Hence, the importance to look at this ultra-microscopic monster from close quarters has taken such a heavy toll on mankind.
There is little reliable information available in the public domain about the virus, its origin, its structure, the peculiarities and its modality of the infection it causes.
The virus from the family of viruses called the coronavirus has been termed Cov 2 which causes the disease Covid 19, as it first appeared in Wuhan, China, in the later part of 2019.
Nor is coronavirus something new. In fact, the first coronavirus was isolated in 1937.
Humans are mostly infected by four types of coronaviruses that cause the third of the most common of cold and flu after rhinoviruses. But they did not spread infection and fatalities as they have now on a wide and extensive scale.
The name stuck when they were for the first time studied under the electron microscope in the early part of 1960s and found that the uniform yellow layer of protein spikes appeared to resemble the corona of the sun that occurs during the solar eclipse.
Coronaviruses are to be found almost everywhere and most of them circulated among camels, cattle, pigs, turkeys, horses, dogs, cats, rats and bats among other animals. And they were not harmful to human beings.
According to the world of virological classification and nomenclature bodies, coronaviruses are found to be of four types—alpha coronavirus, beta coronavirus, delta coronavirus and gamma coronavirus. However, only alpha and beta coronavirus have the capacity to infect humans. These viruses spread through the air and are responsible for upper respiratory infections.
There are altogether seven sub types of coronaviruses in the two broad groups of alpha and beta types. They are HCoV-229E, HCoV-OC43, HCoV-NL63, HCoV-HKU1, SARS-CoV (which causes severe acute respiratory syndrome), MERS-CoV (causes Middle East respiratory syndrome), and now SARS-CoV-2.
Apart from SARS-Cov-2 all others are human pathogens, while the former is zoonotic, which means that there are some animal carriers of the virus which were immune to the adverse effect of the virus while causing infections in humans only.
If we look at the other lethal type of such infections that happened in recent times, two such viruses come up.
The Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV) that killed 774 of the 8,096 people who fell ill in 29 countries and the Middle East Respiratory Syndrome Coronavirus (MERS-CoV) was even more fatal killing about 800 of the 2,000 plus infected.
MERS-CoV is still occurring in the middle-eastern countries. According to a WHO report, SARS-CoV and MERS-CoV spread among people who were in close contact which resulted in many fatalities of healthcare workers.
The ultra structure of the virus had revealed that it is composed of a 32 kilo nucleotide long RNA strand (in fact the largest known RNA virus ) that is surrounded by the protein coat called the capsid, which in turn is surrounded by an additional lipid (fat) layer. However what is unique here is the emergence of the long spikes from the capsid, called the spike proteins.
And these spike proteins are the contrivances that are used like hooks by the virus to latch on the human cell. But then the virus just can’t get latched onto any part of the cell. It needs a special receptor that is recognised by the virus called the ACE 2 (angiotensin converting enzyme ) to which the virus gets latched by help of the S1 protein of the spike. This then facilitates the entry of the virus by endocytosis (a process by the invagination or folding of the cell membrane).
The replication or multiplication process of the coronaviruses is unusual. It is a two step replication mechanism. Most RNA virus genomes contain a single Open Reading Frame (ORF).
The ORF is the beginning point in the RNA sequence from which a protein required for the virus is synthesized. Then it is catalytically cleaved or cut down into smaller functional viral proteins, but coronaviruses can contain up to 10 separate ORFs or ten separate beginning points of protein synthesis at the site of protein synthesis, the ribosomes, both inside and of the host cell.
Interestingly most of the ribosomes translate the biggest one of these ORFs, called replicase, which is twice the size of many RNA viral genomes. The replicase gene encodes a series of enzymes that use the rest of the genome as a template to produce a set of smaller, overlapping messenger RNA molecules, which are then translated into all the proteins—that makes up the different structural and functional ones that ultimately make up the new viral particles.
BAT AND PANGOLIN
When the virus first hit in Wuhan, the Chinese had started sequencing the viral genome. And what was revealed was surprising because first they found that it had almost 96 percent sequence similarity with a bat virus Rhinolopous species.
Then they found that the intermediate host may have been the palm civet. And later on they found that it had much more similarity with a virus found in pangolin that is almost 99 per cent similarity.
And yet later such multiple sequence similarity studies showed that it has 90 per cent similarity with the Malaysian Pangolin.
Such studies have helped the worldwide scientific community theorise that SARS Cov 2 virus may be a chimaeric virus having its origin in two different corona virus that had its genesis in a common host organism. And yet recent studies have shown that it enters and destroys T cells just like HIV virus. And like the latter, it has almost somewhat similar molecular strategy for entry into human cells.
And this makes it highly dangerous to humans.
CHANCES OF COMBATING IT MEDICALLY
Very little is known about the virus, so far as it’s epidemiology and actual mechanism of infection is concerned. Various anti viral drugs and drug combinations seem to give mixed results so far. But the key probably lies in using immuno modulators that would have an enhanced immuno response in the early stages.
On vaccines it is too early to predict whether it would be successful though a lot of work has been going on in various such institutes worldwide with Oxford University already starting clinical studies. This is primarily because we don’t know for certain whether or not its mutation rate is very fast just like HIV.
We can at best just keep our fingers crossed! And gather information on the molecular peculiarities of this wee bit of an entity albeit a deadly pathogen so as to develop a potent strategy for combating and coming out victorious in this war for the time is running out and it’s running out fast!
(The writer teaches Genetics to undergraduate students of Botany and Zoology in Gauhati University)