COVID19 coinfection exacerbates lung inflammation in TB patients

<bold>Introduction:</bold> TB and COVID19 are the two leading causes of mortality among infectious diseases. There is an increasing number of studies trying to elucidate the interactions between <italic>M. tuberculosis</italic> and SARS-CoV2. The mechanism of COVID19 effect on TB progression is not clear. miRs might be involved in the outcome of TB and COVID19, since early work has implicated miRs as regulators of the immune response. <bold>Aim:</bold> Here we investigated expression of miRs in serum of post primary TB patients (with or without COVID19 coinfections) in order to determine markers of TB progression. <bold>Methods:</bold> Serum samples were collected from 30 patients with post primary TB, 20 patients TB-COVID19 (during/after coinfection) and 30 healthy donors. RNA was extracted with TRIzol LS. Pools within each group were analyzed by miScript miRNA PCR Array. Array results were confirmed by TaqMan Assay. miRs expression data were correlated with histopathology of lung tissue. <bold>Results:</bold> Previously we described a set of 5 miRs (miR-155, miR-222, miR-223, miR-191, miR-26a) that could be used to distinguish fibrotic cavitary TB from tuberculoma and also could serve as a biomarker of inflammation activity in TB patients. Co-infection of tuberculoma patients with COVID19 led to a shift in the expression of the miRs set towards FCT pattern. This is in line with histopathology data, when increased inflammation was registered in TB-COVID19 patients as compared with TB patients. <bold>Conclusions:</bold> Our data confirmed the hypothesis of TB inflammation progression in TB-COVID coinfection. We demonstrated significant changes of miRs levels in patients with various forms of active TB-COVID coinfection. These changes involved miRs from inflammatory and the fibrotic pathways.