A new study highlights host-derived lactic acid as an important reason interferon, or IFN, may work less effectively after viral infection. The researchers found that this metabolic byproduct can interfere with IFN's antiviral action while also intensifying inflammatory responses, creating a double challenge during infection.
The findings point to a broader link between metabolism and immune defense. Rather than acting only as a marker of stress in infected tissues, lactic acid appears to actively shape how the body responds to antiviral treatment. That makes it a potential target for improving therapies that rely on IFN.
The study also identified a possible way to counter this effect. According to the report, combining IFN with stiripentol, an approved LDH inhibitor, restored antiviral activity and eased inflammation in viral infection models. This suggests that blocking lactic acid-related pathways could help IFN perform better when the host response is working against it.
Researchers affiliated with Taihe Hospital and Hubei University of Medicine in Shiyan, China, were listed in the report. Overall, the work suggests that managing host metabolism may be an important step in making antiviral treatments more effective and less inflammatory.
