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 pro- and 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.

Background: It has yet to be determined whether the immunocytological profile of the bronchoalveolar lavage (BAL) in respiratory post-COVID syndrome (PCS) reflects the risk of persistent interstitial lung disease (ILD), including pulmonary fibrosis. In this study, we aimed to assess the prognostic value of the BAL cytoimmunologic profile in PCS-related ILD. Materials and Methods: We enrolled 58 non-smoking patients with a history of COVID-19 and new-onset ILD, divided into PCS remission and PCS persistence groups based on clinical data, including repeated computed tomography and pulmonary function tests. We phenotyped BAL major T cell subsets, immune checkpoints (including programmed cell death-1, PD1), and markers of Th1/Th2/Th17 polarization. Results: The PCS groups compared to the control showed increased total cell, lymphocyte, and neutrophil counts and a high BAL neutrophil:lymphocyte ratio (NLR). PCS persistence compared to the controls presented an increased neutrophil count (26 [17–36] vs. 2.6 [1.9–5.4] 103/mL, median [Q1–Q3], p < 0.001) and percentage, BAL NLR (0.77 [0.26–1.63] vs. 0.21 [0.17–0.31], p < 0.0001), CD8+PD1+ cell percentage (43.5 [34–60.5] vs. 24.5 [22–44]%, p = 0.045), and a decreased CD4:CD8 ratio. A high percentage of CD4+CD196+CD183 cells (relevant to Th17 activity, 6.2 [2.0–9.4] vs. 1.2 [0.7–2.7]%, p = 0.02) and increased BAL supernatant elevated IL-8 levels (62.5 [16–243] vs. 10.9 [3.44–32] pg/mL, p = 0.002) were found in the PCS persistence vs. control groups. In the total PCS group, predicted values of Vital Capacity (VC) [16–243] and Diffusing Lung Capacity for CO (DLCO) correlated negatively with BAL NLR; VC correlated negatively with BAL CD8+PD1+; and DLCO correlated positively with the CD4:CD8 ratio. Conclusions: Worse prognosis in PCS is associated with higher BAL NLR, BAL neutrophilia, an elevated percentage of CD8+PD1+ lymphocytes, and a decline in the CD4:CD8 ratio. Th17 cells and IL-8 participate in lung PCS persistence.

Introduction and objective: Obesity is a global civilization disease driven by a positive caloric balance. It leads to severe comorbidities across all organ systems and increases mortality. Current treatment options, including lifestyle changes, surgery, and registered pharmacotherapy (e.g.,...

Background. It has yet to be determined whether the immunocytological profile of the bronchoalveolar lavage (BAL) in respiratory post-COVID syndrome (PCS) may reflect the risk of persistent interstitial lung disease (ILD), including pulmonary fibrosis. We aimed to assess the prognostic value of BAL cytoimmunologic profile in PCS-related ILD. Material & Methods. We enrolled 58 non-smoking patients with COVID-19 history, having new-onset ILD, divided into PCS remission and PCS persistence groups, based on clinical data including repeated computed tomography and pulmonary function tests. We phenotyped BAL major T cell subsets, immune checkpoints (including programmed cell death-1, PD1) and markers of Th1/Th2/Th17 polarization. Results. PCS compared to controls showed increased total cell, lymphocyte and neutrophil count and high BAL neutrophil:lymphocyte ratio (NLR). PCS persistence compared to controls presented increased neutrophil count (26[17-36] vs. 2.6[1.9-5.4] 10³/ml, median[Q1-Q3], p<0.001 ) and percentage, BAL NLR (0.77[0.26-1.63] vs. 0.21[0.17-0.31], p<0.0001) , CD8+PD1+ cell percentage (43.5 [34-60.5] vs. 24.5[22-44]%, p=0.045), decreased CD4:CD8 ratio. High percentage of CD4+CD196+CD183- cells (relevant to Th17 activity, 6.2[2.0-9.4] vs 1.2[0.7-2.7]%, p=0.02 ), and increased BAL supernatant elevated IL-8 levels (62.5[16-243] vs. 10.9[3.44-32]pg/mL, p=0.002) were found in PCS persistence vs. controls. In total PCS, predicted values of Vital Capacity (VC) and Diffusing Lung Capacity for CO (DLCO) correlated negatively with BAL NLR, VC correlated negatively with BAL CD8+PD1+; DLCO correlated positively with CD4:CD8 ratio. Conslusions. Worse prognosis in PCS is associated with higher BAL NLR, BAL neutrophilia, elevated percentage of CD8+PD1+ lymphocytes, decline in CD4:CD8 ratio. Th17 cells and IL-8 participate in lung PCS persistence.