Covid-19 has NOT become more infectious

Covid-19 has NOT become more infectious: Study identifies almost 13,000 coronavirus mutations but none – including the dominant D614G strain – made it better at spreading

  • UCL researchers found 12,706 mutations in 46,723 coronavirus patient genomes 
  • Found than none of the detected mutations made the virus better at spreading  
  • This includes D614G mutation which is the dominant coronavirus strain globally 

Coronavirus has not mutated to become more infectious, according to a scientific study that debunks a widespread theory. 

Most coronavirus cases seen globally feature a specific genetic mutation called D614G which is different to the original strain that emerged in Wuhan last year and experts feared was more infectious than the original version. 

But UCL researchers looked at more than 46,723 cases of Covid-19 from 99 countries and assessed how mutations appeared and if they altered transmissibility. 

Scientists identified 12,706 total mutations in SARS-CoV-2 — the virus which causes Covid-19 — and none of them were found to boost infectivity. 

This includes D614G which is found on the spike of the coronavirus and allows it to bind to human cells, a mechanism which allows it to infect people.  

Other academics doing lab studies, not genetic reviews, had previously found D614G made the virus more infectious but the UCL researchers believe it became dominant by chance, not by design. 

They say their conclusions may disagree with previous findings due to different methodologies and that D614G became so prevalent because it was an early mutation which happened to get carried around the world in the early days of the pandemic, not because it is more infectious. 

UCL scientists found the D614G mutation in 77.8 per cent of all cases but say it does not make the virus more infectious 

The study, published in the journal Nature Communications, explains mutations in coronaviruses can develop in three different ways.

These are: mistakes resulting from copying errors as the virus replicates inside the human body; through interactions with other viruses infecting the same cell; and changes induced by the host’s or a person’s own immune system. 

Most mutations to SARS-CoV-2 are due to the later, the researchers discovered.  

First and corresponding author Lucy van Dorp, of UCL Genetics Institute, added: ‘Fortunately, we found that none of these mutations are making Covid-19 spread more rapidly, but we need to remain vigilant and continue monitoring new mutations, particularly as vaccines get rolled out.’

Based on a modelling of the virus’s evolutionary tree, the scientists said they found no evidence any of the common mutations are increasing the virus’s transmissibility.

Instead, they found most common mutations have a neutral impact on the virus, neither hindering or enhancing its ability to sread. 

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. 

This includes D614G, which is by far the most common strain of coronavirus affecting humans worldwide. 

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 appeared in a European patient in February. 

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

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) at the 614th position on the viral spike, 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 UCL study found it in 77.8 per cent of all cases.

Other studies at individual hospitals have found the D614G strain accounts for more than 99 per cent of all cases. 

In a bid to explain why D614G became ubiquitous, researchers speculated the mutation must make the virus better at spreading than its ancestral variant. 

The orange portion of the graph shows percentage of coronavirus cases which are the original D strain. Blue shows how common the G Strain is. Over time, the G variant supplanted the D strain

These graphs show the ascension of the D614G strain over time. The blue line and coloured area shows how common, as a percentage, the D614G is among all coronavirus cases in different continents. The G strain is now by far the most common, supplanting the original variant, all around the world 

COVID-19 vaccines should NOT be affected by mutations to the coronavirus 

Mutations to the SARS-CoV-2 coronavirus that causes Covid-19 will not affect the effectiveness of vaccines, a study shows. 

The virus has mutated at a critical location since it first emerged in Wuhan late last year, and there were concerns future changes could render vaccines useless.  

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

However, a mutation at one specific location, called position 614, turned one amino acid from a D (aspartate) to a G (glycine), and this ‘G strain’ is now dominant. 

Viral mutations are common and can make creating vaccines difficult as it causes the virus to change shape, rendering previous vaccines useless, as is the case with seasonal flu. 

Researchers were concerned that if this was the case for SARS-CoV-2 a new vaccine would be needed for every time the coronavirus mutated. 

However, a study from the Commonwealth Scientific and Industrial Research Organisation (CSIRO) has found the change from the D to G strain will not impact on vaccine effectiveness. 

They are hopeful that any future mutations will also not impact vaccine efficacy.   

Dr Yixuan Hou, lead author of a previous study from the University of North Carolina conducted a study of the two strains on hamsters and mapped how it spread. 

‘The D614G variant transmits significantly faster and displayed increased competitive fitness than the wild-type virus,’ Hou said .

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

The researchers also used human cells from donors 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. 

But this study did not look at why the G strain was found to be more infectious than the D form.  

Another recent study, published on the pre-print server medRxiv and not yet peer-reviewed, from the University of Leuven in Belgium gave a possible explanation. 

It found the D614G mutation makes the coronavirus thrive at 37°C, human body temperature, whereas the original D strain 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.

But these lab-based studies are at odds with the latest UCL findings, and the researchers say the results of the latest study should be considered carefully.   

In a bid to explain how D614G became so dominant, if it is not more infectious, the researchers write in their study: ‘The abundance of D614G is more probably a demographic artefact: D614G went up in frequency as the SARS-CoV-2 population expanded.’

This states that instead of morphing the coronavirus into a super virulent strain, the D614G mutation may have simply appeared in the right place at the right time to take advantage of the rapidly spreading coronavirus in the early days of the pandemic.  

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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