Jamestown Canyon virus has been circulating in northeastern North American mosquitoes since before the founding of the United States. Few physicians have diagnosed a case. A new study in Current Biology, built on 658 viral genomes sequenced mostly from mosquitoes in the northeastern United States, with additional samples from North Dakota, has produced the most detailed reconstruction yet of the virus’s centuries-long evolutionary history. What it reveals is a pathogen with an unusually complex life cycle, even by the standards of mosquito-borne viruses.
A virus no one was looking for
Jamestown Canyon virus was first isolated from mosquitoes near Jamestown, Colorado, in 1961. Connecticut’s surveillance program found it in 26 mosquito species between 1997 and 2022, and diagnosed human cases have been reported from 26 states, making it one of the most widespread arboviruses in North America. White-tailed deer are the main amplification host in much of the virus’s range. The virus can cause fever, headache and fatigue. In severe recognized cases it can invade the nervous system, causing meningitis or encephalitis. Twelve people have died.
Those numbers, 336 diagnosed cases since 2011 and 227 hospitalizations as summarized by the new study, are almost certainly a vast undercount. After the CDC began routine Jamestown Canyon virus IgM testing around 2013, reported cases jumped seventeen-fold, from an average of fewer than two per year to nearly thirty. Better detection and rising clinician awareness probably explain much of the jump, though surveillance data alone cannot rule out changes in incidence or exposure.
Seroprevalence surveys, which screen blood for antibodies that mark a past infection, suggest the true burden is far larger. A 2025 blood-donor study in selected endemic counties of Massachusetts, Minnesota and Wisconsin found neutralizing antibodies in roughly one in five donors. In Nova Scotia, 88% of deer and 21% of humans tested seropositive. Most infections produce no symptoms, or symptoms indistinguishable from a summer flu, and are never attributed to a cause.
The Lyme disease playbook
The ecological story behind Jamestown Canyon virus will sound familiar to anyone who has followed Lyme disease, though the parallel is looser than it looks. Deer matter to both, but differently. White-tailed deer are the amplification host for Jamestown Canyon virus, the animal in which it multiplies. For Lyme disease, deer feed the adult ticks that carry the bacterium but do not transmit it themselves; the spirochete is maintained by small mammals and birds, especially white-footed mice. What the two share is terrain: the fragmented woodlands and suburban forest edges of the northeastern United States, rebuilt by a transformation that began more than a century ago.
By the late 1800s, deforestation and unregulated hunting had driven deer populations in the Northeast to near zero. Forests were cleared for agriculture and fuel. Then the farms were abandoned, the forests grew back and the deer returned. The same reforestation that helped set the stage for the Lyme epidemic may also have rebuilt habitat important to Jamestown Canyon virus: vernal woodland pools where its key vectors breed, among them Aedes canadensis, Aedes provocans and Aedes abserratus, connected by corridors of regrown forest that deer move through freely.
The new genomic study fits this history, though it cannot by itself show that reforestation caused the virus’s return to Connecticut. The research team, led by Ellie Bourgikos and Nathan Grubaugh at the Yale School of Public Health, estimates that one of the virus’s two major lineages arrived in the Northeast by the early 1700s. Genetic reconstruction places the surviving descendants of that lineage in New York for roughly two centuries before their inferred introduction into Connecticut around the early 1900s, during the broader period of forest regrowth. At least four separate introductions into Connecticut have occurred since.
Frozen in time
The most surprising finding is how slowly this virus evolves. Jamestown Canyon virus accumulates genetic changes 10 to 100 times more slowly per calendar year than dengue, Rift Valley fever or chikungunya. The reason is ecological, not molecular. The virus spends approximately ten months of every year locked inside dormant mosquito eggs that overwinter beneath leaf litter and snow, with little to no viral replication, so few new mutations enter the population. Only during a brief two-month window in late spring and early summer, when those eggs hatch and the emerging mosquitoes begin feeding on deer, does the virus replicate. During that active season its estimated evolutionary rate falls within the range of other mosquito-borne RNA viruses. The annual average is slow because the molecular clock nearly stops for most of the year.
This deep freeze helps make the phylogenetic reconstruction possible. Three centuries of slow evolution have left enough genetic variation to read the virus’s history, but not so much that the signal is overwritten. The same feature that makes Jamestown Canyon virus hard to study by conventional epidemiology — its long, invisible dormancy — is precisely what makes it visible to genomic analysis.
Two cycles, one virus
The study proposes that Jamestown Canyon virus persists through two interlocking transmission cycles, each driven by a different type of mosquito. The maintenance cycle appears to be driven mainly by univoltine Aedes species, mosquitoes that produce a single brood per year. These emerge in spring from woodland pools, feed on deer, and some infected females lay eggs that already carry the virus. The eggs enter dormancy and survive the winter, restarting the cycle the following year. The phylodynamic model inferred that the virus spent roughly 80 to 90 percent of its time in these single-brood mosquitoes.
The diffusion cycle involves multivoltine mosquitoes, especially Anopheles species, which produce several broods across the summer. These amplify the virus and occasionally push it into new territory, but their contribution is episodic. They produce short geographic bursts, not sustained expansion. The virus spreads at roughly 30 to 60 square kilometers per year, a rate more like some slow-moving tick-borne viruses such as Powassan than the mosquito-borne viruses usually used for comparison.
What we still don’t know
We lack the data to say whether Jamestown Canyon virus will become a major public health problem. The virus’s effective population size has been stable across the surveillance period; it is not obviously expanding. But the genomic data come overwhelmingly from the Northeast, where Connecticut’s mosquito surveillance program has been running since 1997. Some of the highest reported case burdens are in the upper Midwest, especially Minnesota and Wisconsin, where genomic data remain much thinner than in Connecticut and the Northeast. We do not know whether the two-cycle transmission model holds there, or whether different mosquito communities produce different dynamics.
What is clear is that the infrastructure of risk is already in place: abundant deer, extensive forest habitat, mosquito species capable of carrying the virus distributed widely across the regions where it has been detected. Jamestown Canyon virus may not be an emerging pathogen in the usual sense. It has been here for centuries. The emergence is in our awareness of it.
