A winter outbreak of tuberculosis (TB) in Los Angeles’ skid row may have exposed up to 4,500 individuals to the bacterium that causes the deadly disease. The outbreak occurred at a time when homeless individuals are driven to crowded shelters, when influenza is peaking and when people’s vitamin D levels, typically boosted by sunlight exposure, are low.
In a new UCLA study, researchers, led by Robert L. Modlin, MD, chief of dermatology, demonstrate that certain bacteria can pretend to be viruses when infecting humans, allowing them to hijack the body’s immune response so that they can hide inside our cells. The findings may also help explain how viral infections like the flu make us more susceptible to subsequent bacterial infections such as pneumonia.
When bacteria pretend to be viruses, the immune system launches an attack with a protein, interferon-beta, that is designed to fight viruses and also blocks the action of interferon-gamma, to the advantage of bacteria. Further, if a real virus were to trigger interferon-beta, it would divert the attention of the immune response, preventing an attack on the bacterial invader. This may explain why flu can lead to a more serious bacteria-based infection like pneumonia.
The team examined the mechanisms by which interferon-beta protein suppresses the interferon-gamma defense response to bacterial infections. As a model, they studied leprosy, which is caused by a bacteria related to TB. The scientists first compared the genetic expression of the virus-fighting interferon-beta protein and the bacteria-fighting interferon-gamma protein in skin lesions from leprosy patients. They found that interferon-gamma was expressed in patients with the milder form of the disease and that interferon-beta was increased in those with the more serious, progressive form of leprosy. The researchers then compared the genes triggered by interferon-beta in these leprosy skin lesions with those found by two other groups of investigators in the blood of TB patients. There was a significant overlap; interferon-beta genes were more frequent in both the skin lesions of leprosy patients with extensive disease and in the blood of TB patients with more severe disease.
The new findings may indicate why, in winter, residents of skid row are at added risk for TB. Because of colder nighttime temperatures, indigent homeless people tend to stay in shelters, where they live closely with others, facilitating the spread of influenza. The body’s immune system could then be diverted by the flu virus to produce interferon-beta, blocking an effective immune response to the TB bacteria. And the drop in vitamin D levels due to decreased sunlight during winter months could further diminish the ability of individuals’ immune systems to kill the TB bacteria.
“Type I Interferon Suppresses Type II Interferon-Triggered Human Anti-Mycobacterial Responses,” Science, March 22, 2013