Nikhil Prasad Fact checked by:Thailand Medical News Team Mar 04, 2026 1 hour, 47 minutes ago
Medical News:
COVID-19 And Migraine Share Hidden Genetic Links
A groundbreaking new genetic study has uncovered surprising biological connections between COVID-19 and migraine, suggesting that the two conditions may share common genetic roots. However, researchers stress that while they found shared genetic patterns, there is no evidence that COVID-19 directly causes migraines — or vice versa.
Shared genes in immune and brain pathways link COVID-19 and migraine without direct causation.
The research was conducted by scientists from the Department of Ultrasound, the Department of Neurology, and the Department of Neurosurgery at The First Affiliated Hospital of Harbin Medical University in Harbin, Heilongjiang Province, China.
Why Scientists Explored This Link
Since the beginning of the pandemic, doctors noticed that many COVID-19 patients reported headaches and worsening migraine attacks. In fact, previous reports suggested that more than one-third of infected individuals experienced migraine-like symptoms. This raised an important question: Is COVID-19 triggering migraines directly, or do both conditions share deeper biological connections?
To answer this, researchers analyzed massive genetic datasets. They examined genetic information from 13,465 migraine patients and 264,662 healthy individuals from the FinnGen consortium. They also studied four different COVID-19 categories from the COVID-19 Host Genetics Initiative: infection, hospitalization, severe disease requiring respiratory support, and comparisons between hospitalized and non-hospitalized patients.
What The Genetic Analysis Revealed
Using advanced genetic tools, the team discovered moderate but statistically significant genetic correlations between migraine and all four COVID-19 categories. This means certain genetic variations increase susceptibility to both conditions.
They identified 13 shared genetic variants and six key shared genes, including DPP9, ELF5, IL10RB, HIST1H1E, HIST1H2BD, and TMPRSS2. Some of these genes are involved in immune system regulation and inflammatory responses — processes that play important roles in both viral infections and migraine attacks.
Further analysis showed that these shared genes are highly active in lung tissue and in the cerebral cortex, a brain region strongly linked to migraine. The genes were also enriched in immune cells such as T cells and B cells, suggesting that immune system activation may connect the two conditions.
The researchers found that these overlapping genes are involved in critical biological pathways, particularly the mTOR pathway and the beta-catenin signaling cascade. Both pathways are known to regulate inflammation, immune responses, and cellular stress — mechanisms that are central to severe COVID-19 outcomes and migraine development.
This
Medical News report highlights that the findings provide a biological explanation for why migraines became more frequent or severe during
the pandemic. Shared immune-inflammatory pathways may make certain individuals more vulnerable to both illnesses.
No Evidence of Direct Causation
Despite the genetic overlap, the study found no evidence that COVID-19 directly causes migraines or that migraines increase the risk of COVID-19 severity. Using a method called Mendelian Randomization, which helps determine cause-and-effect relationships using genetics, researchers found no robust causal link in either direction.
Importantly, the study had strong statistical power for severe COVID-19 comparisons, meaning even small causal effects would likely have been detected. The absence of such findings suggests that any direct effect is minimal.
What This Means for Patients
The conclusions are clear but nuanced. COVID-19 and migraine share genetic foundations, particularly in immune and inflammatory pathways involving the lungs, brain cortex, and specific immune cells. However, having one condition does not genetically cause the other. Instead, both may arise partly from overlapping biological susceptibilities. These insights improve understanding of long-term neurological symptoms seen after COVID-19 and may guide future research into targeted therapies that address shared inflammatory mechanisms without assuming direct causality.
The study findings were published in the peer reviewed journal: Virus Research.
https://www.sciencedirect.com/science/article/pii/S0168170226000250
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