Monocytes: Scientists Just Discovered a Possible Cause of Long COVID

Researchers at the University of Manchester believe that they have found the cause of the mysterious phenomenon of ‘long COVID,’ special immune cells called monocytes.

Key Takeaways:

1. Monocytes Identified as Culprit: Researchers at the University of Manchester have pinpointed monocytes, a type of immune cell, as key players in the phenomenon of long COVID.
2. Abnormal Monocyte Activity: Long COVID patients exhibit abnormal monocyte behavior, with an unusual amount of proteins attached that mislead the immune response, indicating inflammation due to an exaggerated auto-immune reaction.
3. Vicious Cycle of Immune Response: COVID infections attack monocytes, creating a feedback loop that exacerbates the immune response, leading to more severe long COVID symptoms.
4. CXCR6 and CXCL16 Proteins’ Role: The study highlights the increased presence of receptor protein CXCR6 on monocytes and its interaction with CXCL16 in the lungs, contributing to prolonged inflammation and tissue damage associated with long COVID.
5. Pathway to Potential Treatments: Understanding the detailed mechanisms of long COVID opens up avenues for developing targeted treatments, marking a significant step forward in finding a cure for this debilitating condition.
6. Hope for FDA Approval: With advanced biotechnology and pharmaceutical sciences making rapid progress, there’s optimism that a cure for long COVID will soon be developed and undergo FDA approval for patient use.

The Role of Monocytes in Immune Response

Monocytes are immune cells that recognize invading pathogens and call for help from other immune cells. When they send out a signal to the rest of the immune system, other immune cells are funneled towards that signal.

Then those immune cells fight off the pathogen. Without monocytes, the immune system would not function properly.

Long COVID, a debilitating sickness that lingers for months in some unlucky COVID patients, has stumped doctors and researchers since 2020. A recent paper published in the European Respiratory Journal found that long COVID patients had abnormal monocytes.

Various proteins attach to monocytes as part of the normal signaling process to help direct the pathogen-fighting cells. Long COVID patients had an unusual amount of monocytes with these proteins attached. Their monocytes seem to be mistakenly signaling to the rest of the body that there is a pathogen where there is none.

This indicates that long COVID is likely inflammation caused by an exaggerated auto-immune response. Even though the COVID virus itself is gone, the damage it did to the body’s monocytes lingers.

The Feedback Loop Exacerbating Long COVID

The scientists also discovered that there is a feedback loop that makes long COVID even worse. COVID infections attack monocytes, releasing an excess of signaling molecules when they die.

This brings more monocytes and other immune cells that then get attacked by COVID, potentially releasing even more signaling molecules, increasing the immune response further.

The Role of CXCR6 and CXCL16 Proteins

The paper went further than suggesting a vague cause for long COVID as well. The authors found that COVID increased the amount of a specific receptor protein found on the surface of monocytes called CXCR6. CXCR6 binds with CXCL16, a protein produced in the lungs during both acute and long COVID infections.

The researchers hypothesized that this is how the COVID virus causes the symptoms of long COVID. Increased CXCR6 may have caused monocytes to travel to the lungs in greater numbers. They would then bind with the increased concentration of CXCL16, causing prolonged inflammation and eventually tissue damage.

Wrapping Up

This discovery could be a vital step in finding a cure for the debilitating phenomenon of long COVID. With the recent incredible advances in pharmaceutical sciences and biotechnology, a cure may be just around the corner.

Though it will still need to be approved by the Food and Drug Administration before it can be used on patients.

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