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Study reveals COVID-19 could activate TB and other dormant bacterial infections

Many viruses, including SARS-CoV-2, cause a temporary immunosuppressive effect, which causes dormant bacterial infections to come back to life.

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Researchers have found that the SARS-CoV-2 virus that causes COVID-19 may have the ability to reactivate dormant tuberculosis (TB). The study has been conducted by researchers from the Indian Institute of Technology, Guwahati, and the University of Massachusetts.

Many viruses, including SARS-CoV-2, cause a temporary immunosuppressive effect, which causes dormant bacterial infections to come back to life. 

The concerned study showed that infection with a specific coronavirus strain reactivated dormant Mycobacterium tuberculosis (MTB) in mice. If this proves true for human beings too then it is indeed alarming news for countries like India, which accounts for an estimated 40% of the population with dormant or latent TB. 

The results, detailed in The American Journal of Pathology, may pave the way for new vaccines against infectious disease and avoid a potential global TB epidemic.

Earlier, a study conducted in May 2020 also suggested that the long-term impact of the virus could include the activation of dormant bacterial infections like tuberculosis (TB).

According to the World Health Organization (WHO), dormant TB already affects a quarter of the world's population. If the novel coronavirus activates a sizable proportion of these dormant infections, it could severely upset the global health and economic situation.

What study showed

Researchers studied the coronavirus strain murine hepatitis virus-1 (MHV-1) infection in the lung in a mouse model (dMtb) of mesenchymal stem cell (MSC)-mediated MTB dormancy.

This showed 20-fold lower viral loads than the dMtb-free control mice by the third week of viral infection and a six-fold increase of altruistic stem cells (ASCs), thereby enhancing the defense.

TB was reactivated in the dMtb mice, suggesting that dormant TB bacteria hijack these ASCs to replicate in the lung to cause pulmonary TB.

Results suggest that these ASCs are transient and exhibit antiviral activities against MHV-1 by secreting soluble factors.

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