Imagine aging not as a clock winding down, but as a dialogue between your immune system and the microbial world. For Joshua “Scotch” McClure, CEO of Maxwell Biosciences, this isn’t just a metaphor—it’s a scientific hypothesis that could reshape how we think about longevity.
At a recent interview spotlighted on Lifespan.io, McClure laid out a provocative and increasingly evidence-backed claim: infectious disease isn’t just one cause of aging—it might be one of the root causes. Far from being random assaults, pathogens might play a silent yet powerful role in the biological decay we label “getting older.”
Let’s unpack this bold perspective and what it means for the future of medicine, public health, and personal wellness.
A Silent Saboteur: The Latent Impact of Infection
We’re familiar with the toll that acute infections take on the body—fever, fatigue, organ damage. But McClure is more interested in the lingering effects—particularly from viruses that go dormant and remain hidden in our bodies for life. Think Epstein-Barr virus, cytomegalovirus, or herpes simplex. These aren’t occasional guests; they’re permanent residents, quietly nudging the immune system, draining energy, and stoking low-grade inflammation.
According to McClure, these latent pathogens act as “molecular time bombs,” constantly communicating with immune cells and accelerating the underlying processes of aging .
This aligns with a growing body of research linking chronic infection to immunosenescence—the gradual deterioration of the immune system that makes older adults more vulnerable to disease. Persistent infections are also tied to inflammaging, the low-level, chronic inflammation associated with age-related decline.
Biological Age vs. Chronological Age: The Infection Connection
One of the more compelling ideas raised in McClure’s discussion is the difference between how long you’ve lived and how old your body behaves. Biological age—now trackable with epigenetic clocks—doesn’t always match the number on your birth certificate.
Chronic infection can act as an invisible accelerator of biological aging, even in young individuals. Recent studies using methylation markers suggest that people with high viral loads or immune system activation show older biological profiles—regardless of their actual age.
This is more than an academic detail. Your biological age predicts your risk of chronic disease, cognitive decline, and mortality far better than your birthday ever could.
What If Infectious Disease Is the Driver of Aging?
McClure takes it a step further, proposing that aging itself may be a form of chronic infection response. This doesn’t mean that a single virus is the culprit behind wrinkles or joint pain. Rather, it’s the cumulative burden of microbial exposure, immune overactivation, and the molecular debris that pathogens leave behind that drives the degenerative spiral we call aging.
It’s a radical reframing—but one that invites new therapeutic possibilities.
If aging is in part a chronic immune reaction to long-term infections, then targeting those microbes or the immune responses they provoke could slow aging itself.
Introducing the Synthetic Immune System
McClure’s company, Maxwell Biosciences, is developing what he calls a “synthetic immune system”—a suite of small molecules engineered to mimic and augment the body’s natural defenses.
These molecules, called Claromers™, are designed to neutralize a wide range of viruses and bacteria by mimicking the shape and charge of antimicrobial peptides. Unlike antibiotics, which often target specific cellular processes, these Claromers aim to be broad-spectrum and immune-supportive, capable of both killing pathogens and reducing harmful inflammation .
In early lab studies, these compounds have shown promise against viruses like influenza and even coronaviruses, without the resistance concerns seen with traditional antivirals.
If successful, this approach could help reduce the persistent viral load many people carry—a step that McClure believes could translate into healthier aging trajectories.
Echoes from Immunology and Geroscience
McClure’s ideas don’t exist in isolation. They resonate with major themes in immunology, longevity science, and evolutionary medicine.
1. The Inflammaging Hypothesis
Chronic inflammation is increasingly viewed as a central mechanism of aging. It underlies everything from atherosclerosis to neurodegeneration. Many of the inflammatory triggers—damaged cells, misfolded proteins, and yes, infections—stimulate immune pathways like NF-κB and IL-6, which accelerate tissue breakdown over time.
2. Immune Resilience as a Longevity Predictor
Recent research from institutions like the Buck Institute has shown that immune resilience—the ability to return to balance after immune stress—predicts health outcomes more accurately than age. In people with weakened immune flexibility, even mild infections can lead to long-term immune dysfunction and faster biological aging.
3. The Microbiome and Virome in Aging
The gut microbiome has been widely studied in aging, but less attention has been given to the virome—the collection of viruses that live in our bodies. Some of these are benign or even beneficial. Others act as silent agitators of immune response. The composition of one’s virome could explain why some people age more rapidly despite similar lifestyles.
Infection and the Brain: The Cognitive Cost
McClure points to the work of researchers investigating the link between viral infections and cognitive decline. Herpesviruses have been associated with increased Alzheimer’s risk, and certain inflammatory profiles seen in long COVID resemble those of early dementia.
When viral particles linger in the central nervous system, they can activate microglia (the brain’s immune cells), leading to inflammation, myelin loss, and synaptic dysfunction—all contributors to neurodegeneration.
This means the cost of latent infection may be more than physical—it could be neurological and emotional, subtly affecting memory, mood, and mental clarity over time.
Toward a New Paradigm: Longevity Through Anti-Infective Medicine
If McClure is right—and if further research supports the idea that infectious burden is a core driver of aging—then the future of anti-aging medicine may look very different from today’s approach.
Instead of focusing solely on antioxidants, hormone replacement, or nutraceuticals, we may see the rise of preventative antivirals, immune modulators, and claromer-based therapeutics that reduce biological age by reducing infection load.
Imagine a world where instead of fighting aging as an abstract inevitability, we treat it as a chronic, immune-mediated condition—manageable, measurable, and in some ways, reversible.
Practical Implications for Everyday Wellness
While Claromers and synthetic immune systems are still in development, McClure’s message carries immediate value for the wellness-minded individual.
Here are six evidence-based actions you can take today:
- Stay Current on Vaccinations
Preventing infections like shingles, flu, and pneumonia reduces immune stress and may help preserve resilience. - Support Gut Health
A healthy microbiome can prevent systemic inflammation and may buffer the effects of latent viruses. - Practice Safe Hygiene and Travel Health
Avoiding new infections—especially in unfamiliar regions—protects long-term health. - Manage Stress
Chronic stress impairs immune function and reactivates latent viruses like herpes simplex. - Consider Antiviral and Antimicrobial Peptides
Though still emerging, this class of compounds may offer broad-spectrum protection with fewer resistance concerns. - Track Your Biological Age
Epigenetic clocks and blood-based biomarkers can give early warnings of accelerated aging due to infection or inflammation.
Final Reflections: Infection as a Lens, Not a Label
McClure’s central argument—that aging is shaped by infectious disease—challenges us to rethink the boundary between biology and biography. If the body ages partly because it remembers every microbe it has ever battled, then aging becomes not just a matter of time, but of immune history.
This is more than a theory—it’s an invitation to explore a new frontier in longevity science, one that connects virology, immunology, geroscience, and synthetic biology in a shared quest: not just to live longer, but to live clearer, stronger, and freer from the microbial baggage we didn’t know we were carrying.