COVID-19 and tuberculosis (TB) top the list of infectious disease-related causes of death around the globe. But what is the effect of one of these respiratory infections on the other? A team of researchers asked that question, with a focus on the role of a tuberculosis infection, and it’s immune response, on a secondary infection with SARS-CoV-2.

The team used two mouse models of COVID-19, using mice that were chronically infected with Mycobacterium tuberculosis. In both model systems, the mice infected with tuberculosis were, they said, “resistant to the pathological consequences of secondary CoV2 infection, and CoV2 infection did not affect M. tuberculosis burdens.” The findings support the hypothesis that, in mice, the immune response mounted against tuberculosis prevents them from developing COVID-19.

The work is published in PLOS Pathogens in the article, “Mice infected with Mycobacterium tuberculosis are resistant to acute disease caused by secondary infection with SARS-CoV-2.

“TB and COVID are pandemics that affect every part of the world,” Richard Robinson, PhD, associate professor of microbial infection and immunity at the Ohio State University (OSU) noted. “Our study reflects the work of a diverse and talented group of OSU scientists to better understand how these two diseases influence one another, a surprising observation being that mice with TB are resistant to COVID in a lab setting.”

Currently, the bacterium that causes tuberculosis, M. tuberculosis, and the virus that causes COVID-19, SARS-CoV-2, are the leading causes of death from infectious disease worldwide.

Tuberculosis is widespread, and scientists have questioned whether the immune response triggered by this serious respiratory infection might protect people from developing COVID-19. To find out more, researchers worked with two different strains of mice and infected them with M. tuberculosis. Then they exposed the mice to SARS-CoV-2 and monitored them for signs of infection. They discovered that mice with tuberculosis showed no signs of COVID-19, likely because the pre-existing immune response to tuberculosis prevented the virus from proliferating in the lungs.

More specifically, single-cell RNA sequencing of coinfected and monoinfected lungs demonstrated the resistance of M. tuberculosis infected mice is associated with expansion of T- and B-cell subsets upon viral challenge.

The findings demonstrate that tuberculosis infection makes the lungs inhospitable to SARS-CoV-2 in mice. If the same is true for humans, this discovery may be one reason why there have been few reports of individuals with both TB and COVID-19 in the absence of other complications. The findings may also explain why countries tend to have high rates of infection of COVID-19 or TB, but not both. The researchers propose that future research should focus on the interaction between COVID-19 and TB infections in humans.


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