UNIVERSITY PARK, Pa. — When a disease-causing virus or other organism is transmitted from one species to another, most of the time the infection sputters and dies out. On rare occasions, the infection can perpetuate transmission in the new host species and cause a pandemic. For example, scientists are keeping a close eye on H5N1 highly pathogenic avian influenza , which causes bird flu and has been found in cows and humans . But is there a way to anticipate when infections will die out on their own and when they will persist?
New research, led by scientists at Penn State and the University of Minnesota Duluth, identified certain characteristics that could help predict whether the pathogen will stick around. Understanding how a virus spreads and what influences its spread soon after it spills over to a new population could provide information to help stop new diseases from spreading, the team said.
The study was published today (Aug. 21) in the journal PLOS Biology .
"Pandemic prevention efforts largely focus on identifying the next pandemic pathogen, but that's like finding a needle in the haystack," said David Kennedy , associate professor of biology at Penn State and senior author on the paper. "This work helps us figure out which outbreaks to worry about so that we can direct our public health resources where they need to go to prevent and respond to disease emergence."
While pandemics are extremely rare, spillover events — where viruses move between different host species — happen all the time, according to the research team. With so much viral transmission occurring, it's nearly impossible for scientists to pinpoint which spillover events to pay attention to.
"We wanted to know if there is anything we can measure directly after a spillover event or if there are characteristics of a spillover event that would be predictive of whether the virus would or would not persist in a new population," said Clara Shaw , lead author of the study. Shaw was a postdoctoral scholar in biology at Penn State at the time the research was conducted and is now assistant professor of biology at the University of Minnesota Duluth.
The researchers studied viral spillover in a worm model system, which allowed the team to examine disease transmission and emergence at a population level rather than within individual animals, Shaw said. They studied eight strains of worms that belong to seven species of the Caenorhabditis nematode, a model system for disease that shares a large number of genes with humans.
To induce a spillover event, the worms were exposed to Orsay virus, a nematode virus. The species of worms assessed in the study are at least partially susceptible to Orsay virus but vary in their ability to transmit it. The worm populations reproduced and grew for between five to 13 days. Then, the researchers transferred 20 adult worms to a new, virus-free Petri dish where the worms could reproduce and grow again. They repeated this process, transferring worms to new Petri dishes up to 10 times or until the virus was no longer detected in the worms.
The researchers then measured specific traits of the population of worms remaining on the initial plate — what fraction of the population is infected; how much virus is inside of each infected worm; how much virus do they shed; and how susceptible are they to the virus? Using mathematical models, the scientists looked at each trait individually and then together to determine if any of the characteristics were linked to virus emergence as the worms were transferred to new plates.
The researchers found that the dynamics of how the virus spreads during the few days after transmission are important for predicting long-term viral persist. For example, three factors were all positively correlated with whether a virus will take off in the new host population — infection prevalence or the fraction of the exposed population that's infected; viral shedding or the ability to release copies of the virus into the environment; and infection susceptibility or how vulnerable the hosts are to the virus.
Infection prevalence and viral shedding were of particular significance, the researchers said. More than half of the differences seen in whether the virus persists in the worms can be linked to these characteristics that were detected in the initial plate.
"That means these early traits can actually tell us quite a bit about what's going to happen way off in the future," Kennedy said.
The researchers also found infection intensity, or the severity of the infection, did not predict virus persistence.
The researchers said they plan to build on this work. Next, they will explore how pathogens adapt to new hosts to understand the evolutionary changes that occur at the genetic level. For instance, Kennedy said they're interested in understanding what genetic changes allowed the pathogen to persist and when those changes occurred.
Funding from the U.S. National Science Foundation supported this work.
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