the receptor they bind.  SARS CoV has a high affinity for human ACE2 and high infectivity in human cells, and consequently, it was transmitted efficiently between humans. Like the interactions between SARS- Co, and ACE2, the interactions between MERS- Co, and DPP4 have been extensively examined. DPP4 from humans, camels, horses, and bats can function as a receptor for MERS- CoV, whereas DPP4 from mice, hamsters, and ferrets cannot. Isn’t it astonishing that the same protein from other species does allow MERS- CoV binding? Now what type of respiratory illness it is!  Its ARDS in short, viz acute respiratory distress syndrome.

To understand this we need to understand the physiology and function of the lung, let’s do that in pictures (given below).

physiology and function of lung

The second question that arises is since China and the middle east has already suffered Coronavirus before, they must have all the drugs known. So why is it difficult to control it?

According the biophysical and structural analysis, 2019-nCoV has a higher affinity towards binding ACE2 as compared to SARS-CoV. This binding affinity of 2019-nCoV makes it a quick and strong pathogen. Several SARS-CoV specific monoclonal antibodies were tested against 2019-nCoV and no appreciable binding was found.  This suggests that there is least or no cross-reactivity between the SATS-CoV RBD antibody and newly evolving coronavirus like 2019-nCoV. Eventually, the stored antibodies from the previous epidemic are of no good.  2019-nCoV comes back with a new face after a full-fledged evolution, and so a quick treatment or perfect treatment was not possible in the 2019 coronavirus attack.

According to Lancet 2019-nCoV is distinct from SARS-CoV in terms of biological and clinical features. 2019-nCoV and SARS-CoV-2  are not the same and considering them the same is misleading. “As on Feb 17, 2020, 2019-nCoV has caused 71 331 human cases of infections and 1775 deaths in China and 24 other countries. An epidemic virus with international concern deserves a unique name. 2019-nCoV is progressively evolving, and to predict the outcome of the current outbreak will definitely take more time. It is also by some experts that 2019-nCoV may evolve into pathogenic causing less severe disease but may become highly transmissible coronavirus. It may also attain such a biophysical feature that it may return every winter the same as the seasonal influenza virus.  If this remains the case, the name SARS-CoV-2 shall have adverse effects on peoples psychological condition their social stability and economic development in epidemic countries,   perhaps across the world. People are already in a state of panic due to the re-occurrence of SARS.  Tourists and businessmen fear to visit an epidemic country. The majority of people may also believe that 2019-nCoV will not re-emerge once the current outbreak ends as they believed after SARS-CoV ended. People may lose a sense of alert and stay careless and will not be prepared to prevent the next 2019-nCoV infection in the future near.   A sense of alert is very much essential in this world of emerging biological threats, which is ultimately the result of a manmade environment.

Coronavirus Facts

  1. If you have runny nose and sputum you have common old.
  2. Coronavirus pneumonia is a dry cough with no runny nose.
  3. Maintain a fair (10 feet) distance from a sick person around you.
  4. Coronavirus lives for 12 hours on any metal surface, so wash hands with detergent often after coming in contact with metal body
  5. Coronavirus survives on fabric for hours, it can be killed by detergent.
  6. Drinking warm water is effective against all viruses.
  7. Avoid cold beverages.
  8. Avoid less cooked meat
  9. Wash your hands often because the virus can live on hands for a certain time and you can do a lot of things at this time, like rubbing your eyes, touch nose or eat something.
  10. Avoid touching your eyes, nose, and mouth with unwashed hands.
  11. You should also gargle with warm salt water at times.
  12. Drink plenty of water and occasionally warm water.
  13. Eat healthily that will make you immunologically strong.
  14. Maintain social distancing, use a tissue to sneeze or cough, and mostly stay home.


Pneumonia comes with high fever and difficulty breathing within five days of infection.

Coronavirus genome structure and replication.


Brian DA and Baric RS. Curr Top Microbiol Immunol 2005 – Review. PMID 15609507

Hu, B. et al. Discovery of a rich gene pool of bat SARS-related coronaviruses provides new insights into the origin of SARS coronavirus. PLOS Pathog. 13, e1006698 (2017). This paper identifies a gene pool of SARS-CoVs in bats

Lai, M. M. & Cavanagh, D. The molecular biology of coronaviruses. Adv. Virus Res. 48, 1–100 (1997

Hon, C. C. et al. Evidence of the recombinant origin of a bat severe acute respiratory syndrome (SARS)-like coronavirus and its implications on the direct ancestor of SARS coronavirus. J. Virol. 82, 1819–1826 (2008).

Wu, Z. et al. ORF8-related genetic evidence for Chinese horseshoe bats as the source of human severe acute respiratory syndrome coronavirus. J. Infect. Dis. 2013, 579–583

J Virol, 2020,  84 (2), 1198-205 Differential Downregulation of ACE2 by the Spike Proteins of Severe Acute Respiratory Syndrome Coronavirus and Human Coronavirus NL63. Ilona Glowacka 1, Stephanie Bertram, Petra Herzog, Susanne Pfefferle, Imke Steffen, Marcus O Muench, Graham Simmons, Heike Hofmann, Thomas Kuri, Friedemann Weber, Jutta Eichler, Christian Drosten, Stefan Pöhlmann

Iwai, M., and M. Horiuchi. 2009. Devil and angel in the renin-angiotensin system: ACE-angiotensin II-AT(1) receptor axis vs. ACE2-angiotensin-(1-7)-Mas receptor axis. Hypertens. Res. 32:533-536.

Jia, H. P., D. C. Look, P. Tan, L. Shi, M. Hickey, L. Gakhar, M. C. Chappell, C. Wohlford-Lenane,  and P. B. McCray, Jr. 2009. Ectodomain shedding of angiotensin-converting enzyme 2 in human airway epithelia. Am. J. Physiol. Lung Cell. Mol. Physiol. 297:L84-L96.

Kuba, K., Y. Imai, S. Rao, H. Gao, F. Guo, B. Guan, Y. Huan, P. Yang, Y. Zhang, W. Deng, L. Bao, B. Zhang, G. Liu, Z. Wang, M. Chappell, Y. Liu, D. Zheng, A. Leibbrandt, T. Wada, A. S. Slutsky, D. Liu, C. Qin, C. Jiang, and J. M. Penninger. 2005. A crucial role of angiotensin-converting enzyme 2 (ACE2) in SARS coronavirus-induced lung injury. Nat. Med. 11:875-879.

Lambert, D. W., N. M. Hooper, and A. J. Turner. 2008. Angiotensin-converting enzyme 2 and new insights into the renin-angiotensin system. Biochem. Pharmacol. 75:781-786.

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