Molecular and Cellular Mechanisms of M. tuberculosis and SARS-CoV-2 Infections-Unexpected Similarities of Pathogenesis and What to Expect from Co-Infection.

Anna A Starshinova,Piotr Yablonskiy,Vadim Karev,Anna Malkova,Ulia Zinchenko,Angela Glushkova,Irina Dovgalyk,Igor Kudryavtsev,Anastasiya Y Starshinova,Raquel Villar-Hernández,Dmitry Kudlay,Jose Dominguez

doi:10.3390/ijms23042235

Abstract

Tuberculosis is still an important medical and social problem. In recent years, great strides have been made in the fight against M. tuberculosis, especially in the Russian Federation. However, the emergence of a new coronavirus infection (COVID-19) has led to the long-term isolation of the population on the one hand and to the relevance of using personal protective equipment on the other. Our knowledge regarding SARS-CoV-2-induced inflammation and tissue destruction is rapidly expanding, while our understanding of the pathology of human pulmonary tuberculosis gained through more the 100 years of research is still limited. This paper reviews the main molecular and cellular differences and similarities caused by M. tuberculosis and SARS-CoV-2 infections, as well as their critical immunological and pathomorphological features. Immune suppression caused by the SARS-CoV-2 virus may result in certain difficulties in the diagnosis and treatment of tuberculosis. Furthermore, long-term lymphopenia, hyperinflammation, lung tissue injury and imbalance in CD4+ T cell subsets associated with COVID-19 could propagate M. tuberculosis infection and disease progression.

Highlights

Tuberculosis is still an important medical and social problem in many countries of the world [1,2]
An analysis of circulating Th17 cell subsets in COVID-19 revealed a decrease in the proportion of Th17.1 cells, which are capable of producing IFNγ [55], these results are not confirmed by publications of other authors, who found no significant differences in the content of these cells relative to the control group but did report an accumulation of “atypical” Th1 cells that had surface markers more characteristic of Th17, such as CD161 and IL-1RI, in the peripheral blood of severely ill patients with pneumonia [51].Our analysis had shown that the relative number of CCR6+ Th17 cells was decreased within central and effector memory Th cells only in blood samples from patients with severe COVID-19 [46]
A comprehensive analysis and modeling of the effects that the consequences of the COVID-19 pandemic have on the course of tuberculosis, HIV infection and malaria was carried out in one of the most significant publications [18], showing factors influencing the aggravation of the epidemic situation for all diseases being evaluated

Summary

Introduction

Tuberculosis is still an important medical and social problem in many countries of the world [1,2]. Tuberculosis mortality rates increased from 1.1 million in 2010 to a maximum of 1.5 million in 2013 and decreased steadily to 1.3 million in 2020, when most tuberculosis cases were reported in South East Asia (44%) and South Africa (24%), and were three times less in the countries of the eastern Mediterranean (8%), European (3%) and American regions [4]. In 2019, 50% of all MRD-TB and extensively drug-resistant tuberculosis (XDR-TB) cases were reported in India (27%), China (14%) and Eastern European countries (9%) [2]. The WHO reports that millions of people around the world became infected with COVID-19 and millions of patients had died by December 2021 (https://who.sprinklr.com/, accessed on 27 December 2021). It is necessary to expand this strategy by including vaccination against COVID-19 and tuberculosis, taking into account the influx of infected immigrants, re-infection with exogenous tuberculosis and re-infection with COVID-19 after recovery [13]

Tuberculosis Diagnosis in the COVID-19 Pandemic

Findings

Conclusions