Feed a Virus, Starve a Bacterium?
Posted on by Dr. Francis Collins
Yes, the season of colds and flu is coming. You’ve probably heard the old saying “feed a cold and starve a fever.” But is that sound advice? According to new evidence from mouse studies, there really may be a scientific basis for “feeding” diseases like colds and flu that are caused by viruses, as well as for “starving” certain fever-inducing conditions caused by bacteria.
In the latest work, an NIH-funded research team found that providing nutrition to mice infected with the influenza virus significantly improved their survival. In contrast, the exact opposite proved true in mice infected with Listeria, a fever-inducing bacterium. When researchers forced Listeria-infected mice to consume even a small amount of food, they all died.
Just like humans, when mice and other mammals come down with many infectious illnesses, they often lose their appetites and shun food. In the new study reported in the journal Cell, a team led by Ruslan Medzhitov, a Howard Hughes Medical Institute Investigator at Yale University School of Medicine, New Haven, CT, and former Lurie Prize winner from the Foundation for NIH, set out to explore how the presence or lack of nutrition might influence recovery from infections .
In one series of experiments, the researchers infected mice with the influenza virus, which caused potentially life-threatening bouts of the flu. As expected from past observations, the flu-sickened mice reduced their food intake. However, when the researchers pumped more nutrition into some of the sick mice via tube feeding, their odds of survival were significantly better than those who weren’t given the extra nutrition. Further analysis showed that the animals’ survival appeared to hinge on the availability of glucose. When mice suffering from the flu were starved of glucose, they eventually lost the vital ability to control their body temperatures, breathing, and/or heart rates.
Researchers found the situation to be dramatically different in mice that were infected with the bacterium Listeria, an occasional cause of food poisoning in humans. When mice are sickened by Listeria, they tend to stop eating for a while, before eventually resuming eating and recovering. However, in contrast to mice with the flu virus, when researchers gave the Listeria-infected mice even a small amount of nutrition, all the animals died. Again, it was all about sugar. Glucose alone, delivered via tube feeding or injection, was enough to kill Listeria-infected mice. The cause of death wasn’t an inability to clear the infection: they died from changes to their metabolism that made things worse.
PET scans of mice suffering from viral versus bacterial inflammation also revealed significant differences in the way their brains took up glucose. Taken together, these findings suggest that, by taking advantage of key metabolic differences, nutrition (or lack thereof!) may play an important role in helping mammals mount successful responses to different types of infections, just as the old “feed a cold, starve a fever” adage implies.
In light of the findings in mice, a much closer look may be needed to determine what constitutes optimal nutrition for people dealing with a wide range of infectious illnesses. Medzhitov says he and his colleagues are now in the planning stages for a human clinical trial designed to explore that very issue.
So, what to do if you or a loved one comes down with a cold, the flu, or another viral bug this season? Medzhitov wisely hesitates to provide medical advice, noting that mice are not humans and the findings need to be replicated and confirmed in people. But, in the meantime, it appears that giving the patient with a typical viral syndrome a bowl of ice cream or another glucose-rich treat probably wouldn’t hurt—and might even help. Just be sure first that it’s not a serious bacterial infection.
 Opposing effects of fasting metabolism on tissue tolerance in bacterial and viral inflammation. Wang A, Huen SC, Luan HH, Yu S, Zhang C, Gallezot JD, Booth CJ, Medzhitov R.Cell.2016 Sep 8;166:1-14.
Ruslan Medzhitov (Yale University School of Medicine, New Haven, CT)
NIH Support: National Institute of Allergy and Infectious Diseases; National Cancer Institute; National Institute of Arthritis and Musculoskeletal and Skin Diseases; National Institute of Diabetes and Digestive and Kidney Diseases
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