Most Pandemic Viruses Show No Signs of Lab Adaptation — Except This One Historical Outbreak
There has been much debate, both among scientists and the general public, about the origins of some of our planet’s most devastating pandemics. Now, a new genetic analysis of major epidemic viruses challenges a long-held hypothesis about how pandemics start.
According to a study published in CellMany viruses that jump from animals to humans may already be capable of infecting humans without first undergoing particular evolutionary changes. This discovery reshapes the way scientists think about zoonotic diseases and also provides a new tool for investigating the origins of outbreaks, including the virus that causes COVID-19.
“This work is directly related to the ongoing controversy around the origins of COVID-19,” lead author Joel Wertheim said in a press release. “From an evolutionary perspective, we find no evidence that SARS-CoV-2 was shaped by laboratory selection or prolonged evolution in an intermediate host before its emergence. This lack of evidence is exactly what we would expect from a natural zoonotic event – and it represents another nail in the coffin for theories citing laboratory manipulation.”
Learn more: New vaccine platform could reduce development times from months to weeks
How scientists can tell a virus didn’t come from a lab
For years, many scientists believed that animal viruses had to accumulate specific mutations before they could spread between humans. But the new study suggests that this hypothesis does not hold water.
The research team conducted an extensive phylogenetic analysis of viral genomes from several outbreaks, including influenza A virus, Ebola virus, Marburg virus, Mpox virus, SARS-CoV-2, and SARS-CoV-1. They focused specifically on the evolutionary window just before each virus begins spreading among humans. If viruses had undergone significant adaptation before infecting humans, these changes would leave detectable signatures in their genome. But the researchers did not find this signal.
Instead, the selection pressures that shape viruses before they infect humans were essentially the same as those observed during normal circulation in animal reservoirs. Only after viruses began to spread widely among humans did new evolutionary patterns emerge.
“From a general epidemiological perspective, our results challenge the idea that pandemic viruses are evolutionarily special before reaching humans. Rather than requiring rare, finely tuned adaptations in animals, many viruses already possess the basic ability to infect and transmit between humans. What matters most is human exposure to a wide range of animal viruses,” Wertheim explained.
To confirm that their method worked, the researchers also analyzed viruses deliberately propagated in laboratory environments, such as cell cultures or laboratory animals. These viruses produced distinctive genetic signatures – exactly those that scientists would expect to see if a pathogen had been heavily manipulated.
The strange case of the 1977 flu
While most viruses studied have followed the same natural pattern, one historic outbreak stood out.
When researchers looked at the strain responsible for the resurgence of the H1N1 flu virus in 1977, they discovered something unusual. The virus was almost identical to strains circulating in the 1950s. Even more surprising, its evolutionary signature resembled the study’s control viruses grown in the laboratory.
“The story of the 1977 flu is, in many ways, even more compelling than what we discovered for COVID-19,” Wertheim said. “Our results provide new molecular evidence supporting the long-suspected idea that the H1N1 influenza pandemic was triggered by a laboratory strain – perhaps in the context of a failed vaccine trial.”
A new tool for future epidemics
Beyond revisiting historical outbreaks, the researchers say their framework could help scientists assess future pandemics more quickly and more objectively. By establishing what a typical zoonotic spillover looks like at the genomic level, scientists now have a clearer basis for comparison when new viruses emerge.
“Our goal is not just to understand the past, but to be better prepared for the future. By clarifying how pandemics actually start, we can focus our attention where it needs to be: on monitoring, preventing and reducing the possibilities for the virus to continue spreading,” Wertheim concluded.
This article does not offer medical advice and should be used for informational purposes only.
Learn more: What makes the K subclade strain different? Here’s what you need to know about the “super flu”
Article sources
Our Discovermagazine.com editors use peer-reviewed research and high-quality sources for our articles, and our editors review the articles for scientific accuracy and editorial standards. See the sources used below for this article:
