'Wrong' immune response aids TB
Some bacteria, including tuberculosis, are able to invade because the body launches the 'wrong' immune response, say researchers.
Instead of fighting off tuberculosis, people with a severe infection produce a protein which attacks viruses, the journal Science reports.
About 8.7 million people are infected with tuberculosis every year.
The findings may explain why viruses can make people more susceptible to bacterial infections.
A spring peak in tuberculosis infections may be linked to the effects of viruses circulating in winter, experts suggested.
US researchers first identified the phenomenon using leprosy - which is caused by a similar bacterium to tuberculosis.
Looking at skin lesions in leprosy patients, the team found that two different immune proteins were present.
In those with a milder form of the disease, they found a protein associated with a bacterial immune response - interferon-gamma.
Whereas in patients with a more serious form of leprosy, a protein associated with a viral response - interferon-beta - was prominent.
Further work showed the genes for interferon-beta - the virus-fighting protein - were more frequently expressed in the blood of tuberculosis patients with more severe disease.
The researchers said in those with severe disease, the body was responding as if it was attacking a virus, enabling the bacteria to remain hidden and replicate unchallenged within cells.
Not only is interferon-beta an ineffective weapon against bacteria, it can block the action of interferon gamma - which is when bacteria can gain a foothold, the researchers said.
In the face of a real viral infection it may mean that the attention of the immune system is diverted letting a bacterial infection in.
Prof Robert Modlin, a dermatology and microbiology expert at the University of California, Los Angeles, said the study raises the possibility that a decrease or increase of one of these two proteins could shift the balance from mild to more serious disease.
"We may find that therapeutic interventions to block or enhance specific interferon responses may be an effective strategy to alter the balance in favour of protection against bacterial diseases."
The results may also help to explain why outbreaks of tuberculosis in winter such as one currently spreading among homeless groups in Los Angeles are quick to take hold.
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.
"With TB on the rise, this scenario could play out not only in cities in the United States but all over the world," Prof Modlin said.
Prof Ajit Lalvani, director of the Tuberculosis Research Unit at Imperial College London said there is a spring peak in rates of tuberculosis which have been attributed to low levels of vitamin D.
"But this shows there could be at least one other reason - that other viral infections are leading some months down the line to progression from latent to active TB disease.
"The timing fits, but that remains to be proven."