Recombinant M. Tuberculosis Moex antigen

Introduction: The novel coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is responsible for the coronavirus disease 2019 (COVID-19). First COVID-19 case was detected in March, 10, 2020 in Turkey and as of May, 18, 2020 148,067 cases have been identified and 4096 citizens have died. Tuberculosis (TB) is a worldwide public health concern, incidence of tuberculosis (per 100,000 people) in Turkey was reported at 14, 1 in 2018. During pandemic COVID-19 was the main concern in every clinic and as we discuss here overlapping respiratory diseases may result in delaying of the diagnosis and treatment. Methodology: There were 4605 respiratory samples examined between March 23 and May 18 for COVID-19 and 185 samples for Mycobacterium tuberculosis in our laboratory. The Xpert Ultra assay was performed for the diagnosis of pulmonary tuberculosis; SARS-CoV-2 RNA was determined by real-time PCR (RT-PCR) analysis in combined nasopharyngeal and deep oropharyngeal swabs of suspected cases of COVID-19. Results: Both of SARS-CoV-2 and M. tuberculosis tests were requested on the clinical and radiological grounds in 30 patients. Here we discussed 2 patients who were both COVID-19 and TB positive. One patient already diagnosed with tuberculosis become COVID-19 positive during hospitalization and another patient suspected and treated for COVID-19 received the final diagnosis of pulmonary TB and Human Immunodeficiency Virus infection. Conclusions: We want to emphasize that while considering COVID-19 primarily during these pandemic days, we should not forget one of the "great imitators", tuberculosis within differential diagnoses.

Apoptotic and inflammatory pathways play important roles in Mycobacterium tuberculosis-infected macrophages. Sirt1 is a member of the deacetylase family that is known to promote apoptosis resistance in mammalian cells and was recently reported to regulate mycobacterial immunopathogenesis via inflammatory responses. However, the apoptotic role of Sirt1 in the process of M. tuberculosis infection remains unclear. With the help of mouse peritoneal macrophage samples, we have shown that resveratrol, a Sirt1 activator, inhibited M. tuberculosisinduced apoptosis in peritoneal macrophages. Further, we found that Sirt1 activation prompted M. tuberculosis induced GSK3 beta phosphorylation. Further investigation into the possible mechanisms of action showed that Sirt1 directly interacted with GSK3 beta and enhanced GSK3 beta phosphorylation by promoting its deacetylation. Sirt1 activation inhibited M. tuberculosis growth. Thus, it seemed that Sirt1 acted as a novel regulator of apoptosis signaling in M. tuberculosis infection via its direct effects on GSK3 beta. Sirt1 may therefore be a new candidate for the prevention and treatment of tuberculosis.