Immune disorders in pulmonary tuberculosis and concomitant SARS-CoV-2 infection

Abstract

The study aimed to analyze immune-metabolic disorders and biomarkers of endogenous intoxication in patients with pulmonary tuberculosis (TB) caused by different Mycobacterium tuberculosisstrains, including multidrug-resistant TB (MDR-TB), and in cases with concomitant SARS-CoV-2 infection, to assess the impact of coinfection on immune–metabolic homeostasis and systemic inflammation. This prospective study included 191 newly diagnosed TB patients divided into four groups: drug-susceptible TB (n=80), primaryMDR-TB (n=40), acquired MDR-TB (n=49), and TB with SARS-CoV-2 coinfection (n=22). A control group comprised 36 conventionally healthy individuals. A more severe disease course was observed in patients with acquired MDR-TB and SARS-CoV-2 coinfection, associated with decreased CD3⁺, CD4⁺, CD16⁺, and CD8⁺ T lymphocytes. Circulating immune complexes, ESR, acute-phase proteins, and derived hematological indices were elevated in all groups, with the highest levels in coinfected patients. Pro-inflammatory cytokines (TNF-α, IL-6, IL-8) were significantly increased; TNF-αpeaked in acquired MDR-TB, while IL-6 and IL-8 were highest in coinfection. Early detection of MDR-TB and SARS-CoV-2 coinfection, combined with timely immunopathogenic interventions, is essential to modulate immune–metabolic disturbances and improve outcomes in severe TB.