- The coronavirus spread seems to be out of control in certain regions, including several US states, Brazil, India, and other areas.
- The last 1 million confirmed COVID-19 cases were diagnosed over the span of just eight days, compared to more than three months for the first million.
- One reason why the coronavirus transmission is surging in various communities might have to do with a tiny mutation that makes the virus even more contagious than before.
The novel coronavirus needed just eight days to infect the most recent 1 million people, compared to more than three months for the first million recorded cases. More than 10.43 million COVID-19 infections were confirmed as of Tuesday morning, with the illness killing over 510,000 patients so far. While some countries were able to flatten their infection curves and return to some sense of normalcy, others are yet to contain the first wave. The US, Brazil, and India continue to report tens of thousands of new infections per day, with the world having reached a daily record on Sunday when 183,000 cases were recorded globally, according to new stats from the World Health Organization (WHO).
Testing has increased dramatically compared to the first few months of the pandemic, there’s no question about that. But the SARS-CoV-2 virus is highly infectious, especially in densely populated communities where people don’t practice social distancing and refuse to wear masks. Now, it turns out that the reason why the coronavirus spread is out of control in regions that don’t respect any safety measures might be a small mutation that may have made the virus more contagious.
This isn’t the first time we’ve heard about the D614G mutation, which was detailed in several COVID-19 studies in the past few months. But more researchers believe this mutation is mainly responsible for the emergence of a dominant version of SARS-CoV-2 that is more infectious than the original virus that came out of Wuhan late last year.
As The Washington Post explains, some 1,300 amino acids are part of the proteins on the surface of the virus. One of these amino acids mutated — number 614 — switching from “D” (aspartic acid) to “G” (glycine). This change alone, also known as the “G” mutation, might have made the virus more efficient at hooking up to ACE2 receptors and binding to cells in the human body.
The mutation affected the spike proteins, which are found at the exterior of the virus. These protruding structures are what allow the pathogen to hook up to healthy cells. Once that’s done, the RNA information in the virus is decoded, and the cells are hijacked to mass-produce large quantities of the virus. The replicas are released out of the dying cells, and the process is repeated over and over.
Of the nearly 50,000 virus genomes that were uploaded online, some 70% of them carry the G mutation, the Post reports. Four new studies indicate the variation makes the virus more infectious, but the work has not been peer-reviewed. A different study says patients infected with the G mutation have more virus in their bodies, so they’re more likely to spread it to others. If the G mutation gives the virus a better chance to hook up to cells, then the virus could multiply easier than the D version.
The good news is that the G mutation doesn’t make people sicker or more deadly. Also, the mutation doesn’t hinder vaccine work so far. It might just make the virus more contagious.
“The epidemiological study and our data together really explain why the [G variant’s] spread in Europe and the US was really fast,” Scripps Research virologist Hyeryun Choe said. “This is not accidental.”
The researcher explained that the original spike protein of the SARS-CoV-2 featured two parts that don’t always hold well together. The outer part frequently broke off in the original, which means the virus had a harder time infecting cells. Choe found that the G version of the virus featured more spike proteins, and the outer parts were less likely to break off. This change was enough to make the study 10 times more infectious in lab experiments.
A geneticist at the New York Genome Center and New York University was studying the genes that allow the virus to infiltrate human cells. But Neville Sanjana’s experiments failed when using a gene sequence from a Wuhan patient. Switching to the G mutation increased the virus’s capabilities to infect cells. “We were shocked,” Sanjana said. The team repeated the experiment on various types of cells, and every time the G mutation was many times more infectious.
While Choe thinks the spike protein is more stable because of the G mutation, the Sanjana team believes the mutation helps with the actual process of invading the human cell. Jeremy Luban from the University of Massachusetts Medical School has a third hypothesis. The G variation lets the spike protein change shape as it attaches to the ACE2 receptor, and that’s what allows it to fuse better with the membrane of the cell.
It was previously theorized that the D614G mutation is to blame for the virus’s increased infectivity, as researchers posted such studies back in April. But others disputed the findings, saying there may have been issues with the data collected. Reduced access to testing in America, as well as the fact that the G mutation came to the States from Europe, could have impacted the April research.
The increased number of studies of the D614G mutation could provide the answers officials and doctors need to continue to fight the pandemic. In case this tiny mutation is responsible for the increased contagiousness of the virus, then outbreaks might be even more challenging to control. Social distancing, face masks, and regular hand washing could still help reduce the risk of transmission and buy more time until more meds are available.