The Atlantic waters around Cape Cod are home to two familiar seals, harbor seals and gray seals. Both can contract influenza, but something unusual happens.
Harbor seals often become sick and may even die, while gray seals appear unaffected. This curious difference has drawn scientists into a deeper investigation.
Milton Levin is an associate research professor of pathobiology and veterinary science at the University of Connecticut.
“That’s the big question we’re trying to understand – why is there a difference in the response in two different species that occupy the same space; why is one susceptible to the disease?”
Levin’s team began to explore cytokines, small proteins produced by immune cells that regulate inflammation and immune defense. These molecules normally spark an immune reaction and then switch it off once the danger is gone.
Infectious disease naturally shapes wildlife populations, but human-driven changes have increased outbreak intensity. Climate change, pollution, and habitat disruption now amplify disease spread in marine ecosystems.
Marine mammals, especially seals, serve as sentinel species. Their long lifespans and high position in food webs make them indicators of ecosystem health.
Influenza A virus has triggered mass deaths in seals before, with harbor seals suffering severe losses. Gray seals, however, appear to act as reservoirs, carrying the virus with little sign of illness.
The researchers tested whether cytokines played a role in the contrasting responses. Surprisingly, they discovered no difference in cytokine profiles between gray seal pups infected with influenza and those without.
The results suggest that the seals’ immune systems are either ignoring the virus or the virus is muting their responses beyond detection.
“Right now, it seems that the seals are not responding at all to influenza, and that’s probably why we’re not seeing clinical signs and why they don’t die,” said Levin.
This outcome challenges expectations. In most animals, viral infection usually alters cytokine activity in measurable ways. To reach their conclusion, Levin’s team collected blood from more than 100 gray seal pups and used a canine-designed kit to test for 13 cytokines.
Previous work confirmed the kit’s effectiveness for seals, given their evolutionary relationship with dogs.
The broader study also examined whether age, molt stage, or overall body condition influenced cytokine levels. None of these factors showed significant effects.
The lack of strong inflammatory signals suggests gray seals may have evolved a different strategy to manage infections.
Levin believes the muted cytokine response might actually protect gray seals. In humans, the opposite sometimes occurs. When the body encounters a pathogen, it can trigger a “cytokine storm,” an overreaction that harms the body more than the virus itself.
“If we can understand why gray seals don’t generate that response, that could tell us more about the immune response in general in marine mammals versus other species,” Levin says.
The study also noted that pro-inflammatory molecules like IL-6 and KC-like were less frequently detected in infected gray seal pups.
These molecules often correlate with severe disease in humans and other animals. Their reduced presence could explain why gray seals avoid the harmful consequences of influenza.
Another explanation could be viral host shutoff, a process where influenza suppresses the host’s gene expression to favor viral replication.
This may incidentally shield gray seals from excessive immune activation. While the virus manipulates cells for its own gain, the host avoids dangerous inflammation.
The next phase involves studying harbor seals. Collecting samples, however, presents challenges. Gray seal pups separate early from their mothers and remain accessible on beaches.
Harbor seal pups, in contrast, stay with their mothers longer, and adult seals are far too large to safely handle.
For over a decade, Levin and collaborators have sought to understand how viruses circulate in marine populations. Their work extends beyond seals themselves, touching on broader ecological and even human health questions.
“We’re trying to understand how pathogens, viruses, and influenza in particular, are being passed between species and if it is being transmitted to humans or are humans transmitting it to seals,” said Levin.
Understanding gray seals’ resilience could also help predict the effects of climate-driven disease outbreaks. As emerging infections sweep across oceans, knowing why some animals resist illness may guide conservation efforts and public health protections.
The study is published in the Journal of Wildlife Diseases.
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