Arthritis drugs may weaken the antiviral defenses that block influenza and COVID-19
NTNU researchers found JAK inhibitors, used for rheumatoid arthritis, can suppress antiviral genes and may help viruses like influenza and SARS-CoV-2 spread.
Summary
Janus kinase (JAK) inhibitors are widely prescribed to calm inflammation in rheumatoid arthritis and other autoimmune conditions. Researchers at the Norwegian University of Science and Technology report that these drugs, including baricitinib, can also turn down an immune signaling pathway that normally protects healthy cells from viruses. When that pathway is dampened, genes that fight infection become less active, and viruses may find it easier to establish infection and spread between cells. The viruses highlighted include influenza A, SARS-CoV-2, adenovirus and Rift Valley fever virus. The work, published in NAR Molecular Medicine, points to a trade-off: the same mechanism that reduces damaging inflammation also lowers a layer of antiviral defense. For people managing autoimmune disease, especially older adults who already face higher infection risk, the finding is a reminder to weigh benefits against infection vulnerability and to discuss vaccination and monitoring with a physician.
Detailed Summary
Many adults manage chronic inflammatory disease with drugs that quiet the immune system. Janus kinase (JAK) inhibitors are one of the most widely used classes, prescribed for rheumatoid arthritis and other autoimmune and inflammatory conditions. Because immune function declines with age while inflammatory disease and infection risk rise, understanding how these drugs shape antiviral defense matters for healthy aging.
Researchers at the Norwegian University of Science and Technology, led by Professor Denis Kainov, studied how JAK inhibitors affect the body's ability to resist viruses. Their study, published in NAR Molecular Medicine, found that these drugs, including baricitinib, suppress an important immune signaling pathway that helps protect healthy cells from viral attack. As a result, the activity of genes that normally fight viral infections is reduced.
The team reports that this weakened defense may make it easier for several viruses to infect cells and spread. Those named include influenza A, adenovirus, Rift Valley fever virus and SARS-CoV-2, the virus that causes COVID-19. The researchers describe the effect as a surprising and potentially serious side effect, because the very mechanism that makes JAK inhibitors effective against inflammation also interferes with a first line of antiviral protection.
The practical message is about trade-offs rather than abandoning treatment. These drugs can be highly effective for people with debilitating autoimmune disease, and stopping them without medical guidance can carry its own risks. Patients and clinicians may want to consider infection risk, keep vaccinations current, and act early when respiratory symptoms appear.
Several caveats apply. The article excerpt does not describe the experimental models in detail, so it is unclear how strongly the laboratory findings translate into real-world infection rates in patients. The magnitude of risk, differences between individual JAK inhibitors, and the role of dose and duration remain to be established. Readers should consult the original paper and their physician before changing any medication.
Key Findings
- JAK inhibitors, including baricitinib, suppress an immune pathway that normally shields healthy cells from viral attack.
- Reduced activity of antiviral genes may make it easier for viruses to infect cells and spread.
- Viruses highlighted include influenza A, SARS-CoV-2, adenovirus and Rift Valley fever virus.
- The drugs are prescribed for rheumatoid arthritis and other autoimmune conditions, so the anti-inflammatory benefit carries an infection trade-off.
- The findings were published in NAR Molecular Medicine by researchers at the Norwegian University of Science and Technology.
Methodology
This is a news report summarizing a peer-reviewed study in NAR Molecular Medicine from the Norwegian University of Science and Technology, distributed via ScienceDaily. The excerpt gives no details on experimental models, sample sizes or doses, so the strength of evidence cannot be fully judged from the article alone.
Study Limitations
The article excerpt is truncated and does not describe the study design, whether findings come from cell models or patients, or the size of any infection risk. Real-world risk differences between specific JAK inhibitors, doses and patient groups are not addressed. Verify details in the original NAR Molecular Medicine paper.
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