Introduction. Coronaviruses (CoVs) are positive-strand RNA viruses with the largest genome among all RNA viruses. They are able to infect many host, such as mammals or birds. Whereas CoVs were identified 1930s, they became known again in 2003 as the agents of the Severe Acute Respiratory Syndrome (SARS). The spike protein is thought to be essential in the process of CoVs entry, because it is associated with the binding to the receptor on the host cell. It is also involved in cell tropism and pathogenesis. Receptor recognition is the crucial step in the infection. CoVs are able to bind a variety of receptors, although the selection of receptor remains unclear. Coronaviruses were initially believed to enter cells by fusion with the plasma membrane. Further studies demonstrated that many of them involve endocytosis through clathrin-dependent, caveolae-dependent, clathrin-independent, as well as caveolae-independent mechanisms. Objectives. The aim of this review is to summarise current knowledge about coronaviruses, focussing especially on CoVs entry into the host cell. Advances in understanding coronaviruses replication strategy and the functioning of the replicative structures are also highlighted. The development of host-directed antiviral therapy seems to be a promising way to treat infections with SARS-CoV or other pathogenic coronaviruses. There is still much to be discovered in the inventory of proand anti-viral host factors relevant for CoVs replication. The latest pandemic danger, originating from China, has given our previously prepared work even more of topicality.

This study aimed to assess the efficacy and safety of the approved in our Hospital thromboprophylaxis algorithm. Thrombotic events, with higher than usual occurrence, are commonly reported in COVID-19 patients. Until now limited data exist to guide the intensity of antithrombotic prophylaxis. We declare that the risk of arterial and venous thromboembolic events in COVID-19, according to our protocol, can be reduced by more carful optimalization of low molecular heparin administration with a good safety profile.

INTRODUCTION    Interleukin 27 (IL‑27) is a cytokine secreted mostly by antigen‑presenting cells. It is important for the immune polarization of T helper‑1 (Th1) cells, and its role in interstitial lung diseases (ILDs) and lung cancer has been investigated. OBJECTIVES    We assessed IL‑27 expression in the lower airways of patients with selected ILDs and early‑stage non-small cell lung cancer (NSCLC). PATIENTS AND METHODS    IL‑27 concentrations were examined by an enzyme‑linked immunosorbent assay in bronchoalveolar lavage (BAL) fluid supernatants collected from patients with pulmonary sarcoidosis (PS; n = 30), extrinsic allergic alveolitis (EAA; n = 14), idiopathic pulmonary fibrosis (IPF; n = 12), nonspecific interstitial pneumonia (NSIP; n = 14), and NSCLC stages I to IIa (n = 16) with peripheral localization, and in controls (n = 14). The major lymphocyte subsets in BAL fluid were phenotyped, and intracellular IL‑27 expression was evaluated by flow cytometry.  RESULTS    IL‑27 concentrations in BAL fluid supernatants were significantly increased in Th1‑mediated conditions such as EAA and PS, but not in IPF or NSIP. The highest IL‑27 levels (median [SEM], 16.9 [17.5] pg/ml) were reported for NCSLC, and the lowest-for controls (median [SEM], 0.4 [0.2] pg/ml). IL‑27 was undetectable in corticosteroid‑treated patients with PS. Both CD4+ and CD8+ lymphocytes were positive for IL‑27; they were a possible local source of IL‑27 because the cytokine levels were positivelysignificantly correlated with the total number of lymphocytes, including CD4+ cells. CONCLUSIONS    Our results support the Th1‑linked activity of IL‑27in ILDs. Early‑stageNSCLC is characterizedby high IL‑27expression in the lower airways. IL‑27 is produced by a high percentage of CD4+ and CD8+ cells in BAL fluid, both in patients and controls.

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biotherapy -induced sarcoidosis) in the lungs. 8 However, to our knowledge, the actual expression of both types of checkpoints in patients with lung granulomatous disease has not been fully established.A particularly useful method for the examination of interstitial lung diseases in situ is bronchoalveolar lavage (BAL). This technique facilitates diagnosis and helps to assess the local cellular reaction as well as the release of inflammatory mediators. 9 We aimed to determine the expression of ICPs on bronchoalveolar lavage lymphocytes in HP and sarcoidosis, in association with immunological and clinical data. Patients and methodsWe enrolled patients suspected to have interstitial lung diseases. In the diagnostic procedure we followed the European Respiratory Society guidelines; details were described previously. 4 The exclusion criteria comprised: 1) treatment with systemic corticosteroids, methotrexate, azathioprine, biological drugs (eg, infliximab for sarcoidosis), or any other medication known to potentially cause interstitial lung pathology or influence the cytoimmunological BAL profile 8 2) respiratory failure, heart failure (New York Heart Association class IV), or acute coronary syndromes; 3) poor technical quality of the BAL material (eg, BAL fluid recovery <30% of instilled volume, percentage of contaminating epithelial cells >3% of BAL cells). 9 Hypersensitivity pneumonitis (n = 14) was diagnosed on the basis of clinical data, including typical symptomatology following allergen

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