In 1971, a patient identified only as John Cunningham gave his initials to one of the most quietly prevalent viruses in the human body. The JC virus, formally known as human polyomavirus 2, is estimated to have infected between 50 and 90 percent of adults worldwide. Most will never know it. A small number will wish they hadn’t.
The virus spreads through the fecal-oral route, appearing in urine and stool. Researchers hypothesize that initial infection happens at the tonsils or the gastrointestinal tract, likely early in life. That first encounter produces no symptoms. What remains is what scientists call the archetype JC virus — a persistent, silent passenger that sits in the cells without doing anything detectable. For the overwhelming majority of carriers, that silence is permanent.
For a few, it isn’t.
Under conditions of severe immune suppression, the archetype virus can apparently awaken, rearrange its genetic material, and transform into something categorically different — a variant that crosses into the brain and begins destroying it. The resulting disease, progressive multifocal leukoencephalopathy, or PML, attacks the cells that form the myelin sheaths protecting nerve fibers, causing demyelination, nerve death, and lesions visible on brain imaging. Symptoms can look like a stroke, or multiple sclerosis, or both at once: speech impairments, visual defects, motor dysfunction, seizures.
PML was first identified in 1958 in a cancer patient and remained extremely rare until the HIV/AIDS crisis of the 1980s, when it became an AIDS-defining illness. Between 2 and 5 percent of HIV-infected patients developed it in the early epidemic years, and at that point it was uniformly fatal. The introduction of highly active antiretroviral therapy in 1996 changed that calculus — PML cases dropped, and survival became possible, though often with significant lasting neurological damage. Since then, PML has been understood as a disease of profound immune collapse, appearing mainly in people with HIV/AIDS, certain cancers, or those taking powerful immunosuppressive drugs for conditions like multiple sclerosis.
Globally, PML is estimated to occur in roughly 2 in 100,000 people.
That framing may now need revisiting. According to a case study published this week in the Annals of Internal Medicine Case Reports, researchers at a New York hospital documented PML in a 72-year-old man without the severe immune suppression previously considered a prerequisite. His underlying condition was stage-5 chronic kidney disease — the point at which the kidneys have effectively failed. He arrived at the hospital after a week of word-finding difficulty, confusion, and general weakness. Physicians initially attributed his neurological decline to uremic encephalopathy, a loss of brain function caused by toxin accumulation from kidney failure.
Testing eventually pointed elsewhere. The researchers note that chronic kidney disease, which affects approximately 10 percent of adults worldwide, allows toxins to build up in the blood that impair immune cells, promote chronic inflammation, and reduce the body’s ability to detect and suppress viral activity. That degraded surveillance, they argue, may have been enough for the JC virus to activate and make its way into the brain — without the profound immunosuppression that PML has always required, according to existing understanding.
The case does not establish a new rule. It raises a possibility about a condition that 800 million people currently live with.
Photo by Risto Kokkonen on Unsplash
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