Research suggests why the ‘Alpha’ Coronavirus Variant Became So Powerful

In December, British researchers discovered that a new variant was sweeping through their country. When it arrived in other countries, the variant, now known as Alpha, tended to become more common in its new homes as well. By April, it had become the dominant variant in the United States, and it has remained so ever since.

Alpha’s swift success has left scientists wondering how the variant conquered the world. A new study points to one secret to its success: Alpha disables the first line of immune defense in our bodies, giving the variant more time to multiply.

“It’s very impressive,” said Dr. Maudry Laurent-Rolle, a physician and virologist at the Yale School of Medicine who was not involved in the new study. “Any successful virus has to get beyond that first defense system. The more successful it is at doing that, the better off the virus is.”

The report was posted online on Monday and has not yet been published in a scientific journal.

Alpha has 23 mutations that set it apart from other coronaviruses. When the variant started to surge in Britain, researchers began inspecting these genetic tweaks to look for explanations as to why it was spreading faster than other variants.

A lot of researchers focused their attention on the nine mutations that alter the so-called spike protein that covers the coronavirus and allows it to invade cells. One of those mutations helps the virus bind more tightly to cells, potentially improving its chances of a successful infection.

But other scientists have focused on how Alpha affects the human immune response. Gregory Towers, a virologist at the University College London, and his colleagues grew coronaviruses in human lung cells, comparing Alpha-infected cells with those infected with earlier variants of the coronavirus.

They found that lung cells with Alpha made drastically less interferon, a protein that switches on a host of immune defenses. They also found that in the Alpha cells, the defensive genes normally switched on by interferon were quieter than in cells infected with other variants. ...