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Three years into the pandemic, COVID-19 is still going strong, causing wave after wave as cases rise, fall, then rise again. But last fall there was something new – or rather something old: the return of the flu. In addition, the respiratory syncytial virus (RSV) – a virus that doesn’t make much headlines in normal years – ignited in its own wave, causing a ‘tripleemia’.
The spikes in these old foes were especially striking as flu and RSV all but disappeared during the first two winters of the pandemic. Even more surprising is that some version of the flu may have died out during the early COVID pandemic. The World Health Organization’s surveillance program has not definitively detected the B/Yamagata flu strain as of March 2020. “I don’t think anyone is going to stick their neck out and say it’s gone already,” said 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 occurrence, Webby says.
But yes, the past few years have been highly unusual times for human-virus relationships, and lockdowns and masks have greatly contributed to keeping flu and RSV from entering human nostrils. Still, Webby thinks another factor has kept them at bay as COVID raged. It’s called viral interference and it simply means that the presence of one virus can block the other.
Viral interference can occur in individual cells in the lab, and in individual animals and humans exposed to multiple viruses, but it can also occur in entire populations, if enough people get one virus to massively hinder the flowering of others. This results in waves of infections by individual viruses that dominate in turn. “Looking back over the past few years, I’m very confident that COVID can definitely block flu and RSV,” says Webby.
It wouldn’t be the first time scientists have observed such patterns. In 2009, the virus to be afraid of was swine flu, for example, which had jumped from pigs to humans in the spring of that year. It seemed that it would increase in the fall, but suddenly it stagnated in some parts of Europe. The rhinovirus, responsible for the common cold and likely spread by children going back to school, took center stage for several weeks before swine flu took hold. That flu strain then delayed the typical fall rise in RSV by as much as two and a half months.
Ongoing interference
There are a number of ways that interference can occur in the body. One occurs when two viruses use the same molecule to access host cells. If virus A gets there first and grabs onto all those molecular doorknobs, then virus B is out of luck.
Another kind of interference can occur when two viruses compete for the same resources in the cell, such as the machinery to make new viral proteins or the means to escape from that cell to infect others. “Think of it as a race between two viruses,” says Webby.
But the best-understood method of interference involves a defense molecule called interferon that’s made by cells of all backbone animals (and possibly some invertebrates, too). Indeed, viral interference is why interferon got its name to begin with. When a cell senses a virus, any virus, it starts making interferon. And that, in turn, activates a whole host of defensive genes. Some of the products of those genes act inside the cell or at its boundaries, where they prevent additional viruses from entering the cell and prevent viruses already present from replicating or leaving the cell.
Cells secrete interferon into their environment, warning other cells to be wary. The result of all this: if a second virus shows up, cells have already activated their defenses and may be able to shut it out.
