Mycobacterium tuberculosis may induce resistance to secondary SARS-CoV-2 infection

NewsGuard 100/100 Score

A team of United States-based scientists recently conducted a study to evaluate the effect of Mycobacterium tuberculosis infection on the pathogenesis of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.

The findings of this study, which is published on the preprint server bioRxiv*, reveal that mice infected with Mycobacterium tuberculosis are resistant to SARS-CoV-2 infection. This resistance is induced by expansion of T- and B-cell subsets in the lungs upon secondary viral challenge.

Study: Mice infected with Mycobacterium tuberculosis are resistant to secondary infection with SARS-CoV-2. Image Credit: Kateryna Kon / Shutterstock.com

This news article was a review of a preliminary scientific report that had not undergone peer-review at the time of publication. Since its initial publication, the scientific report has now been peer reviewed and accepted for publication in a Scientific Journal. Links to the preliminary and peer-reviewed reports are available in the Sources section at the bottom of this article. View Sources

Background              

Mycobacterium tuberculosis is a pathogenic bacterium belonging to the family Mycobacteriaceae. Like SARS-CoV-2, the causative pathogen of coronavirus disease 2019 (COVID-19), Mycobacterium tuberculosis causes severe and often fatal lung infection called tuberculosis.

Both tuberculosis and COVID-19 are associated with high mortality rates in humans. Interestingly, there is evidence suggesting that the mortality rate of COVID-19 is relatively low in countries where tuberculosis is prevalent.

In the current study, the scientists investigate the clinical consequences of mycobacterium tuberculosis and SARS-CoV-2 co-infection in mice.

About the study

The scientists developed two mouse models of COVID-19 using mice that were chronically infected with Mycobacterium tuberculosis. To this end, human angiotensin-converting enzyme 2 (ACE-2)-expressing mice were infected with low-dose mycobacterium tuberculosis via aerosol-based delivery.

After 30 days, secondary SARS-CoV-2 infection was induced in these mice through the intranasal route. The researchers subsequently assessed the clinical consequences of co-infection at days 4, 7, and 14 post-viral challenge. The controls in this study were mice infected with either Mycobacterium tuberculosis or SARS-CoV-2.

Clinical consequences of co-infection

The highest reduction in body weight was observed in mice infected with only SARS-CoV-2. Interestingly, co-infected mice did not show any significant body weight loss and were comparable to mice infected with only Mycobacterium tuberculosis.

A significantly lower lung viral load was observed in co-infected mice compared to SARS-CoV-2-infected mice. Moreover, no change in the growth of Mycobacterium tuberculosis was observed in the lungs, liver, and spleen after the viral challenge.  

Immune response to co-infection

The challenge of mice with SARS-CoV-2 caused a significant increase in the levels of proinflammatory mediators including interferon g (IFN-g), interleukin-6 (IL-6) and IL-1b. Mice infected with Mycobacterium tuberculosis only exhibited even higher levels of inflammatory mediators in the lungs.

Importantly, the levels remained unchanged upon challenge with SARS-CoV-2. The resistance of Mycobacterium tuberculosis-infected mice to SARS-CoV-2 was not associated with an elevated expression of anti-inflammatory mediators.  

Regarding histopathological changes, SARS-CoV-2-infected mice showed significant levels of alveolar necrosis and infiltration of proinflammatory mediators. A significantly higher level of pneumonia and hyaline membrane formation was observed in the lungs of SARS-CoV-2-infected mice. However, these changes were not seen in the lungs of co-infected mice.

The viral resistance due to Mycobacterium tuberculosis infection observed in ACE-2-expressing mice was also observed in mice infected with mouse-adapted SARS-CoV-2. Immune cells isolated from the lungs of mice infected with mouse-adapted SARS-CoV-2, Mycobacterium tuberculosis, or both were subjected to single-cell ribonucleic acid (RNA) sequencing to determine the mechanism of Mycobacterium tuberculosis-induced viral resistance.

The findings of RNA sequencing revealed that the immune environment in the lungs of co-infected mice was similar to that observed in the lungs of Mycobacterium tuberculosis-infected mice, with the exception of expanded B-cell and T-cell subsets.

Study significance

The current study reveals that mice infected with Mycobacterium tuberculosis are resistant to secondary SARS-CoV-2 infection and COVID-19-related pathologies. To this end, the Mycobacterium tuberculosis infection appears to create an inflammatory microenvironment in the lungs, which is unfavorable for SARS-CoV-2 propagation.

The presence of a wide variety of innate immune cells due to Mycobacterium tuberculosis infection may prevent SARS-CoV-2 infection. In addition, Mycobacterium tuberculosis-induced adaptive immune response may cross-react with viral antigen to induce resistance. The expansion of B-cell and T-cell subsets after the SARS-CoV-2 challenge supports the explanation of Mycobacterium tuberculosis-induced SARS-CoV-2 resistance.

This news article was a review of a preliminary scientific report that had not undergone peer-review at the time of publication. Since its initial publication, the scientific report has now been peer reviewed and accepted for publication in a Scientific Journal. Links to the preliminary and peer-reviewed reports are available in the Sources section at the bottom of this article. View Sources

Journal references:

Article Revisions

  • Apr 28 2023 - The preprint preliminary research paper that this article was based upon was accepted for publication in a peer-reviewed Scientific Journal. This article was edited accordingly to include a link to the final peer-reviewed paper, now shown in the sources section.
Dr. Sanchari Sinha Dutta

Written by

Dr. Sanchari Sinha Dutta

Dr. Sanchari Sinha Dutta is a science communicator who believes in spreading the power of science in every corner of the world. She has a Bachelor of Science (B.Sc.) degree and a Master's of Science (M.Sc.) in biology and human physiology. Following her Master's degree, Sanchari went on to study a Ph.D. in human physiology. She has authored more than 10 original research articles, all of which have been published in world renowned international journals.

Citations

Please use one of the following formats to cite this article in your essay, paper or report:

  • APA

    Dutta, Sanchari Sinha Dutta. (2023, April 28). Mycobacterium tuberculosis may induce resistance to secondary SARS-CoV-2 infection. News-Medical. Retrieved on May 28, 2024 from https://www.news-medical.net/news/20211114/Mycobacterium-tuberculosis-may-induce-resistance-to-secondary-SARS-CoV-2-infection.aspx.

  • MLA

    Dutta, Sanchari Sinha Dutta. "Mycobacterium tuberculosis may induce resistance to secondary SARS-CoV-2 infection". News-Medical. 28 May 2024. <https://www.news-medical.net/news/20211114/Mycobacterium-tuberculosis-may-induce-resistance-to-secondary-SARS-CoV-2-infection.aspx>.

  • Chicago

    Dutta, Sanchari Sinha Dutta. "Mycobacterium tuberculosis may induce resistance to secondary SARS-CoV-2 infection". News-Medical. https://www.news-medical.net/news/20211114/Mycobacterium-tuberculosis-may-induce-resistance-to-secondary-SARS-CoV-2-infection.aspx. (accessed May 28, 2024).

  • Harvard

    Dutta, Sanchari Sinha Dutta. 2023. Mycobacterium tuberculosis may induce resistance to secondary SARS-CoV-2 infection. News-Medical, viewed 28 May 2024, https://www.news-medical.net/news/20211114/Mycobacterium-tuberculosis-may-induce-resistance-to-secondary-SARS-CoV-2-infection.aspx.

Comments

The opinions expressed here are the views of the writer and do not necessarily reflect the views and opinions of News Medical.
Post a new comment
Post

While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. We do not provide medical advice, if you search for medical information you must always consult a medical professional before acting on any information provided.

Your questions, but not your email details will be shared with OpenAI and retained for 30 days in accordance with their privacy principles.

Please do not ask questions that use sensitive or confidential information.

Read the full Terms & Conditions.

You might also like...
COVID-19 survivors show lasting brain function alterations, fMRI study finds