A class of antibiotics used to treat bacterial infection is found to work by stimulating host cells, thereby creating an antiviral state that reduces host vulnerability to infection by herpes, influenza and Zika viruses in mice, reports a paper published online this week in Nature Microbiology.
Antibiotics are widely used to treat bacterial infections in humans, yet their direct effects on our body are poorly understood. One class of antibiotics - the aminoglycosides - is used in hospitals mostly to treat life-threatening bacterial infections because of their potential toxicity, but also as a topical ointment for ear, eye and oral infections.
Akiko Iwasaki and colleagues report that the topical use of aminoglycosides in the vagina and nose before viral infection increases host resistance to herpes simplex, influenza A and Zika viruses. This antibiotic acts directly on the mouse cells and does not depend on the animal’s microbiota. The authors find that aminoglycosides cause dendritic cells - the ‘sentinels’ of the immune system - to secrete signalling proteins, thus inducing antiviral resistance in the vaginal and lung mucous membranes. This effect is shown only to occur when the antibiotics are administered prior to viral infection. Moreover, the effect is transient, so the use of aminoglycosides to treat viral infections is unwarranted (although ointments containing aminoglycosides may provide some protection from viruses as a side-benefit). Rather, this study highlights how antibiotics can directly affect patient bodies and reveals an unexpected new way to activate antiviral defences. The findings could aid the development of new, more potent and less toxic compounds that can mimic the aminoglycoside effect to act as broad-spectrum antivirals.
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