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Study: Tuberculosis takes tricky advantage of antiviral response

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According to UC researchers, the medling bacterial interloper may be something of an opportunist, gaining access as body defenses are distracted, and employing immune-response trickery to multiply while masquerading as a virus.

A new study discovered that when a person is infected with certain severe forms of  leprosy or tuberculosis, the immune response is "to produce lots of interferon-beta, a virus-destroying protein. There's just one problem. Those diseases are bacteria, not viruses," notes io9.

Researchers at the University of California Los Angeles first discovered this unusual property while studying leprosy. Patients whose immune systems were dealing with a milder form of the disease produced interferon-gamma, which is the correct protein to ward off bacterial infections. But when the leprosy was more severe, interferon-beta became more prominent.

Not only is this antiviral protein useless in fighting off bacterial infection, it also can jam the proper working of interferon-gamma, meaning the bacteria has free rein to spread and multiply within the body.

In the original publication last month in Science, researchers say the "inverse correlation" findings suggests  "the differential production of IFNs contributes to protection versus pathogenesis in some human bacterial infections."

Production of the appropriate protein to combat bacteria — interferon-gamma — may be disrupted by the production of the other protein, leaving the body vulnerable for TB to traipse in.

The BBC says the findings may explain why viruses can make people more susceptible to bacterial infections, and offers a possible explanation for spring spikes in tuberculosis infections that follow a winter wash of viruses.

Prof Robert Modlin, a dermatology and microbiology expert at the UCLA said the study results may also help to explain outbreaks among, say, homeless populations in Los Angeles.

A potent combination of people sleeping in close quarters in shelters, flu outbreaks diverting the body's immune response to the viral setting and a lack of vitamin D from sunlight, which also impacts the immune response, may be to blame, they suggested.