The Herpes simplex virus hides in plain sight. For most, it’s a fleeting nuisance — a tingling lip, a blister, a cold sore. But new research suggests that herpes simplex virus type 1 (HSV-1), carried silently by billions, may leave a far more lasting imprint deep within the brain: an increased risk of Alzheimer’s disease.

A growing faction of scientists suspects that Alzheimer’s may not begin in the brain, but rather with the body’s reaction to something far more common — infection. A new study highlights HSV-1, the common Herpes simplex virus, as one of the prime suspects.

Viruses and the brain

Alzheimer’s is one of the most horrifying diseases out there. It’s a slow-burning catastrophe. It devours memories, burdens families, and steals away patients’ sense of self. Alzheimer’s disease affects over 55 million people worldwide and is the leading cause of dementia, accounting for 60–80% of cases. With aging populations, the global burden is expected to triple by 2050, straining healthcare systems and families alike.

It’s also a costly disease. In the US alone, it costs over $305 billion a year. Most research has focused on the brain’s internal failings — those toxic amyloid-beta plaques and tau tangles that choke neurons over time.

The new study, led by researchers from Gilead Sciences and the University of Washington, crunched insurance claims data from over 344,000 people diagnosed with Alzheimer’s and an equal number of matched controls. Their question was simple: Were HSV-1 infections more common in those who developed Alzheimer’s?

The answer, apparently, is also simple: yes. Alarmingly, people who had HSV-1 infections were far more likely (80%) to develop Alzheimer’s.

The association goes even deeper. Those who took antiviral drugs after their HSV-1 diagnosis were 17% less likely to get Alzheimer’s compared to their HSV-1-infected peers who didn’t get treatment.

“This is a well-conducted study adding to strong data in the field linking HSV-1 and other viral infections to increased risk of developing Alzheimer’s disease, but it is important to note that HSV-1 infection, which is extremely common in the population, is by no means a guarantee that someone will develop Alzheimer’s,” says Tara Spires-Jones, Director of the Centre for Discovery Brain Sciences at the University of Edinburgh, who was not involved in the study.

What the numbers are really saying

On its face, an 80% increased risk sounds terrifying. But you have to keep in mind that this is relative risk. About 1 in 9 people age 65 and older (11%) has Alzheimer’s. So, an 80% increase on that takes it to 19.8%.

But it also gets a bit stranger. Out of 344,628 Alzheimer’s patients in the dataset, just 1,507 — about 0.44% — had a recorded HSV-1 diagnosis. That’s still far below the estimated prevalence of HSV-1 in the general population. So, what gives?

Most people with HSV-1 never get formally diagnosed. They don’t see a doctor for it, and if they do, it might not be recorded properly in an insurance database.

“Despite the large sample size, this research has limitations partly due to only using health records and administrative claims data. Most people infected with HSV-1 don’t have any symptoms so some infections might not have been recorded. Infections predating the information recorded are also not available. Although cases were matched with controls, diagnosing Alzheimer’s disease, especially in the early stages, remains a challenge,” noted Dr. Sheona Scales, Director of Research at Alzheimer’s Research UK, who wasn’t involved in the study. “This study doesn’t tell us if infections are causing the risk, it only shows an association.”

In other words, we may be looking at the tip of an iceberg. Or we may be chasing a ghost. This study doesn’t definitively clarify the problem. However, the idea that viruses may be causing problems like Alzheimer’s is not new.

Viral defenses gone wrong

Back in 2010, researchers discovered that amyloid-beta — the protein long blamed for Alzheimer’s — also happens to have antimicrobial properties. It seems to be one of the brain’s ways of defending itself, forming plaques to trap invading microbes like HSV-1.

The mechanism, in time, could become a liability. If repeated infections or reactivations of HSV-1 nudge the brain’s immune system into overdrive, this could slowly create the conditions for cognitive decline.

“This is a well-conducted study adding to strong data in the field linking HSV-1 and other viral infections to increased risk of developing Alzheimer’s disease, but it is important to note that HSV-1 infection, which is extremely common in the population, is by no means a guarantee that someone will develop Alzheimer’s,” says Tara Spires-Jones, Director of the Centre for Discovery Brain Sciences at the University of Edinburgh.

“Why viral infections may increase risk of dementia is not fully understood, but the most likely explanation is that infections increase inflammation in the body and contribute to age-related brain inflammation.  More research is needed to understand the best way to protect our brains from Alzheimer’s disease as we age, including a better understanding of links between viral infection and Alzheimer’s risk.”

There’s also another theory that genetics plays a role. In particular, the ApoE-ε4 gene could play a role. This gene is a known risk factor for Alzheimer’s, and it is also linked with more severe HSV-1 outbreaks. The virus, it seems, might hit their brains harder, or linger longer.

Some scientists are skeptical

Not everyone is convinced that these findings are ready for prime time. Dr. David Vickers from the University of Calgary didn’t mince words: “This pharma-funded research exaggerates the role of HSV-1, failing to appreciate its absence in 99.56% of Alzheimer’s cases. The observed 17% hazard reduction with antiherpetic drugs translates to a mere nine-month delay in AD onset, offering no meaningful relief to the US$305 billion costs for treatment.”

It’s a fair critique. The study was funded by Gilead Sciences, which manufactures antiviral drugs. And observational studies based on insurance data come with baggage: misdiagnoses, inconsistent record-keeping, and the fact that correlation isn’t causation.

Still, others argue the findings are too consistent — and too important — to ignore.

“Smaller but significant effects are also seen for HSV-2 and varicella zoster virus (VZV). With many GPs and the population being unaware of the dementia related benefits of treating HSV infections and preventing VZV activation through vaccination, it is time to call for actions informing those working in primary care as well as the population at large,” adds Cornelia van Duijn, Professor of Epidemiology at the Nuffield Department of Population Health, University of Oxford.

So where does this all leave us?

This study won’t be the last word on the issue. There’s much we don’t know. But it moves the conversation in a compelling direction. There’s an increasing amount of evidence that suggests our body’s response to certain viruses could put us at an increased risk of developing Alzheimer’s disease in later life. It’s not a clear risk factor for now, but it’s definitely something worth exploring more.

Future research needs to answer the big questions. Do antivirals work long-term? Should they be given preventively to people at genetic risk? Could vaccines against HSV-1 reduce Alzheimer’s cases? And how exactly do viruses interact with the aging brain?

That said, the stakes are enormous. Even a modest delay in the onset of Alzheimer’s — say, one or two years — could have huge public health benefits if applied across millions of people.

In the meantime, if you’re carrying an infection, you’re probably best off trying to treat it properly. Research is increasingly showing that infections just cause acute illness — they can leave behind long-term damage. Chronic hepatitis can lead to liver cancer. HPV infections can trigger cervical cancer. Even seemingly minor bugs like Helicobacter pylori can inflame the stomach lining and increase the risk of ulcers and gastric cancer.

Infections are not always fleeting; sometimes, they lay the groundwork for diseases that emerge years or even decades later.

The study was published in the British Medical Journal.