‘Wrong’ immune response aids TB
Some bacteria, including tuberculosis, may be able to invade since the body launches the ‘wrong’ immune response, say researchers.
Instead of fighting off tuberculosis, those with a severe infection produce a protein which attacks viruses, the journal Science reports.
About 8.7 million persons are infected with tuberculosis per annum.
The findings may explain why viruses could make people more prone to bacterial infections.
A spring peak in tuberculosis infections could be associated with the consequences of viruses circulating in winter, experts suggested.
US researchers first identified the phenomenon using leprosy – that is resulting from an analogous bacterium to tuberculosis.
Looking at skin lesions in leprosy patients, the team found that two different immune proteins were present.
In people with a milder sort of the disease, they discovered a protein linked to a bacterial immune response – interferon-gamma.
Whereas in patients with a more serious type of leprosy, a protein linked to a viral response – interferon-beta – was prominent.
Further work showed the genes for interferon-beta – the virus-fighting protein – were more frequently expressed within the blood of tuberculosis patients with more severe disease.
The researchers said in people with severe disease, the body was responding as though it was attacking an epidemic, enabling the bacteria to stay hidden and replicate unchallenged within cells.
Not only is interferon-beta an ineffective weapon against bacteria, it may block the action of interferon gamma – that is when bacteria can gain a foothold, the researchers said.
In the face of a true viral infection it’s going to mean that the awareness of the immune system is diverted letting a bacterial infection in.
Prof Robert Modlin, a dermatology and microbiology expert on the University of California, La, said the study raises the chance that a decrease or increase of 1 of those two proteins could shift the balance from mild to more serious disease.
“We may find that therapeutic interventions to dam or enhance specific interferon responses could be a great method to alter the balance in favour of protection against bacterial diseases.”
The results might help to give an explanation for why outbreaks of tuberculosis in winter corresponding to one currently spreading among homeless groups in L. a. are quick to take hold.
A potent combination of individuals sleeping in close quarters in shelters, flu outbreaks diverting the body’s immune response to the viral setting and an absence of vitamin D from sunlight, which also impacts the immune response, is also accountable, they suggested.
“With TB at the rise, this scenario could play out not just in cities inside the United states of america but around the globe,” Prof Modlin said.
Prof Ajit Lalvani, director of the Tuberculosis Research Unit at Imperial College London said there’s a spring peak in rates of tuberculosis which were attributed to low levels of vitamin D.
“But this shows there may well be at the least an additional reason – that other viral infections are leading some months down the road to progression from latent to active TB disease.
“The timing fits, but that continues to be to be proven.”