Plate Nº 19 · recorded October 30, 2026
Health & Medicine ResearchReported finding
Common Arthritis Drugs May Help Dangerous Viruses Spread, Study Finds
NTNU researchers found JAK inhibitors, common rheumatoid arthritis drugs, suppress antiviral genes and may ease the spread of influenza A and SARS-CoV-2.
By Marcus Bennett4 min read744 words
In brief
- NTNU study in NAR Molecular Medicine (DOI 10.1093/narmme/ugaf017) links JAK inhibitors to faster viral spread.
- Affected viruses include influenza A, SARS-CoV-2, adenovirus, and Rift Valley fever virus.
- The drug baricitinib was among the JAK inhibitors tested.
- Experiments used lung, eye, and brain cells plus lab-grown organoid models.
- Funding came largely from NTNU's Magnar Bjørås plus four Norwegian and Swedish research bodies.

A class of widely prescribed anti-inflammatory drugs may make it easier for dangerous viruses — including influenza A and SARS-CoV-2 — to infect cells and spread through the body, according to researchers at the Norwegian University of Science and Technology (NTNU).
The study, published in NAR Molecular Medicine, found that Janus kinase inhibitors, known as JAK inhibitors, suppress genes that normally fight off viral infections. The finding matters for anyone prescribing or taking these drugs, because it points to a hidden risk during flu seasons, outbreaks, or active infections.
What did the researchers find?
The NTNU team discovered that JAK inhibitors can weaken a crucial layer of the body's innate immune defense — the fast, first-line response that protects healthy cells before adaptive immunity kicks in.
"We have found a surprising and potentially serious side effect of a class of anti-inflammatory drugs. They can help viruses spread more easily in the body," says Denis Kainov, a professor at NTNU's Department of Clinical and Molecular Medicine.
Among the viruses that spread more easily under the influence of these drugs are:
- Rift Valley fever virus
- Influenza A
- Adenovirus
- SARS-CoV-2, the virus that causes COVID-19
"Among the viruses that more easily affect the body with the help of these drugs are Rift Valley fever virus, influenza A, adenovirus and SARS-CoV-2, the virus that causes COVID-19," Kainov says.
Each of these pathogens can cause significant illness, which makes any treatment that boosts their ability to spread a genuine clinical concern.
Why do arthritis drugs weaken antiviral defenses?
JAK inhibitors, including the medication baricitinib, are prescribed for autoimmune and inflammatory conditions such as rheumatoid arthritis. They work by calming overactive immune signaling — effective for inflammation, but a trade-off for infection defense.
"JAK inhibitors are often prescribed for autoimmune diseases and inflammatory conditions such as rheumatoid arthritis," says Erlend Ravlo, a PhD research fellow at NTNU and first author of the paper.
The drugs suppress an important immune signaling pathway that helps protect healthy cells from viral attacks. "In particular, the drugs suppress an important immune signalling pathway that helps protect healthy cells from viral attacks," Ravlo said.
When that pathway falters, the activity of antiviral genes drops.
"These genes play a crucial role in the body's response to viral infections," said Aleksandr Ianevski, an NTNU researcher and coauthor of the study.
Without the usual defensive response, viruses find it easier to establish an infection and move between cells.
How did the team test this?
The researchers combined advanced virology methods with gene expression analysis and organoid technology — miniature, lab-grown organ models that mimic real human tissue.
Their experiments covered cells from the lungs, eyes, and brain, allowing the team to track how JAK inhibitors affect antiviral defenses across different tissue types rather than in a single cell line.
"Although JAK inhibitors are effective in the treatment of inflammation, this shows that they can pose a hidden risk for patients who have latent or active viral infections," Ravlo says.
Takeaway: lab-grown tissue models from three organs showed the same pattern — the drugs removed barriers that normally hold viruses in check.
What does this mean for prescribing?
The results suggest clinicians should weigh the timing of JAK inhibitor prescriptions carefully, particularly when a patient already has a viral infection or when a virus is circulating widely in the community.
The researchers stop short of calling for anyone to stop treatment. The findings are preliminary in the sense that they come from laboratory models, not from clinical trials in patients, and the authors themselves frame their recommendation as a call for further study.
"We recommend further studies to better understand how the drugs can be used optimally, especially during virus outbreaks or pandemics," says Ianevski.
There is also a research upside. The same immune-suppressing properties that create risk in patients could help scientists under controlled laboratory conditions — for example, in developing vaccines or evaluating candidate antiviral drugs.
Who funded the work?
Professor Magnar Bjørås of the Department of Clinical and Molecular Medicine provided significant scientific expertise and secured most of the funding. Additional support came from the Central Norway Regional Health Authority, the South-Eastern Norway Regional Health Authority, the Research Council of Norway, and the Swedish Research Council.
For prescribers, the practical point is simple: JAK inhibitors work well against inflammation, but during an outbreak or an active infection, their antiviral cost deserves a second look.
via norwegianscitechnews.com (Original)
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News editor covering regulation, policy and their impact on general science news at SciBeat.
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