Fifty-eight individuals in the U.S. have contracted the H5N1 avian influenza virus this year. Nearly all had close contact with poultry or cattle, the primary animal hosts for this strain. This indicates the virus primarily spreads through direct animal contact, not human-to-human transmission.
However, a December 5th *Science* journal publication reveals concern: the H5N1 strain affecting U.S. cattle is only one mutation away from readily binding to human cells, a crucial step for human-to-human transmission, according to study co-author James Paulson of Scripps Research.
Currently, H5N1 infects animals more effectively than humans. It has impacted millions of birds and cows across over 700 U.S. dairy herds but relatively few people.
Most human cases involve close contact with infected animals. This suggests that while H5N1 struggles to infect humans, it can succeed with high exposure, explains Troy Sutton of Penn State University. Because it doesn’t readily grow in human nasal and throat tissues, it’s unlikely to spread through coughing or sneezing like seasonal flu, Sutton adds.
If H5N1 adapts to readily infect, grow in, and spread among humans, “that’s how a pandemic starts,” Paulson warns.
Paulson’s team investigated the initial stage: the viral changes needed for efficient human cell binding. They studied a synthetic gene from the bovine strain, introducing targeted mutations to assess their impact on human cell attachment. The surprising result, Paulson notes, was that a single mutation appeared sufficient, contradicting prior research suggesting more changes would be needed.
“The emergence of a bovine H5N1 virus capable of recognizing human receptors may be closer than previously thought,” observes Yoshihiro Kawaoka of the University of Wisconsin-Madison, in an email to TIME.
This is a “striking” finding, Sutton agrees, emphasizing the need to prevent further human cases. Federal health officials recommend high-risk individuals, such as farmworkers, use protective equipment and antiviral medications (effective against bird flu) following potential exposure.
Paulson stresses that a pandemic isn’t imminent. The currently circulating virus hasn’t evolved for efficient human infection. Public health authorities confirm no human-to-human transmission and a low risk to the general public.
More changes might be required for a true pandemic threat. Efficient human cell binding—as tested by Paulson’s team—is only the first step towards widespread person-to-person transmission. Further changes are likely needed for significant contagiousness.
Kawaoka concurs. Over 50 U.S. cases without human-to-human spread suggest that “additional mutations are likely necessary for the virus to achieve efficient human-to-human transmission,” he wrote.
Health officials are closely monitoring the situation. A Canadian teenager’s H5N1 case resulted in hospitalization. Analysis revealed a mutation potentially increasing human transmissibility, similar to Paulson’s findings (though no secondary infections occurred).
Kawaoka also studied a strain from a U.S. farmworker. It grew in human lung cells due to a mutation promoting mammalian viral growth; however, this mutation wasn’t found in the bovine strains studied in October.
Despite the lack of human-to-human spread, Paulson advocates for preparedness. Stockpiling antivirals and planning distribution strategies are crucial preventative measures.
Continued virus monitoring is essential, Sutton adds. However, he notes a crucial concern: “what’s alarming to me is that we often realize we have a pandemic after the pandemic has started,” he says. “If we started to see this mutation, would it already be too late? We don’t know the answer to that.”