A coronavirus is a subfamily of viruses, so named because they have large bulbous spikes from their envelope, which the virologist naming the virus thought resembled a monarchical crown. These projections are key to CoV infection.
“The term ‘protein corona’ refers to the layer of proteins that adhere to the surfaces of nanostructures when they encounter biological fluids,” explains Swedish virologist Kariem Ezzat. These proteins are strategically perched on the outside of a virus, acting as intelligence agents and first-contact specialists. “The importance of the corona layer is that it constitutes the actual surface of interaction with biological membranes or ‘what the cell sees’,” furthers Ezzat.
Coronaviruses are the viral family responsible for the “common cold.” By slight contrast, a distinct family of viruses cause influenza (the “flu”). Both viral families are enveloped RNA viruses. Symptoms of cold and flu are often selfsame.
Coronaviruses primarily infect the upper respiratory and digestive tract of mammals and birds. In people, coronaviruses are responsible for an unhealthy percentage of common colds. Coronaviruses also cause pneumonia and bronchitis.
Coronavirus disease was first described in 1931, with the viruses themselves first seen in 1965, having been taken from the nasal cavities of people with the common cold and put under an electron microscope.
Various coronaviruses are widespread among birds and mammals. Like all other viruses, coronaviruses opportunistically speciate by adaptively acquiring (via infection) or problem-solving new proteins which provide better tools for infection.
Coronaviruses have the ability to proofread their genome during replication and make corrections. Coronavirus mutation rates are thereby lower than other RNA viruses.
There are over 2 dozen coronaviruses. 7 known strains infect humans. The 6th to emerge was SARS-CoV-1 (V1), which hosted an epidemic in China in the winter of 2002. V1 caused a disease called SARS, which an acronym for “severe acute respiratory syndrome.” With its high mortality rate, SARS was scary.
V2 evolved from V1. V2 is the 7th, and latest, coronavirus. V2 causes the disease covid-19. The 19 stands for 2019, the year in which V2 made its human pandemic debut.
Both V1 and V2 have 29,891 nucleotides – twice as large as an influenza virus genome.
Most coronaviruses are not dangerous. But those that cause Middle East respiratory syndrome (MERS), SARS, and now covid-19, can be deadly.
Many mammalian coronaviruses originated with bats. Humans first encountered coronaviruses roughly 2 centuries ago from eating infected cattle. Modern outbreaks of new variants typically happen from eating infected animals.
V1 probably originated in bats and spread to humans through the civet cat, which was sold in wildlife markets and eaten as a delicacy in southern China. Civets were slaughtered en masse after the SARS outbreak.
Strong evidence indicates that V2 originated in horseshoe bats (Rhinolophus shameli) by 2010. V2 or a selfsame virus “has been circulating unnoticed in bats for decades,” reports a team of virologists.
Indonesia still runs wildlife meat markets. Along with dogs, Tomoho in central Indonesia sells bats, rats, lizards and snakes. “The market is like a cafeteria for animal pathogens,” said Indonesian epidemiologist Wiku Adisasmito, who has urged the government to close the country’s wildlife markets. “Consuming wild animals is the same as playing with fire.”
Chinese and Western researchers link SARS-CoV-2 to the pangolin: a mammal illegally trafficked in huge numbers for the reputed (but superstitious) healing qualities of its scales and meat. But pangolins may not be the source of SARS-CoV-2. The research published on the origin of the virus so far is inconclusive, other than to point to bats as the mammalian origin, with some intermediary mammal as the source of human infection.
British environmental scientist Thomas Lovejoy, who coined the term “biological diversity” in 1980, said of covid-19: “This pandemic is the consequence of our persistent and excessive intrusion in Nature and the vast illegal wildlife trade. It was just a matter of time before something like this was going to happen.”
The Chinese government belatedly cracked down on the wildlife trade believed to be behind the viral outbreak. On 17 February 2020, Chinese president Xi condemned the “major hidden danger” of eating wild animals. On 3 July China announced phasing out the sale and slaughter of live poultry at food markets. China subsequently banned the sale of wildlife.
English medical researcher Tom Jefferson argues that the common attribution of China as the origin point is only speculative. There is evidence of V2 in Spain, Italy, and Brazil months before the publicized outbreak in China. V2 was found in Barcelona waste water collected in March 2019, 9 months before the covid-19 outbreak in China.
Viruses of all kinds take atmospheric transport to spread across the globe. V2 is likely to have been one of them.
CoV2 (V2) has caused the most extensive global pandemic in recent history. The virus’ success owes to its saltational innovations, especially asymptomatic contagion. V2 achieved this by the exacting manipulation and deception.
V1 didn’t make it very far because it was not especially infectious. V1’s top spread (R0 (pronounced “R-naught”)) was only 0.5: every 2 cases of SARS resulted in only 1 additional infection. By contrast, V2’s R0 may reach 6 or even higher. In comparison, a typical seasonal flu virus has an R0 of 1.3.
Endemic viruses – those that become enduring invaders of their hosts – commonly have an evolutionary vector: they become less lethal and more infectious than their ancestors.
Herpes is a hoary virus that has been infecting most life forms from their early emergence. This ancient virus is exemplary in taking up residence in their hosts and commonly causing only modest discomfort during their stay – though the “settling in” of initial infection typically acts as a temporary disease.
Saltation is the attribution evolutionary biologists use for organisms which make seemingly sudden evolutionary leaps. Turtles are an example of saltation, in having suddenly appeared in the fossil record. Bones being well preserved, proto-turtles would have been discovered. The striking varieties of orchids is another example of saltation. In its rapid adaptations for asymptomatic infectiousness and prolonged virulence, V2 is a viral example of saltation.
V2 opportunistically adapted much faster than SARS did. It took SARS 3 months to mutate to human-to-human transmission; a feat that took covid-19 only 1 month.
V2 has also managed to infect numerous other mammals, including felines (cats), canines (dogs), and minks. Repeated covid outbreaks among minks on farms in Denmark, Spain, the Netherlands, Greece, Sweden, and the USA has caused considerable consternation, as minks have spread the disease back to people. Denmark decided to cull its entire herd of mink due to the risk of V2 mutations from minks making any vaccine ineffective.
V2 was a considerable evolutionary advance on V1 in being much more contagious yet far less lethal (~0.4% in V2 versus 9.6% in V1). This was achieved by ramping viral load quicker, before symptom onset. Whereas V1 viral loads did not peak until the 2nd week of illness, V2 viral load peaks before or around the time of any symptom onset.
The protein spikes that V2 sport are a critical factor in their naughty R-naught. “Viruses with more functional spikes on the surface would be more infectious,” said virologist Michael Farzan.
V2 has 4-5 times as many spikes as V1, and they are more robust. A V2 virion sports 20-40 spikes which end with a club-like shape ~20 nm in length.
V2 uses its spikes to detect target cells in a host. V2 evolved greater sophistication in being able to flexibly attach to host cells and infect than has been seen with other coronaviruses. Virologist Maolin Lu: “The spike protein constantly changes shape. This shape-shifting feature not only allows the virus to enter host cells, it also helps the virus escape from being attacked or recognized by antibodies.”
V1 spikes tended to break off after some use, debilitating the virus for finding its targeted host cell via a signifier on the cell termed ACE2. Besides being much more abundant, and thereby more attentive to the mission of infection, V2 spikes have more staying power.
A V2 spike is flexibly connected to the viral surface by 3 hinges that disguise themselves from antibody detection via glycosylation. Sugar molecules swirl around the surface of a protein-laden spike, creating a cloak which hides the virus from being detected by host antibodies.
Multiple spikes act in concert to conformationally engage onto the flat surface of a host cell: an ideal configuration for rapid reading of a possible entry site. The optimality of these innovations is impressively saltational.
The robust spikiness of V2 seemingly emanates from a single modest genic mutation that causes the 614th amino acid in the spike protein to be D rather than G. “The D614G mutation increases the infectivity of SARS-CoV2,” Australian evolutionary virologist Eddie Holmes said. “That’s the incredible thing about viruses. Small changes can amplify quite dramatically,” marveled American virologist Michael Letko.
The image above is a side view of the V2 spike protein, with section 1 in green and section 2 in purple. This 2-piece appendage is not as stable as a single section would be. The D614G mutation both stiffens this system and sensitizes it to ACE2 reception. V2 “figured out how to hold on better and not fall apart until it needs to. The virus has made itself more stable,” remarks American virologist Michael Farzan. “D614G began spreading in Europe in early February, and when introduced to new regions it rapidly becomes the dominant form,” notes American computational biologist Bette Korber.
Not all virologists are wowed about the D614G mutation being the key to V2’s worldwide success. The skepticism is well grounded, as asymptomatic infection has been the real key to becoming a global pandemic.
Upon sensing the possibility of reaching its destination, a little hook at the end of a spike protein flips up above the sugar shield to suss the situation. If it encounters a particular protein on the surface of a host cell, it sets off a series of reactions that allows the virus to fuse to a cell membrane and inject its sentient package of genetic material.
The RNA that comprises V2 is just artifactual. “You have a lot more information stored in how it’s shaped,” informs structural microbiologist Sylvi Rouskin. The root of V2’s success is the energetic intelligence behind the virus, not the molecules themselves.
A ribosome is the organelle within a cell that manufactures proteins and other bioproducts that a cell needs. Viruses hijack ribosomes to produce copies of themselves rather than provisioning the host cell.
V2 RNA is precisely structured to fit neatly into a ribosome. Precise conformational geometry to ribosomal machinery is how V2 is able to replicate so quickly.
V2 replicates 3 times faster than V1, thus enhancing its virulence by dint of spreading within a host before the immune system has the opportunity to respond. The reproductive speed of V2 also smacks of saltation.
The viral RNA is read by a ribosome in a convoluted way. A ribosome reads V2 RNA strands like a roller coaster car rolling along a track, obtaining the chemical formula for producing what the virus wants.
Specific loops in the viral RNA throw the roller coaster reader off its track, jumping it to a spot thousands of positions away. Other loops force the ribosome to back up a bit and then move forward again in its interpretive reading. These viral guides make it possible for entirely distinct proteins to be produced from the same stretch of RNA: an incredible economy in using the same genetic material multiplicitively.
Creating a new, viable virus does not just spontaneously happen. A team of some half-dozen distinct proteins coordinate assembly of a new V2 virus.
This freshly minted virus is then packed into a robust droplet. This droplet form helps hide the pathogenic identity of the virus from the immune system.
Droplets are tightly sealed with an innocuous membrane. A viral protein within the droplet can pop open the droplet when conditions warrant. The viral droplets get coughed or sneezed out, along with and encased in phlegm. Viral droplets may also exude from the skin, fomenting fomite contamination.
The ability to rapidly reproduce but not disrupt host functioning is the saltational genius of V2. This owes to V2’s ability to confound the host immune system, thereby weakening its response.
Researchers have identified a specific V2 protein, termed Nsp1, that instructs ribosomes to make virual bioproducts while neglecting built-in programming or instructions from the host cell. The ribosome is duped into not warning its own cell that it has been hijacked.
Camouflage is V2’s secret weapon. V2 makes an enzyme which fools its host cell into thinking that the virus is native, not something of concern.
Viruses are cellular mavens. Nucleic acids are their stock in trade, proteins their handicraft. The innovations of V2 were decisions by the coherent intelligence that appears as a virus.
“Biological evolution is an economic process in which the entities of life – all organizational units from genes to species – change through time according to the circumstances in which they live and which they helped to create. It is a process governed by opportunities, challenges, and limitations. Feedbacks between life and its environment effect evolution,” observed Dutch evolutionary biologist Geerat Vermeij.
Like other coronaviruses, V2 thrives in colder environments. Hence food markets where products are kept cool and meat-processing plants have been a popular hangout for the virus. A computer simulation study in Japan found that air humidity lower than 30% more than doubles the potential volume of V2 aerosol particles compared to 60% humidity or higher. The dry conditions found indoors in winter provide considerable potential for abetting V2 transmission.
Unlike other coronaviruses, V2 has done quite well in warmer climes. Retaining vivacity despite warmer temperature is an impressive innovation in a viral family typically thermally sensitive in preferring being cool. The V2 virus did not miss a beat during the summer heat.
American computational biologist Bette Korber thinks V2 is working toward a “fitness advantage.” American virologist Stanley Perlman, “It certainly looks more readily transmissible. Viruses mutate to become more transmissible, but not generally to become more virulent (unless this enhances transmissibility).” “It is in the virus’ interest to infect more people but not to kill them because a virus depends on the host for food and for shelter,” remarked infectious disease researcher Paul Tambyah.
V2 has many variants, and the virus continues to evolve to improve its infectiousness. V2 “differs not only on a country and regional basis but even among cities,” reports Turkish virologist Sadrettin Pençe. “The evolution and demography are complex,” adds American biostatistician Marc Suchard. This variability lessens the reliability of tests and the prospect of a vaccine having any longevity in effectiveness.
Variants commonly carry a package of innovations, including many which change the structure of the spike protein on the surface of the virus, enhancing V2’s ability to bind to human cells. People infected with the variant have higher viral loads, indicating greater viral productivity. Those infected shed more virus when coughing or sneezing – leading to its increased contagiousness.
Virologists suspect that recent V2 variants are partly aimed at making children “as equally susceptible as adults,” said English virologist Wendy Barclay.
V2’s wiles in asymptomatic transmission seems something of a conundrum because the symptoms in its victims, when they do appear, are so diverse and can be devastating: affecting both respiratory and circulatory systems. While increasing infectiousness is relatively easy, as V2 exemplifies, it takes a long time for a virus to learn how to minimize its damage to its host system. Compassion is not a viral priority.
V2 does not make healthy people sick, or they are inconvenienced by a mild cold at worst. The root problem of severe covid is autoimmune response. In unhealthy people, V2 alarms the immune system such that it kicks into overdrive and wrecks havoc. People who have a chronic health condition, are overweight and/or physically out-of-shape are susceptible to covid sickness.
Thanks to V2’s ambition and adaptations, covid-19 looks to be a never-ending pandemic.
Ishi Nobu, “Coronavirus pandemic news,” (updated daily).
Ishi Nobu, “Viral engineering,” (10 March 2020).
“A trove of bat coronaviruses,” Nature (17 March 2021).
Carl Zimmer, “The coronavirus unveiled,” The New York Times (9 October 2020).
B. Korber et al, “Spike mutation pipeline reveals the emergence of a more transmissible form of SARS-CoV2,” bioRxiv (5 May 2020).
Lizhou Zhang et al, “The D614G mutation in the SARS-CoV2 spike protein reduces S1 shedding and increases infectivity,” Scripps Research (12 June 2020).
“Mutated coronavirus shows significant boost in infectivity,” Scripps Research (12 June 2020).
Benedict Carey & James Glanz, “Mutation allows coronavirus to infect more cells, study finds. Scientists urge caution,” The New York Times (12 June 2020).
Ishi Nobu, The Elements of Evolution, BookBaby (2019).
Ishi Nobu, “Viruses,” (8 February 2020).
Ishi Nobu, “Viral engineering,” (10 March 2020).