Janus kinase inhibitors, prescribed for rheumatoid arthritis and other inflammatory diseases, suppressed antiviral genes in laboratory experiments and let viruses including influenza A and SARS-CoV-2 spread more easily. The work comes from Denis Kainov’s group at the Norwegian University of Science and Technology and covers cells and lab-grown mini-organs, not patients.
Tech news in one quick read: Get the most interesting stories in startups, tech and programming, each with a short TLDR, in one daily email from TLDR.
We may earn a commission if you sign up.
Baricitinib was the drug the researchers highlighted. The paper’s authors recommend caution, particularly during outbreaks, and further study before any change in prescribing.
Baricitinib and the antiviral genes it quiets
JAK inhibitors work by blocking Janus kinase enzymes that relay inflammatory signals, which calms overactive immune responses in autoimmune disease. The same signaling system switches on a first line of antiviral defense inside ordinary cells. The study, JAK inhibitors remove innate immune barriers facilitating viral propagation, appeared in NAR Molecular Medicine in 2025 and combined virology, gene-expression analysis and organoid technology to compare antiviral defenses across human tissues.
The team worked with cells from the lung, eye and brain and with organoids. In those models, JAK inhibitors including baricitinib reduced the activity of genes involved in antiviral defense, which weakened an immune signaling layer and made it easier for viruses to establish infection and move between cells. The viruses named in the work were Rift Valley fever virus, influenza A, adenovirus and SARS-CoV-2.
Limits of the NTNU laboratory models
Kainov described the result, in a university-supplied account, as a surprising and potentially serious side effect of a class of anti-inflammatory drugs. First author Erlend Ravlo said the drugs suppress an important immune signaling pathway that helps protect healthy cells from viral attacks, and that they can pose a hidden risk for patients who have latent or active viral infections. Aleksandr Ianevski, a coauthor, called for further studies on how the drugs can best be used.
Several limits apply. The summaries do not name the affected genes, give effect sizes or report any patient infection rates. Only baricitinib is named, so applying the finding to every drug in the class goes beyond what has been shown. Cells in a dish lack the rest of the immune system, and a drug dose reaching a lung in a patient differs from one added to cultured cells. Nothing in the laboratory data shows how often a patient on one of these drugs catches influenza or COVID-19 more severely, which is the question a clinician would need answered.
The research group is large: the paper lists 20 authors, among them Magnar Bjørås, who the university account says supplied significant scientific expertise and secured most of the funding. Ravlo, Ianevski and Kainov form the core named in the release, and the work crossed virology, immunology and tissue engineering. A study built across lung, eye and brain cells is meant to test whether the effect is tissue-specific, though the summaries do not report results tissue by tissue or say which tissues responded most strongly to the drugs.
Labels already warn about other risks
JAK inhibitors are not new to safety scrutiny. In September 2021 the Food and Drug Administration required revised boxed warnings for tofacitinib (Xeljanz), baricitinib (Olumiant) and upadacitinib (Rinvoq), covering serious heart-related events, cancer, blood clots and death. That communication does not describe viral infections as a new finding, so the Norwegian result adds a mechanism-level question rather than a new regulatory conclusion.
For patients, the practical relevance sits in the respiratory season. The Centers for Disease Control and Prevention lists people who take immune-suppressing drugs for chronic conditions among those with a weakened immune system and at higher risk of flu complications. It recommends a yearly flu vaccine for everyone aged 6 months and older, especially higher-risk people, and prompt antiviral treatment when a higher-risk person has or may have flu.
A side effect that may also be a research tool
The same effect could have a use. The researchers note that suppressing these antiviral genes might help in controlled laboratory settings, such as vaccine development or antiviral drug screening, where a virus that spreads easily is an advantage. That framing shows how the team sees the finding: as a property of the drugs to be understood, not as a reason to stop treatment.
Arthritis treatment itself is built around controlling joint damage. The CDC describes disease-modifying antirheumatic drugs as the main class, with biologics prescribed when initial treatment fails, and says those drugs aim to slow progression and prevent deformity. Patients on any of them face a trade-off between joint protection and infection risk, and the decision belongs to a rheumatologist.
The ScienceDaily page that surfaced the work on October 27, 2026 repeats the 2025 findings and adds no new data. What remains unknown is whether the gene suppression seen in organoids translates into measurable differences in infections among people taking baricitinib, a question only studies in patients can resolve. Until such work appears, the finding stays a laboratory warning flag about a drug class already carrying heavy label warnings.
This article was produced with the assistance of AI and reviewed by Morning Overview editors prior to publication.
Tech news in one quick read: Subscribe to TLDR →
We may earn a commission if you sign up.
More from Morning Overview
- Long use of a common prostate pill is tied to a higher chance of glaucoma
- Ford is recalling 223,472 F-150 pickups because the fuel tank can leak or detach
- Hybrids have 15% fewer problems than gas cars, while EVs and plug-in hybrids have about 80% more, Consumer Reports finds
- Regulators cleared the first U.S. small modular reactor, 4 months early
