Ever since viruses came to light in the late 1800s, scientists have set them apart from the rest of life. Viruses were far smaller than cells, and inside their protein shells they carried little more than genes. They could not grow, copy their own genes or do much of anything. Researchers assumed that each virus was a solitary particle drifting alone through the world, able to replicate only if it happened to bump into the right cell that could take it in.

This simplicity was what attracted many scientists to viruses in the first place, said Marco Vignuzzi, a virologist at the Singapore Agency for Science, Research and Technology Infectious Diseases Labs. “We were trying to be reductionist.”

That reductionism paid off. Studies on viruses were crucial to the birth of modern biology. Lacking the complexity of cells, they revealed fundamental rules about how genes work. But viral reductionism came at a cost, Vignuzzi said: By assuming viruses are simple, you blind yourself to the possibility that they might be complicated in ways you don’t know about yet.

For example, if you think of viruses as isolated packages of genes, it would be absurd to imagine them having a social life. But Vignuzzi and a new school of like-minded virologists don’t think it’s absurd at all. In recent decades, they have discovered some strange features of viruses that don’t make sense if viruses are lonely particles. They instead are uncovering a marvelously complex social world of viruses. These sociovirologists, as the researchers sometimes call themselves, believe that viruses make sense only as members of a community.

Granted, the social lives of viruses aren’t quite like those of other species. Viruses don’t post selfies to social media, volunteer at food banks or commit identity theft like humans do. They don’t fight with allies to dominate a troop like baboons; they don’t collect nectar to feed their queen like honeybees; they don’t even congeal into slimy mats for their common defense like some bacteria do. Nevertheless, sociovirologists believe that viruses do cheat, cooperate and interact in other ways with their fellow viruses.

The field of sociovirology is still young and small. The first conference dedicated to the social life of viruses took place in 2022, and the second will take place this June. A grand total of 50 people will be in attendance. Still, sociovirologists argue that the implications of their new field could be profound. Diseases like influenza don’t make sense if we think of viruses in isolation from one another. And if we can decipher the social life of viruses, we might be able to exploit it to fight back against the diseases some of them create.

Under Our Noses

Some of the most important evidence for the social life of viruses has been sitting in plain view for nearly a century. After the discovery of the influenza virus in the early 1930s, scientists figured out how to grow stocks of the virus by injecting it into a chicken egg and letting it multiply inside. The researchers could then use the new viruses to infect lab animals for research or inject them into new eggs to keep growing new viruses.

In the late 1940s, the Danish virologist Preben von Magnus was growing viruses when he noticed something odd. Many of the viruses produced in one egg could not replicate when he injected them into another. By the third cycle of transmission, only one in 10,000 viruses could still replicate. But in the cycles that followed, the defective viruses became rarer and the replicating ones bounced back. Von Magnus suspected that the viruses that couldn’t replicate had not finished developing, and so he called them “incomplete.”

In later years, virologists named the boom and bust of incomplete viruses “the von Magnus effect.” To them, it was important — but only as a problem to solve. Since no one had seen incomplete viruses outside of a lab culture, virologists figured they were artificial and came up with ways to get rid of them.

“You have to eliminate these from your lab stocks because you don’t want them to interfere with your experiments,” said Sam Díaz-Muñoz, a virologist at the University of California, Davis, recalling the common view within the field. “Because this is not ‘natural.’”

Researchers in the 1960s observed that incomplete viral genomes were shorter than those of typical viruses. That finding strengthened the view of many virologists that incomplete viruses were defective oddities, lacking the genes needed to replicate. But in the 2010s, inexpensive, powerful gene-sequencing technology made it clear that incomplete viruses were actually abundant inside our own bodies.

In one study, published in 2013, researchers at the University of Pittsburgh swabbed the noses and mouths of people sick with the flu. They pulled out the genetic material from influenza viruses in the samples and discovered that some of the viruses were missing genes. These stunted viruses came into existence when infected cells miscopied the genome of a functional virus, accidentally skipping stretches of genes.

Other studies confirmed this discovery. They also revealed other ways that incomplete viruses can form. Some kinds of viruses carry garbled genomes, for example. In these cases, an infected cell started copying a viral genome only to reverse partway through and then copy the genome backward to its starting point. Other incomplete viruses form when mutations disrupt the sequence of a gene so that it can no longer make a functional protein.