-Diganta Paul
A significant super-spreader event took place in a hotel in 2002, causing the hotel guests to unknowingly become global carriers of a virus. This virus resulted in 774 deaths as well as staggering economic losses within the span of six months. The virus had a global economic impact with the Asian Development Bank recording losses of 59 billion USD. This was the outbreak of SARS-CoV (Severe Acute Respiratory Syndrome Coronavirus) viruses causing SARS (Severe Acute Respiratory Syndrome). A few years later, the first case of MERS-CoV (Middle East Respiratory Syndrome Coronavirus) viruses was found and documented in Saudi Arabia. The MERS-CoV virus was sequenced and identified as related to SARS-CoV virus. Due to the known pandemic potential of SARS-CoV in addition to the annual religious pilgrimage to Mecca, MERS-CoV triggered global health security concerns. However, epidemiological reports showed that MERS-CoV is less contagious and has a lower pandemic potential than SARS-CoV. Despite the lower pandemic potential, MERS-CoV, like SARS-CoV, also had a global impact. Travel restrictions were applied to all travellers in the infected area by interfering with the normal traffic to and through the region.
Late December 2019, Wuhan, China: People started to fall sick having fever associated with cough, dyspnea and muscle aches. ‘Viral Bilateral Pneumonia’ cases started to knock doctors’ doors. The knocks looked familiar because the disease was thought to be ‘Pneumonia’. Soon the knocks seemed to be alarming because the number of cases embarked to go up rapidly. Deep dive into the cause of the sickness unveiled the shattering truth that a disease in pneumonic disguise had been creeping down the lungs towards gastrointestinal organs of human body. Sixteen years after the attack of SARS-CoV, the human respiratory systems were noticed to carry a previously undetected virus from ‘Nidovirales’ order based on the taxonomical analysis of viruses. Though the virus was an RNA virus (because its genetic material was ‘Ribonucleic Acid’ or ‘RNA’), unlike many known RNA viruses such as HIV [Human Immunodeficiency Virus causing AIDS (Acquired Immune Deficiency Syndrome)], this virus was not transforming its RNA to DNA (Deoxyribonucleic Acid) to insert that DNA to the host-cell’s DNA. Rather, after entering the host-cell, this virus was placing its RNA to act as ‘messenger RNA’ (mRNA) for the host-cell’s ‘Ribosome’ to translate this mRNA into two large overlapping polyproteins. One of those polyproteins splits into sixteen nonstructural proteins that help to produce new viral RNAs through replication and transcription processes.
The microscopy image of the virus-particle showed club-shaped spikes of protein projected from its particle-membrane and resembled ‘Solar Corona’. This view confirmed the virus to be a newly discovered member from ‘Coronaviridae’ family which consists of four genera – ‘Alphacoronavirus’,’Betacoronavirus’,’Gammacoronavirus’ and ‘Deltacoronavirus’.
The contagious disease caused by this virus was named as ‘Coronavirus Disease-2019’(COVID-19) and it spread all over the globe resulting in more than 722,435 confirmed infection-cases and at least 33,997 reported deaths distributed across more than 114 countries as of 30th March, 2020. As this virus caught the attention of Mankind for the first time, it was named ‘Novel Coronavirus’ initially but later, based on about 70% similarity of its genome (the collection of all the possible genes is called ‘Genome’ of an organism) sequences and its degree of relatedness to the SARS-CoV virus, this virus was called ‘Severe Acute Respiratory Syndrome Coronavirus-2’ (SARS-CoV-2).
This virus has been comprehended to be a sibling strain to the SARS-CoV virus under ’Betacoronavirus’ genus, ‘Sarbecovirus’ subgenus and ‘Severe acute respiratory syndrome-related coronavirus’ species.
SARS-CoV-2 Particle Structure and the Way It Penetrates Human Cell:
Each SARS-CoV-2 virion (the microorganism is called ‘Virus’ when it is inside host’s cell but called ‘Virion’ when it is either outside host body or at the intercellular gap of host-body) is approximately 50–200 nanometres in diameter. Like other Betacoronaviruses; SARS-CoV-2 has four structural proteins – S (spike), E (envelope), M (membrane) and N (nucleocapsid) proteins. The N protein holds the RNA genome and the S, E, and M proteins together create the viral envelope. SARS-CoV-2 has shown sufficient affinity to the ACE2 enzyme (Angiotensin Converting Enzyme 2) of human cells. ACE2 enzyme is most abundant in the type II alveolar cells of the lungs. ACE2 is also abundantly expressed in the glandular cells of gastric, duodenal and rectal epithelium as well as endothelial cells and enterocytes of the small intestine. The virion connects to the ACE2 using the ‘Spike Protein’ of its surface. After connecting to the ACE2, the virion can enter cell in two ways – a) it can enter the ‘Endosome’ (an endosome is a membrane-bound compartment inside a eukaryotic cell) of the host-cell by fusion of the viral envelope with the ‘Endosomal Wall’ or b) it can enter the host-cell directly by fusion of the viral envelope with the host-cell membrane.
Symptoms of COVID-19:
Reported illnesses have ranged from mild symptoms to severe illness and death for confirmed COVID-19 (Coronavirus Disease 2019) cases.
Below-mentioned symptoms may appear 2-14 days (Incubation Period) after exposure to the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) causing COVID-19 disease-
- Fever
- Cough
- Shortness of breath
- Muscle Aches
Warning Signs for COVID-19:
Some warning signs may pop up before completion of the incubation period of SARS-CoV-2 virus –
- Persistent pain or pressure in the chest
- Bluish lips or face
(This list may not be all inclusive because COVID-19 is a new disease and we are continuing to understand this disease every day.)
People Who Are at Higher Risk of Severe Illness Due to COVID-19:
COVID-19 is a new disease and there is limited information currently regarding risk factors.
Those who are at high-risk of severe illness from COVID-19 include –
- People aged 65 years and older.
- Other high-risk conditions may include:
- People with chronic lung disease or moderate to severe Asthma.
- People who have heart disease with complications.
- People who are immunocompromised.
- People of any age with severe obesity (body mass index [(BMI)≥40]) or certain underlying medical conditions, particularly if not well controlled, such as those with Diabetes, renal failure, or liver disease may also be at risk.
- People who are pregnant should be monitored since they are known to be at risk with severe viral illness.
Many conditions can cause a person to be immunocompromised. These include Cancer treatment, bone marrow or organ transplantation, immune deficiencies, poorly controlled HIV or AIDS, and prolonged use of corticosteroids and other immune weakening medications.
How does COVID-19 spread?
The virus SARS-CoV-2 is thought to be natural and has an animal origin through spillover infection.
‘Spillover Infection’, also known as ‘Pathogen Spillover’ and ‘Spillover Event’, occurs when a reservoir population with a high prevalence of a particular species of pathogens (bacteria or viruses or other microorganisms that can cause disease) comes into contact with a novel host (host of a particular species that is new to be infested with the pathogens) population. The pathogens, transmitted from the reservoir population to the novel host population, may or may not be transmitted within the novel host population.
The reservoir population of SARS-CoV-2 viruses is still not known. It is being assumed that animals became their novel hosts somehow and then human beings became the same.
Person-to-person spread
The viruses have been thought to spread from person-to-person in following ways –
- Between people who are in close contact with one another (within about 6 feet).
- Through respiratory droplets produced when an infected person coughs or sneezes. These droplets can land in the mouths or noses of people who are nearby or possibly be inhaled into the lungs.
Spread from contact with contaminated surfaces or objects
It may be possible that a person can get COVID-19 by touching a surface or object that has the virus on it and then touching his/her own mouth, nose, or possibly his/her eyes.
Estimation of the rate of decay of these viruses suggests that the viruses may remain viable up to 18 hours on copper, 55 hours on cardboard, 90 hours on stainless steel, and over 100 hours on plastic. The viruses remain viable in aerosols for 3 hours. The viruses have also been found in faeces.
A Probable Way Needing Investigation to Cure COVID-19:
We have already known the guidelines to follow to avoid exposure to SARS-CoV-2 viruses from various sources. Now let us look into a possible way to get rid of this virus. We have known that SARS-CoV-2 virus is of ‘Severe acute respiratory syndrome-related corona virus’ species. I am going to propose a probable way that Doctors and Scientists may investigate to stop the viruses of ‘Severe acute respiratory syndrome-related corona virus’ species from multiplying in human cell. To make understand the way, first let me explain the process how the viruses of this species multiply in human cell:
Process of Multiplication of Severe Acute Respiratory Syndrome-Related Coronavirus in Human Body
After the virus enters human cell by fusion, the virus’ ‘Nucleocapsid’ passes into the human cell’s cytoplasm where the viral genome is released. The genome acts as a ‘messenger RNA’ (mRNA) and the human cell’s ‘Ribosome’ translates two-thirds of the mRNA into two large overlapping polyproteins – ‘pp1a’ and ‘pp1ab’. The polyproteins contain their own enzymes ‘Proteases’, ‘Papain’ and ‘3CLpro’ which cleave the polyproteins. The cleavage of polyprotein ‘pp1ab’ yields 16 nonstructural proteins (‘nsp1’, ‘nsp2’, ‘nsp3’,…….,‘nsp16’). A number of nonstructural proteins among them act as replication proteins. A number of those nonstructural replication proteins coalesce to form a multi-protein ‘Replicase-Transcriptase Complex’ (RTC). The main Replicase-Transcriptase Protein in that complex is the ‘RNA-dependent RNA polymerase’(RdRp) or ‘nsp12’. ‘RdRp’ or ‘nsp12’ is directly involved in the replication and transcription of new viral RNA from an existing viral RNA strand. The other nonstructural proteins in the complex also assist in the replication and transcription process. ‘nsp1’ protein promotes human mRNA degradation, blocks translation process in the human cell and also blocks innate immune response of human body. ‘Papain’ enzyme-domain of the polyprotein ‘pp1ab’ also blocks human’s innate immune response.
Counteracting the ‘Papain’ Enzyme Produced by Severe Acute Respiratory Syndrome-Related Coronavirus in Infected Human Cell ‘Papain’ is derived chiefly from the unripe fruit of the papaya or pawpaw tree. Its enzymatic properties have found application in the food and drug industries such as clearing cloudy contact lenses, tenderizing meat, lysing wound adhesions, treating Hymenoptera and jellyfish stings and as additives in laxatives, tooth powders, digestive tablets and skin lotions. Many people who work in these industries have to get exposed to ‘Papain’ and many of them suffer from dyspnea, cough and chest tightness which are some of the symptoms of COVID-19 caused by SARS-CoV-2 viruses. So, the ‘Papain’ enzyme-domain of ‘pp1ab’ polyprotein, generated in the infected human cells by the virus, may be a cause of dyspnea, cough and chest tightness in COVID-19 patients. If we can apply anti-enzyme (a substance especially an antibody or an enzyme which counteracts the effects of another enzyme) for ‘Papain’ enzyme to the COVID-19 patients, that may be helpful. As per the multiplication process discussed above, ‘Papain’ enzyme-domain of ‘pp1ab’ polyprotein is an important element for Severe Acute Respiratory Syndrome-Related Coronavirus to multiply in human body and so counteracting the ‘Papain’ enzyme-domain of ‘pp1ab’ polyprotein in infected human cell may stop the multiplication of the virus. The bodies of some people working in the above-mentioned ‘Papine’ dependent industries for long may have produced such a type of anti-enzyme and that is a matter of investigation.
