Another danger of obesity
Obesity has made the flu more dangerous and helped its spread
Scientists from St. Jude Children's Research Hospital have found out how overweight individuals in the population contribute to the virulence of the influenza pathogen and what exactly leads to this. They published an article about their research in the journal mBio (Honce et al., Obesity-Related Microenvironment Promotes Emergence of Virulent Influenza Virus Strains – VM).
The obesity epidemic is an ever-growing threat to public health: today, 50% of the adult population worldwide is overweight or obese. This is a serious factor that explains, among other things, the statistics of the incidence of influenza. Previous studies have shown that obese people, exhaling, emit more viral particles, and also release the pathogen into the external environment for longer.
Warning that it is impossible to completely extrapolate the results of the experiment on mice to humans, the researchers note that the probability of similar reactions is very, very high. Cells behave in a similar way in a "fatty" environment, and it seems that it is because of this that obese people do not have good antiviral reactions. The immune response is delayed and blunted.
The authors of the work suggested that the microenvironment in obesity contributes to the rapid variability of influenza strains. To test the hypothesis, they infected lean and obese mice with the same type of causative agent of this disease, giving it three days to reproduce in their organisms. Then the scientists extracted virus samples from obese and thin rodents and successively infected the pathogen from thin mice, again, thin, and taken from fat – fat. Three days later, virus samples were also extracted from these "intermediate hosts" and the cycle was repeated again. Thus, the authors modeled the spread of the flu epidemic in human societies – in the population with normal weight and in the population with obesity.
It turned out that during the time that the pathogen spent in mouse organisms, it managed to create mutations. And the viruses eventually obtained from the obese population were more virulent than those from which ordinary mice suffered. When cells interact with the infectious agent of influenza, the body normally issues an interferon-mediated response to stop the reproduction and spread of the virus. The data from this work show that this emergency response was weakened in obese mice. The increased diversity of the viral population in obese mice correlated with a decrease in responses to type I interferon, and treatment of obese rodents with recombinant interferon reduced the diversity of the pathogen. In this regard, the authors suggest that such delayed antiviral responses, manifested in obesity, may contribute to the emergence of a more virulent population of the influenza pathogen.
In the future, the researchers plan to study how similar processes occur in humans at the population level. "Do we see this increase in viral diversity in obese people in what they secrete? Is obesity one of the reasons that we now see so much viral drift every season (changes in viral antigens due to mutations during replication – ed.), and why we should constantly update our vaccines?" – says the main author of the work, Dr. Stacy Schultz-Cherry. Researchers will also analyze what is happening in humans at the cellular level in order to influence the pathogen itself and advance the creation of vaccines and possible drugs for therapy.
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