Jack | amatica health Profile picture
Sep 4 23 tweets 4 min read Read on X
🔬Viruses don’t just cause short-term illness.

Many stay in your body for life.

They speed up the aging process - in your immune system, organs, and even your DNA.

Here’s some examples, and why stopping them could help extend lifespan🧵 Image
Common long-term viruses include:

- CMV (cytomegalovirus)

- HSV (herpes simplex, cold sores)

- EBV (Epstein-Barr, mono)

- HIV

- HBV and HCV (hepatitis B and C)

These viruses often remain in the body for years, even decades.
They cause damage over time, even when you don’t feel sick.

Researchers have found that these viruses speed up many of the same processes that happen during normal aging.
One example: telomeres - protective caps at the ends of your DNA.

They get shorter as you age.

People with chronic infections have much shorter telomeres, especially in their immune cells, even at younger ages.
Short telomeres mean cells can’t divide properly.

This leads to weaker immune function, more inflammation, and higher risk of age-related diseases.
Viruses also cause some cells to enter a “shutdown” state.

These are called senescent cells.

They don’t die, but they release harmful signals that affect nearby healthy cells.
This contributes to chronic inflammation in tissues - seen in diseases like arthritis, heart disease, and Alzheimer’s.

Some viruses cause this directly. For example, COVID-19 can trigger senescent cells in the lungs.
Mitochondria - the energy source in your cells - also take a hit.

Viruses like HIV and hepatitis C damage mitochondria in immune cells, leading to more stress, less energy, and faster aging.
This results in “tired” immune cells that don’t work as well, similar to those found in much older people.
Many viruses also keep the immune system constantly activated.

This causes long-term, low-level inflammation - sometimes called “inflammaging.”
For example, people with CMV (a very common lifelong virus) have higher levels of inflammatory molecules in their blood.

This increases the risk of heart disease, diabetes, and other chronic conditions.
Some viruses even change how your genes are regulated - what’s known as epigenetic aging.

People with HIV or CMV often show signs of being biologically years older than their actual age.
These epigenetic changes can affect how your body repairs itself, fights disease, and maintains organ function.

And they can last even after the virus is under control.
Let’s look at some examples from human studies:

People with high numbers of chronic infections have shorter telomeres.

HIV+ people, even on treatment, show signs of faster aging (in immune function, inflammation, and DNA changes).

CMV is linked to poor vaccine response and higher frailty in older adults.
In animal studies:

- Infected monkeys age faster at the genetic and immune level.

- Mice with long-term viral infections have more inflammation and die younger.

- Infected fruit flies lose gut function earlier and have shorter lifespans.
So what can be done?
There are ways in development that may reduce or slow down this virus-driven aging - through prevention, treatment, and new therapies.
CRISPR-based gene editing is being tested to remove viruses from the body entirely.

- Early HIV trials show partial success.

- Lab studies show this could work for herpes and hepatitis B as well.
Senolytics - drugs that remove senescent cells - may help reverse some of the damage.

In mouse studies, they reduced lung damage caused by COVID by clearing these aged, damaged cells.
Researchers are also working on immune-boosting therapies to help the body better control chronic viruses without ongoing damage.
In short:

Chronic viruses can quietly speed up aging in the immune system, liver, brain, and elsewhere.

They make your body behave like it’s older than it is.
Preventing and controlling these infections could become part of how we slow down aging, reduce disease risk, and extend healthy lifespan.
This is just another example of how viruses cause negative effects in the human body past the acute illness phase.

Research into post viral diseases like Long COVID & ME/CFS may also help uncover mechanisms in which viruses continue to effect individuals post infection.
You can follow our research @amaticahealth on our website and join the projects yourself to help progress research:

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More from @JackHadfield14

Sep 5
🧵 T cell exhaustion - possibly one of the drivers of chronic infections in Long COVID & ME/CFS.

What is it, what genes are involved, and how we can gain insights with available testing.

Let’s break it down. 🧵 Image
T cells are immune cells that normally help fight infections and cancer.

But when T cells are exposed to a threat for too long - like a virus or tumor that doesn’t go away - they can enter a state called “exhaustion.”
Exhausted T cells (Tex) don’t die, but they stop working properly.

They lose their ability to kill infected or cancerous cells.

They stop multiplying.

They start expressing signals that suppress the immune system.
Read 25 tweets
Sep 4
🔬A major new study shows clear evidence of immune overactivation, energy metabolism failure, gut issues, and worsening after exercise in ME/CFS.

Importantly - patients separated into subgroups, a focus by us @amaticahealth

Let’s break it down in simple language 🧵 Image
@amaticahealth Researchers studied 56 people with ME/CFS and 52 healthy controls. Blood samples were taken before and after an exercise challenge that typically triggers post-exertional malaise (PEM), a core symptom of ME/CFS.

They looked at immune responses, proteins, and metabolites.
@amaticahealth Before exercise, people with ME/CFS had much stronger immune responses to bacterial and fungal mimics in lab tests. Their immune cells released more inflammatory chemicals like IL-6, TNF-alpha, and others - especially in women.

This suggests heightened immune sensitivity.
Read 23 tweets
Sep 3
🔬Interesting aging study - removing a single protein (FTL1) from the brain of old mice restores memory and brain function.

It also improves how brain cells use iron and energy.

Aging reversal is hope for me losing years to chronic illness - let’s break it down.🧵 Image
As mice age, a protein called FTL1 builds up in the hippocampus, a brain region essential for learning and memory.

FTL1 helps store iron. That’s normal. But in older mice, too much FTL1 is a problem.
The researchers found that higher levels of FTL1 in the brain were linked to worse memory.

So they asked: what happens if you artificially raise FTL1 in young mice?
Read 20 tweets
Sep 1
🔬Most people think mast cells are only involved in allergies or rare conditions like MCAS or mastocytosis. That’s incorrect.

Research shows mast cells are active in many diseases, including neurodegenerative, autoimmune, infectious, heart, gut, and mental health conditions🧵 Image
Mast cells sit in tissues like the skin, gut, and around blood vessels and nerves. When triggered, they release a large mix of chemicals: histamine, tryptase, chymase, cytokines (like TNF and IL-6), prostaglandins, and more.

These chemicals affect nearby cells and tissues.
They don’t just respond to allergens. They’re activated by stress, infections, tissue damage, antibodies, and even certain hormones.

Once activated, they can increase inflammation, damage tissue, recruit other immune cells, and change blood vessel function.
Read 25 tweets
Aug 30
A new study identifies a protein called SMPDL3B as a possible key factor in Myalgic Encephalomyelitis (ME/CFS).

It could explain immune problems, symptom severity, and even point to new treatments.

Here’s a full breakdown - our preliminary RNA data supports this finding: 🧵 Image
First, what is SMPDL3B?

It’s a protein found on the surface of immune cells. It plays a role in controlling inflammation and responding to viruses. It also helps manage how lipids (fats) behave in cells.
This protein exists in two forms:

- Membrane-bound: attached to immune cells

- Soluble: floating freely in the blood
Read 24 tweets
Aug 29
🔬 A major international study looked at what COVID-19 does to your blood vessels over time.

It found that people who had COVID - especially women - had “older” and stiffer arteries, even months later.

Here’s a simplified breakdown of what they found 🧵 Image
The CARTESIAN study followed nearly 2,400 people from 18 countries.

They compared:
People who never had COVID
People who had mild COVID (not hospitalized)
People hospitalized with COVID
People who were in the ICU with COVID
Researchers measured something called “pulse wave velocity” or PWV.

It checks how stiff your arteries are.

Stiffer arteries = worse long-term heart and blood vessel health.

Higher PWV means your arteries are aging faster than normal.
Read 18 tweets

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