D614G coronavirus strain 'more infectious than original version'

Most common strain of coronavirus found in 85% of all cases worldwide mutated from the original version to be MORE infectious – but not more deadly, study finds

  • D614G is found in more than 85 % of global coronavirus patients, data shows 
  • Scientists tried to find why mutant is so dominant compared to original strain
  • New study shows the mutated strain is more infectious and better at spreading 
  • However, no evidence it increases the risk of death or serious symptoms  

A mutated version of the coronavirus, dubbed D614G, is found in 85 per cent of global cases and researchers believe this version is so common because its genetic modification makes it more infectious and better at spreading. 

However, analysis from experts at the University of North Carolina found the change did not make it more deadly or likely to cause severe symptoms. 

D614G is by far the most common strain of coronavirus affecting humans worldwide and first appeared in February in Europe.

International travel allowed this variant to spread across the continent and into the Americas, Oceania and Asia within weeks. 

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D614G mutation is the most common variant of the coronavirus,  found in 85 per cent of global cases, and researchers believe this mutant version thrives because its modification made it more infectious and better at spreading

In the early days of the Covid-19 pandemic, the dominant guise of the virus was a variant now called the ‘D strain’. 

However, the D614G mutation sprung up at one specific location, position 614, on the spike protein of the virus, in a European patient. 

This viral spike hijacks the human receptor ACE2 and this is how it infects human cells. 

The location of the mutation sits at a critical juncture which affects how the virus cleaves in half after infiltrating a cell.

The mutation is very small and simple, one amino acid is changed from a D (aspartate) to a G (glycine), hence the moniker D614G.  

As Italians, Britons and others from coronavirus hotspots travelled to Asia, Australia and America, the D614G virus then took hold in these regions. 

Data from a study published last month shows a spike of the G strain in Europe at the start of February, followed by another resurgence of the G variant a fortnight later. 

By the start of March, cases of D614G were spotted around the world and this specific mutation made up around a quarter of all cases.  

It continued to take over and constituted more than 70 per cent of all cases by May, and the number is now thought to exceed 85 per cent.  

Scientists have been trying to determine why the D614G strain emerged as the principle form of SARS-CoV-2, the virus which causes Covid-19. 

The latest study, published in the journal Science, created a lab-built version of the mutant virus and watched how it infected mice and hamsters modified to have the human version of the ACE2 receptor.

ACE2 has been dubbed the ‘gateway to the cell’ for the coronavirus and the interaction between it and the viral spike is the focus of much research. 

Yixuan Hou, lead author of the study, at the University of North Carolina, says the amount of virus an animal became infected with was similar whether it was the D or the G strain. 

How one amino acid led to a major mutation in SARS-CoV-2

The study by the Royal Society’s SET-C (Science in Emergencies Tasking – COVID-19) task force also studied the one major mutation SARS-CoV-2 underwent. 

It is located on the S-protein which sticks out from the surface of the virus. 

This spike latches on to the ACE2 receptor of human cells, tricks it into opening the cell, and allows the pathogen to infect a person. 

At one specific location — residue 614 on the S1 terminus — the original form of the coronavirus had the amino acid aspartate, labelled with a D.

However, a random mutation saw this amino acid replaced with a glycine, labelled with a G. 

The so-called D614G mutation was seen in barely any samples taken in February. 

However, by March, more than a quarter (26 per cent) of isolated SARS-CoV-2 strains contained the mutation. 

By May this figure had reached 70 per cent. 

The D614G mutation i the most dominant one seen globally. 

This mutation appears to help more virus infect a person and for more efficient infection of cells. 

The D614G virus is also almost always accompanied with three other minor mutations. The role  of these changes remains unknown. 

‘However, the D614G variant transmits significantly faster and displayed increased competitive fitness than the wild-type virus in hamsters. 

‘These data show that the D614G substitution enhances SARS-CoV-2 infectivity, competitive fitness, and transmission in primary human cells and animal models.’ 

The hamsters with the mutated strain lost slightly more weight than those with the original variant but the authors say it is negligible and that, overall, the D614G substitution does not significantly enhance virus pathogenesis. 

The variant did transmit significantly faster in hamsters, which, the authors believe, indicates the virus evolved not for greater pathogenicity, but for better human transmissibility. 

These findings, although not in humans, offer some of the most convincing evidence yet that the mutation spread rapidly due to improvements in its transmissibility. 

The researchers also used human cells from doors to see if the mutated strain was better at infecting cells and found it was. 

Both the ancestral and mutated version were injected into cells and after three days, the G strain was overwhelmingly dominant in the cultures.

This happened ‘regardless of whether the [original] virus was at a 1:1 or 10:1 ratio over the isogenic D614G mutant’, the researchers say.   

While the study confirms the mutation is more infectious, it does not come to a conclusion as to why. 

However, a recent study, published on the pre-print server medRxiv and not yet peer-reviewed, from the University of Leuven in Belgium discovered the D614G mutation makes the coronavirus thrive at 37°C, human body temperature. 

It is more stable at this temperature than the original D strain, which prefers 33°C. 

This difference makes the new variant more stable at the exact temperatures seen in the human respiratory tract. 

The mutation is also associated with increased ability to manipulate proteases, enzymes in cells which destroy proteins, to facilitate infection. 

‘Collectively, our findings indicate how the coronavirus spike protein is fine-tuned towards the temperature and protease conditions of the airways, to enhance virus transmission and pathology,’ the academics write.

WHAT IS AN ACE-2 RECEPTOR AND WHAT DOES IT HAVE TO DO WITH COVID-19? 

ACE-2 receptors are structures found on the surface of cells in the lungs and airways which work with an enzyme called ACE (angiotensin-converting enzyme) to regulate blood pressure.

Its exact function in the lungs is not well understood but studies suggest it is protective against lung damage and low levels of it can worsen the impact of viral infections.

Scientists say that the coronavirus which causes COVID-19 enters the body through the ACE-2 receptor, which the shape of it allows it to latch on to.

This means that someone with more ACE-2 receptors may be more susceptible to a large viral load – first infectious dose of a virus – entering their bloodstream.

People who have higher than usual numbers of ACE-2 receptors may include those with diabetes or high blood pressure because they have genetic defects which make them produce more.

High levels of ACE-2 receptors may also be protective, however.

They are thought to be able to protect the lungs during infection and a study on mice in 2008 found that mice which had ACE-2 blocked in their bodies suffered more damage when they were infected with SARS, which is almost identical to COVID-19.

Smoking has in the past been repeatedly linked to lower than normal levels of ACE-2 receptors, potentially increasing the risk of lung damage from COVID-19.

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