Three years into the pandemic, COVID-19 is still going strong, causing wave after wave as the number of cases spikes, falls, and then rises again. But this past fall saw something new, or rather, something old: the return of the flu. In addition, the respiratory syncytial virus (RSV), a virus that makes few headlines in normal years, flared on its own rise, creating a “triple epidemic.”
The surges in these old foes were particularly surprising because influenza and RSV all but disappeared during the first two winters of the pandemic. Even more surprising, a particular version of the flu may have died out during the first COVID pandemic. The World Health Organization’s surveillance program hasn’t definitively detected the B/Yamagata flu strain since March 2020. “I don’t think anyone would take a chance and say it’s gone,” says Richard Webby, a virologist at St. Jude Children’s Research Hospital in Memphis. But, he adds, “we hope it’s squeezed out.” Such an extinction would be a super rare event, Webby says.
But then, the last few years have been very unusual times for human-virus relationships, and lockdowns and masks went a long way toward preventing the flu and RSV from infiltrating human nostrils. Still, Webby thinks another factor may have kept them at bay as COVID raged. It’s called viral interference, and it simply means that the presence of one virus can block another.
Viral interference can occur in individual cells in the laboratory, and in individual animals and people who are exposed to multiple viruses, but it can also affect entire populations, if enough people contract one virus to hinder the flourishing of others on a large scale. . This results in waves of individual virus infections taking turns to dominate. “Looking back at the last two years, I’m pretty sure COVID can certainly block the flu and RSV,” Webby says.
It would not be the first time that scientists have observed such patterns. In 2009, for example, the virus to fear was swine flu, which jumped from pigs to people in the spring of that year. It seemed about to rise when autumn came, but suddenly, in some parts of Europe, it stagnated. The rhinovirus, responsible for the common cold and likely spread by children returning to school, took center stage for a number of weeks before swine flu regained dominance. That flu strain then delayed the typical fall RSV surge by up to two and a half months.
There are several ways that interference can occur in the body. One occurs when two viruses use the same molecule to enter host cells. If Virus A gets there first and grabs onto all those molecular doorknobs, then Virus B is out of luck.
Another type of interference could occur if two viruses compete for the same resources within the cell, such as the machinery to make new viral proteins or the means to escape from that cell and infect others. “Think of it like a race between two viruses,” says Webby.
But the best-understood method of interference concerns a defensive molecule called interferon that is produced by the cells of all animals with backbones (and possibly some invertebrates as well). In fact, viral interference is the reason interferon got its name to begin with. When a cell detects a virus, any virus, it begins to produce interferon. And that, in turn, turns on a whole host of defensive genes. Some of the products of these genes function within the cell or at its boundaries, where they prevent additional viruses from entering and block the replication or exit of viruses already present from the cell.
Cells secrete interferon into their environment, warning other cells to raise their guard. The result of all this: if a second virus appears, the cells already have their defenses activated and it is possible that they can block it.