- Researchers looked at the coronavirus strain of more than 5,000 Houston cases
- Found that 99.9 per cent of the strains discovered were the D614G variant
- This appeared in Europe in February and rapidly became dominant globally
- Other studies have found this strain is more infectious than the original variant
A mutated version of the SARS-CoV-2 coronavirus which now dominates the world may be more infectious than the original version.
A study of more than 5,000 Covid-19 patients at a hospital in Houston, Texas, revealed that 99.9 per cent of infections were caused by this altered version of the virus, called D614G.
The finding adds credence to the theory the mutation, which accounts for 85 per cent of global cases, is more contagious than the original strain.
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.
Scientists are still trying to determine why the D614G strain has become the principle form of SARS-CoV-2, and think it may be due to the mutation increasing the amount of virus in the upper respiratory tract.
This makes it more likely to spread when the infected person talks, coughs or sneezes.
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, called position 614, on the spike protein of the virus.
This 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.
It is believed the D614G strain emerged first in Europe at the start of February 2020 and spread quickly.
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 week 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.
However, in some localised areas the virus is almost ubiquitous. A September study from the US found 99 per cent of cases in a New York hospital were of the G strain, similar to the latest figures from Houston.
The latest study, which was was led by the Houston Methodist Hospital and has been published in the peer-reviewed journal mBIO, found that, during the initial wave of the pandemic in the spring, 71 per cent of cases were D614G.
By the time the second wave of the outbreak hit Houston during the summer, this variant had leaped to 99.9 per cent prevalence.
'The virus continues to mutate as it rips through the world,' says co-author of the Houston study Dr Ilya Finkelstein from the University of Texas at Austin.
There is much debate over why the D614G mutation became dominant but the prevailing theory is that it is more infectious than the original version.
While the new research does not show a direct link between the amount virus in the upper respiratory tract and the likelihood of it spreading, several studies have hinted that the D614G mutation is more contagious.
In August, Paul Tambyah, senior consultant at the National University of Singapore and president-elect of the International Society of Infectious Diseases, made headlines when he said D614G makes the virus more infectious but less deadly.
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.
Many in the scientific community decried his comments as premature and founded in speculation not evidence, but recent research shows he may have been at least partially correct.
A study published last week by the University of Texas looked at how the D and G strains compared with each other and how they altered the trajectory of a coronavirus infection.
It found the G strain is more infectious and 'enhances viral loads in the upper respiratory tract of COVID-19 patients'.
The researchers studied the two strains in a laboratory in both hamsters and human cell models.
'We demonstrated that the spike substitution D614G enhanced SARS-CoV-2 replication in the upper respiratory tract through increased virion infectivity,' the authors write.
'The replication differences were more dramatically observed in the human airway culture, with up to a 13.9-fold advantage in a head-to-head competition test.'
The authors of this previous study speculate that the G strain causes more virus to be produced in the nose and throat, but not in the lungs.
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) found the change from the D to G strain will not impact on vaccine effectiveness.
If this was to occur, it could mean a new vaccine would be needed every time a new mutation emerged, similar to seasonal flu.
Experts are also hopeful that any future mutations will also not impact vaccine efficacy.
'Despite this D614G mutation to the spike protein, we confirmed through experiments and modelling that vaccine candidates are still effective, said Professor Seshadri Vasan from CSIRO, who led the study.
'We've also found the G-strain is unlikely to require frequent "vaccine matching" where new vaccines need to be developed seasonally to combat the virus strains in circulation, as is the case with influenza.'
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.