Jack - amatica health
@jackamatica.bsky.social
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ME/CFS patient and researcher Co founder of amatica health https://amaticahealth.com
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jackamatica.bsky.social
This is just one example of research papers we can review to gain insights from in relation to RNA data.

You can test all your RNA (20,000 markers per person) and see how you compare to Herberg et al., findings below:

amaticahealth.com/me-cfs-long-...
jackamatica.bsky.social
Important note:

These are preliminary. They rely on a simplified 2-gene model and only reference ranges from 3 control. More genes, controls, clinical data, and lab results will strengthen the interpretation.

Study tracked children with active fevers; relevance to adults without fever is unknown
jackamatica.bsky.social
This method doesn’t require identifying the pathogen itself.

It’s based on how the immune system responds.
jackamatica.bsky.social
Summary:

C2 & C5 = viral

C3 & C4 = bacterial

C1 = unclear (possibly mild viral)

These groupings are based solely on gene expression patterns of IFI44L and FAM89A discussed in Herberg et al.
jackamatica.bsky.social
Interestingly, the person in C5 had improvements from COVID Monoclonal Antibodies (mAbs), consistent with persistent viral load.
jackamatica.bsky.social
🟡 C5: Viral

C5 has very high IFI44L and only moderate FAM89A.

This produces a strongly “viral” signal.

The interferon-driven IFI44L is strongly induced here.
→ Fits the viral subset.
jackamatica.bsky.social
🟢 C4: Bacterial

C4 also shows elevated FAM89A and minimal IFI44L.

Though less extreme than C3, the imbalance points toward a bacterial immune signature.
jackamatica.bsky.social
🟢 C3: Bacterial

C3 has high FAM89A and very low IFI44L.

This pattern matches the typical bacterial infection response.
jackamatica.bsky.social
🔵 C2: Viral

C2 shows elevated IFI44L with low FAM89A.

This matches the viral infection pattern seen in Herberg et al.’s work.

Fits into the viral infection group.
jackamatica.bsky.social
🟣 C1: Unclear (borderline viral)

C1 has modest expression of both genes. IFI44L is slightly higher than FAM89A.

→ Slight viral tilt, but not enough to say confidently.

Possibly an indeterminate or mild infection.
jackamatica.bsky.social
The key idea is this:

- High IFI44L, low FAM89A → viral infection

- High FAM89A, low IFI44L → bacterial infection

We applied this rule to each preliminary cluster to infer possible infection type.
jackamatica.bsky.social
This classification uses a method from Herberg et al. (JAMA, 2016). They showed that expression levels of just two genes (RNA) can help separate viral from bacterial infections in children with fever.

The RNA are available to be tested here:
amaticahealth.com/me-cfs-long-...
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20,000 results in one test - understand your disease while helping advance research
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jackamatica.bsky.social
🔬We identified five preliminary immune clusters (C1–C5) in our Long COVID & ME/CFS cohort using two RNA markers: IFI44L and FAM89A.

Research shows these genes can help distinguish bacterial from viral infections.

Let’s break down which clusters likely fall into each category.
jackamatica.bsky.social
All markers above can be tested through our full RNA seq panel - 20,000 results per participant:

amaticahealth.com/me-cfs-long-...

For Research Use Only - not for use in diagnostic procedures. Results are educational, not medical advice, and not validated to assess BBB function.
jackamatica.bsky.social
Here’s the key study on Long COVID, brain fog, and blood–brain barrier disruption using blood RNA profiling:

www.nature.com/articles/s41...
jackamatica.bsky.social
A carefully chosen gene panel (like the one above) helps researchers focus on meaningful BBB signals - even when they’re low in abundance.

As more studies are done, this approach may help monitor or predict brain conditions from a simple blood test.
jackamatica.bsky.social
This suggests a systemic response - possibly due to vascular stress or early BBB damage in Alzheimer’s.

Even in chronic diseases, blood gene expression can reflect changes in brain vascular health and BBB stability.
jackamatica.bsky.social
Study 4: Alzheimer’s & Vascular Genes

Researchers looked at VEGF-related gene expression in blood and brain. They found:

- Higher PGF and VEGFB in blood

- Lower expression in brain

This imbalance was linked to faster cognitive decline.
jackamatica.bsky.social
This study shows that blood RNA changes reflect the inflammatory response after stroke - especially the response that damages the BBB and allows immune cells into the brain.

The method used is directly applicable to tracking BBB injury over time.
jackamatica.bsky.social
Study 3: Intracerebral Hemorrhage (Stroke)

Researchers sequenced blood RNA at 24h and 72h after stroke.

At 72h, they found:

- Increased IL8, MMP9, NF-κB, ICAM1

All tied to immune-driven BBB damage.
jackamatica.bsky.social
Study 2: Repeated Blast Exposure

Military breachers (who experience repeated low-level blasts) showed changes in blood RNA:

- Immune genes like LILRB5, CD200

- A brain-specific gene CNTNAP2

This suggests chronic stress or damage to brain barriers.
jackamatica.bsky.social
They also showed that these patients’ blood cells stuck more strongly to lab-grown brain endothelial cells, and their serum caused inflammation in those cells.

The changes in blood RNA reflected inflammation and damage at the BBB.
jackamatica.bsky.social
Study 1: Long COVID + Brain Fog

Researchers sequenced immune cells from Long COVID patients with brain fog. They found:

Increased clotting and complement genes

Decreased adaptive immune genes

This matched signs of a leaky BBB on MRI.
jackamatica.bsky.social
Now let’s look at how this has been used in real research.

Studies have used blood RNA sequencing to detect changes in BBB-related genes in humans - both in acute injuries and chronic brain conditions.