Minute yet Mighty: The Coronavirus

By: Maria Rizwan
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‘It’s really the survival of the fittest’- Dr. Adam Lauring, Associate Professor of Microbiology and Immunology at the University of Michigan in Ann Arbor.
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​COVID-19, a descendant of the seven-member nuclear family of corona viruses (CoVs), has been the star of town for quite a while now, and according to some sources, won’t be leaving town anytime soon. It’s the day to day news, chit, and chatter, but how well exactly did you absorb the information? Let’s take a look at its simply complex nature, step by step.

Meet the Family
The family of Coronaviruses are, by no surprise, quite infectious. 2 of them evolved to become what we came to know as SARS (severe acute respiratory syndrome) and MERS (Middle East respiratory syndrome). Consequently, titling the novel coronavirus as the ‘severe acute respiratory syndrome 2’ (SARS-Cov-2).

Discovered in the mid-1960s, the family of coronaviruses were named after their ‘crown-like spikes’ and were further classified into a family known as the Orthocoronavirinae. This particular family is divided into four genera, one of which SARS-Cov-2 resides in, namely the Betacoronaviruses (β-CoVs). These also happen to include SARS and MERS CoVs and are commonly known to infect humans and /or various other mammals. Virologists also firmly believe that the β-CoVs genera are a descent of the bat gene pool, thus allegedly leading us to the controversial ‘bat soup’ speculations. This lineage of β-CoVs have wracked chaos in our world and have yet to be detained. 

A Microscopic Glimpse
Now that we know of its relatives, let’s dive deeper into its replication mechanism. How exactly does this acellular, minute of a particle send our body into a frenzy? 

It all begins when these microscopic particles waft through the air and enter our body during inhalation, subsequently attaching itself to the surface cells in our airway. The (S1) crown-like spikes surprisingly, have a high binding capacity with the ACE2 molecules present on the cells. Locked in, these particles invade the cells through endocytosis (engulfment of material by cell membranes), enabling the virus to enter our cells.

Once settled in and cosy, the virus takes advantage of the genetic machinery of the cell. It releases a strand of RNA (Ribonucleic Acid), a fraction of the viral genetic material, and begins the synthesis. Encompassing the gear, the protein synthesis creates fresh new viral proteins ready to conquer a multitude of cells.

Do note that, one infected cell has the capability to generate millions of viral copies before it becomes of no use!

Symptoms
The most communal symptoms of SARS-CoV-2 seen in the public are of pneumonia, dry cough and fever. The pneumonic symptoms can be owed to the nature of the virus. SARS and MERS CoV both are sources of atypical pneumonia, which accounts for a mild fever (36-37℃) and dry cough. Due to the SARS-CoV-2 possessing > 70% of the same genetic sequence as the SARS-CoV, it only makes sense that the range of symptoms align to be parallel.

If you scroll up, you’d re-encounter the infamous entry cell receptor, ACE2. Research shows that although, SARS-CoV and SARS-CoV-2 are astonishingly similar, the ‘corona’ spikes of the latter have approximately a 10-20-fold higher affinity to bind with ACE2 than the afore mentioned. Causing this pandemic to be exceedingly contagious and taut.

Upon entrance of the viral copies in the alveolar epithelial cells (located in lungs), rapid replication transpires, and an immune response is triggered. An extremely strong immune response, at that. Like many of us, cells tend to overreact and push the red button. Which, in this case, would be a cytokine storm. A cytokine is a signalling protein produced by threatened cells to prompt an immune response. However, overproduction and release of these proteins can be fatal. The cytokine storm syndrome (CSS) can lead to fatigue, high fever and Hypercytokinaemia which in turn, instigates multiple organ failure. According to the PMC, from the first 99 patients of COVID-19, 17% displayed signs of ARDS (acute respiratory distress syndrome), a symptom of CSS, among whom 11% had passed away due to multiple organ failure.

Overall, this dynamic of symptoms affects our immune system collectively. It tires out our immune cells, specifically the T cells. T cells aim to adapt and mediate pathogenic invasions. With lack of full vigil, primary and secondary immune responses are slowed down, paving way for the virus to thrive.

Resilience
Although Coronaviruses fall under the category of ‘enveloped viruses’, their nature deems to be quite resistant. Their lifestyle alone as non-living particles stem a variety of problems. However, let’s first peer at this from a generic perspective.

The afore mentioned category also accounts for large particles. Yes, CoVs are large, enveloped viruses. Large in comparison to other viruses, not the microorganic domains! Owing to that, and the fact that they encompass none of the hallmarks of living things (disregarding sensitivity), the bar has been raised. 

Generally, viruses are impervious pathogens due to their idiosyncratic ways of living. They hijack our genetic material and photocopy of our host cells. Due to them seizing our cells and becoming one, anti-viral drugs are difficult to propose. If they intend to dissolve these parasites, they will consequently eradicate our somatic and gamete cells.
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Why can’t we utilize the anti-viral drugs formulated for SARS-CoV or MERS? A common question, with a paradoxical answer. From one virus to another, innumerable differences prevail. Like an enzyme to its substrate, a virus is specific to its own anti-viral drug. The former anti-viral drugs may engender side effects or perhaps relieve symptoms, in some cases.

Withal these frustrating impediments, mutations have seen a drastic accretion throughout the recent months. Mutations are changes, rather mistakes created during the DNA replication process. Although, being unfavourable, they may also result to be propitious. Thus, scientists are unsure of the evolving nature of the virus. Despite that, it does arise problems as they gradually become harder to identify. The S1 crownlike spikes may reform into distinctive shapes and inhibit the impact of contemporary developing vaccines as our bodies’ antibodies may remain oblivious due to the lack of antigens.

Inhibition
Speaking of anti-viral therapy, several have been clinically tested to investigate (in)direct effects on the SARS-CoV-2. A strategical approach the majority first leaned towards was the concept of drug repurposing. Dr. Sumit K. Chanda’s, a virologist at Sanford Burnham Prebys Medical Discovery Institute in La Jolla, Calif, team, led this initiative. 

The most eminent tactic was to test previous proven-effective anti-viral drugs, the ones of Ebola or SARS, perhaps. The infamous anti-viral, Remdesivir, had high expectations from the medical community, but isn’t as efficacious as they hoped it to be. Though on the bright side, Dr. Anthony S. Fauci, America’s leading infectious disease specialist, announced that it reduced mortality rates and duration of SARS-CoV-2.

Another team of researchers directed by Dr. Nevan Krogan, a molecular biologist at UCSF, are continuing a study on 69 compounds. They limited it to these compounds as they found that they worked in a similar manner of that of the virus. They targeted similar proteins and gave a possibility to battle the virus. In further examination, about 60 of the candidates failed the expectations, however the remaining 9 deemed promise. The 9 drugs ensued great impact as it was said to be: ‘10 to a hundred times more potent than Remdesivir’, according to Dr. Krogan. The future of these 9 awaits trial and errors, reforming our hopes.

Precautions
In wait of the pending answer, general instructions have been initiated by the public. Though hand washing seeming to be the universal go-to. However, do you know the chemistry behind it? 

Soap molecules are pin-shaped and pointed, rupturing. Since viruses and bacteria contain an oily lipid membrane that holds them intact, their Achilles heel is quite apparent. The water-repelling end of the soapy molecule, a hydrophobic tail that can bind with fatty substances, jabs at the membrane puncturing it. Hence, leaving a disarray of organelles and a deflated particle.
Alcohol is a potential candidate as well. Nonetheless, they usually exist to be in quantities <60% in disinfectants. Moreover, they can’t outdo the dual nature of soaps. Chemically both achieve desired effects, but soaps prove to be more effective in physically extracting substances off our skin. The hydrophilic (water-loving) molecules’ heads grasp to contact water molecules, though their tails refrain from doing so. To avoid contact, they curl inwards, consequently scooping up minute bubble captures known as micelles. Thus, cleansing the tested surfaces.

Antibacterial soaps/gels are furthermore of no use either, as they fail to penetrate viruses. In bacterial cases, at times it may also develop a resistance due to mutations during DNA replication or via evolution-led natural selection. 

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To conclude, I’d like to highlight that this is a time of uncertainty and clouding doubts. It’s a time of lively deaths and deadly lives. The path ahead remains unclear and may deem to be a mirage. An illusion to our eyes, questioning anything and all. Nevertheless, this mirage is wholely dependant on your vision, on your actions.
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Remain clam and refrain from panic. Pay heed to precautionary measures, as they’re instructed for solely you, and your loved ones’ benefit. See to be updated and help if you’re able. However, do not see to exhort human interaction and rather, branch out virtually to lend a hand to those lacking or needing. It’s a time for us to coherently depend on one another and unite, from a distance.

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Sources:
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Li, Heng, et al. “Coronavirus Disease 2019 (COVID-19): Current Status and Future Perspectives.” International Journal of Antimicrobial Agents, Elsevier B.V. and International Society of Chemotherapy., May 2020, www.ncbi.nlm.nih.gov/pmc/articles/PMC7139247/.
“Betacoronavirus.” Wikipedia, Wikimedia Foundation, 29 May 2020, en.wikipedia.org/wiki/Betacoronavirus.
 “How Soap Kills COVID-19 on Hands.” UNESCO, 24 Apr. 2020, en.unesco.org/news/how-soap-kills-covid-19-hands.
Zimmer, Carl. “Old Drugs May Find a New Purpose: Fighting the Coronavirus.” The New York Times, The New York Times, 30 Apr. 2020, www.nytimes.com/2020/04/30/health/coronavirus-antiviral-drugs.html.
Schraer, Rachel. “Coronavirus Mutations: Scientists Puzzle over Impact.” BBC News, BBC, 6 May 2020, www.bbc.com/news/health-52557955.

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Author

Maria Rizwan is a sophomore in UAE, passionate about STEAM and Innovation. She's particularly drawn towards Microbiology and relevant fields, hoping to learn and shed light on the basis of life and disease. You can also find her in a variety of other organizations, i.e GiWC, Steam On, Lilac, etc., involved in either Arts, Poetry or Science. If not napping, you can find her indulged in the world of arts, painting away :)