The SARS-CoV-2 virus, which produces COVID-19, may be capable of reactivating latent tuberculosis (TB). In new research published in The American Journal of Pathology, scientists discovered that infection with a particular coronavirus strain reactivated latent Mycobacterium tuberculosis (MTB) in mice. This insight might aid in developing new COVID-19 vaccines and avoiding a worldwide TB outbreak.
Stem Cells Can Be Helpful In Developing New Vaccines Against COVID-19
The COVID-19 pandemic produced by the SARS-CoV-2 virus illustrates an emerging virus’s capacity to harm large numbers of people while also straining and disrupting contemporary healthcare systems throughout the world. A substantial proportion of COVID-19-infected people have recovered. A putative host defense or antiviral mechanism against the virus, on the other hand, has yet to be found. Concerns have been raised that, in the long run, the virus may reactivate dormant bacterial diseases such as tuberculosis (TB) in select affected persons, even though TB is already prevalent in one-quarter of the world’s population.
Viral infections, such as the influenza virus or SARS-CoV-1, produce temporary immune suppression, resulting in the reactivation of latent bacterial infections. Patients with TB had the greatest death rate during the 1918 Spanish flu pandemic. Patients with TB or multidrug-resistant TB had a poorer prognosis than others during the 2009 influenza A (H1N1) pandemic.
To avoid a potential global TB pandemic, there is an urgent need to study the association of COVID-19 with dormant TB reactivation, according to lead investigator Bikul Das, MD, PhD, Department of Stem Cell and Infectious Diseases, KaviKrishna Laboratory, Guwahati Biotech Park, Indian Institute of Technology, Guwahati, India; and Department of Stem Cell and Infection, Thoreau Lab for Global Health. Understanding the host defensive mechanism against this disease is critical for developing a better vaccination and/or therapy.
As a result, they hypothesized that, like bacteria, adult stem cells could have an altruistic defensive mechanism to preserve their niche from external threats.
According to Bikul Das, proving altruism in mammalian cell biology is difficult because they encountered years of pushback from peers. Altruism is based on group selection, which is difficult to establish at the molecular level. However, the notion of altruism that they are discussing here is the philosophical perspective of Vedic Jiva Upakarvada (Vedic altruism), a component of Vedantic thinking that claims that amid stress, the living organism attains a higher condition known as Avatar.
The coronavirus strains murine hepatitis virus-1 (MHV-1) infection in the lung of a mouse model (dMtb) of mesenchymal stem cell (MSC)-mediated MTB dormancy was investigated. By the third week of viral infection, these mice had 20-fold lower viral loads than the dMtb-free control animals and a six-fold increase in altruistic stem cells (ASCs), boosting defense. Tuberculosis was reactivated in dMtb mice, suggesting that latent TB bacteria hijack these ASCs and multiply in the lung, causing pulmonary TB.
The findings indicate that these ASCs are transitory (they grow for two weeks before undergoing apoptosis or cellular death) and have antiviral activity against MHV-1 through secreting soluble substances.
These results are significant because they indicate a unique ASC defensive mechanism against mouse coronavirus infection, which might be utilized to create innovative COVID-19 treatment methods, Bikul Das said. The discovery of TB reactivation in a stem cell-mediated Mtb dormancy animal model after MHV-1 coronavirus infection suggests that the SARS-CoV-2 virus may activate latent bacterial illnesses in the long term, post-pandemic.
This is an important discovery in light of the current coronavirus pandemic, in which many people in India and other poor nations with latent tuberculosis may see an upsurge in active TB cases following COVID-19. The ASC-mediated defense mechanism might be used to produce vaccines against viral infections and avert a worldwide TB epidemic.