Lung Inflammation Signature in Post-COVID-19 TB Patients.

Tuberculosis (TB) remains a leading cause of infectious disease mortality worldwide, despite the COVID-19 pandemic. The mechanisms by which SARS-CoV-2 affects tuberculosis progression have not yet been established. Here, we compared the level of inflammation in the wall of the tuberculoma and in the parenchymal lung tissue of 30 patients diagnosed with tuberculoma without a history of COVID-19 and 30 patients diagnosed with tuberculoma 3 months after COVID-19. We also characterized TB activity in these patients using a panel of TB-associated miRNAs. Histopathological changes were examined in the resection material, and the expression level of cytokine/chemokine genes was determined by qRT-PCR. In patients with a history of COVID-19, the histological data obtained suggested activation of tuberculosis. In the same group of patients, as opposed to those without a history of COVID-19, equally high levels of pro-inflammatory cytokines/chemokines were expressed both in the tuberculoma wall and in the periphery of the resected specimen. A full set of miRNAs (miR-191, miR-193a, miR-222, miR-223, miR-155, miR-26a, and miR-150) were downregulated in the sera of patients with TB and active COVID-19 co-infection compared to controls. Our observations indicate signs of tuberculosis activation resulting from COVID-19 infection.

Morphologically, immunohistochemically and PCR proven lymphocytic viral peri-, endo-, myocarditis in patients with fatal COVID-19.

BACKGROUND: Despite a reported cardiac injury in patients with new coronavirus infection, the possibility and specifics of genuine viral myocarditis in COVID-19 remains not fully clear. PURPOSE: To study the presence of SARS-CoV-2 in the myocardium and the morphological properties of myocarditis in patients with severe coronavirus infection (COVID-19). METHODS: Autopsy data of eight elderly patients (75.6 ± 7.4 years), four male and four female, with severe new coronavirus infection were studied. The lifetime diagnosis of COVID-19 is based on a positive result of the PCR study. The inclusion criterion was the presence of morphological signs of myocarditis according to the Dallas criteria. A standard histological examination included staining by hematoxylin and eosin, toluidin blue and Van Gieson. An immunohistochemical study was performed using antibodies to CD3, CD 68, CD20, perforin, toll-like receptor (TLR) types 4 and 9. PCR in real-time was performed to determine the viral RNA in the myocardium. RESULTS: All patients had severe bilateral viral pneumonia. In all cases, myocarditis was not clinically diagnosed. Morphological examination of the heart found signs of active lymphocytic myocarditis. PCR identified the SARS-Cov2 RNA in all cases. There were also signs of destructive coronaritis in all cases, thrombovasculitis, lymphocytic pericarditis (in 3 cases) and endocarditis (in 2 cases). The absence of neutrophils confirms the aseptic nature of inflammation. An immunohistochemical study showed the CD3-positive T lymphocytes in the infiltrates. Increased expression of TLR type 4 and less 9 was also detected. CONCLUSION: Morphological and immunohistochemical evidence of myocarditis in COVID-19 was presented. Lymphocytic infiltrations and positive PCR confirm the viral nature of inflammation. Myocarditis in COVID-19 is also characterized by coronaritis with microvascular thrombosis and associated with lymphocytic endo- and pericarditis.