The worst fears of epidemiologists have been realised: Covid-19 has mutated, and the strain now dominating the world is up to six times more infectious.
New research published in the science journal Cell cites laboratory research as identifying small changes in the proteins that protrude from the surface of the Covid-19 virus. These changes, which have evolved during the past six months, enhance its abilities to jump between humans – but have not increased or reduced its symptoms.
The public face of the United States' fight against the exploding pandemic, Dr Anthony Fauci, told the American Medical Association at the weekend the findings – while unconfirmed – could be significant.
"I think the data is showing that there is a single mutation that actually makes the virus be able to replicate better, and maybe have high viral loads," he said.
Viral load refers to the amount of virus colonising a sufferer.
The study was conducted by the Los Alamos National Laboratory in New Mexico, the Duke University in North Carolina and the University of Sheffield's Covid-19 Genomics UK research group.
The team studied 999 British patients being treated for severe infections, as well as conducting laboratory experiments on how effective the virus was at breaching the defences of human cells.
The researchers revisited their initial work in June after the scientific peer-review process challenged the extent of their findings. The revised results indicate the current strain – D614G – is between three and six times more infectious than the original first detected in the Chinese city of Wuhan.
But exactly how this mutated protein affects the transmission of Covid-19 outside a laboratory environment is yet to be determined.
"We don't have a connection to whether an individual does worse with this [strain] or not," Fauci said.
"It just seems that the virus replicates better and may be more transmissible."
Hopes for a successful vaccination remain high. But the chances of populations suffering through a Covid-19 outbreak emerging with a degree of "herd immunity" have been dealt a serious blow.
A series of new studies suggest our immune systems are so strained fighting the coronavirus they don't produce enough antibodies to resist reinfection longer than a few weeks or months.
It's all related to a specific protein receptor. Such receptors cover cells. They receive chemical "keys" from the body to turn on or off specific functions. One such "lock" – ACE2 – is found on many different kinds of human cells across the body.
And Covid-19 has a copy of the ACE2 protein "key". And once Covid-19 breaks into a cell, it's dead.
Cells with ACE2 receptors can be found in the nasal passage in an area associated with smell. But it's also in some lung, heart, kidney, liver, gastrointestinal and blood vessel cells.
We're not certain how the virus gets to these vital organs in some people, but not others.
But research suggests our immune systems are not helping. It can overreact. It can fight back so hard, it can cause intense inflammation.
In severe cases, the immune system ends up damaging the same lungs, kidneys, heart – and the smallest of blood vessels, such as those found in toes – it's supposed to protect.
Virologists say this is not entirely unusual. Other viruses can also trigger overreactions, such as influenza and brain swelling. What is unusual is Covid-19 itself. It's new. It's nasty. And we're not yet certain of how it works.