SARS-CoV-2 can infiltrate the lower respiratory tract, resulting in severe respiratory failure and a high death rate. Normally, the airway and alveolar epithelium can be rapidly reconstituted by multipotent stem cells after episodes of infection. Here, we analyzed published RNA-seq datasets and demonstrated that cells of four different lung epithelial stem cell types express SARS-CoV-2 entry factors, including Ace2. Thus, stem cells can be potentially infected by SARS-CoV-2, which may lead to defects in regeneration capacity partially accounting for the severity of SARS-CoV-2 infection and its consequences.

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus that causes coronavirus disease 2019 , has led to an unprecedented public health emergency worldwide. While common cold symptoms are observed in mild cases, COVID-19 is accompanied by multiorgan failure in severe patients. Organ damage in COVID-19 patients is partially associated with the indirect effects of SARS-CoV-2 infection (e.g., systemic inflammation, hypoxic-ischemic damage, coagulopathy), but early processes in COVID-19 patients that trigger a chain of indirect effects are connected with the direct infection of cells by the virus. To understand the virus transmission routes and the reasons for the wide-spectrum of complications and severe outcomes of COVID-19, it is important to identify the cells targeted by SARS-CoV-2. This review summarizes the major steps of investigation and the most recent findings regarding SARS-CoV-2 cellular tropism and the possible connection between the early stages of infection and multiorgan failure in COVID-19. The SARS-CoV-2 pandemic is the first epidemic in which data extracted from single-cell RNA-seq (scRNA-seq) gene expression data sets have been widely used to predict cellular tropism. The analysis presented here indicates that the SARS-CoV-2 cellular tropism predictions are accurate enough for estimating the potential susceptibility of different cells to SARS-CoV-2 infection; however, it appears that not all susceptible cells may be infected in patients with COVID-19.

An increased frequency of B-cell lymphomas is observed in human immunodeficiency virus-1 (HIV-1)-infected patients, although HIV-1 does not infect B cells. Development of B-cell lymphomas may be potentially due to the action of the HIV-1 Tat protein, which is actively released from HIV-1-infected cells, on uninfected B cells. The exact mechanism of Tat-induced B-cell lymphomagenesis has not yet been precisely identified. Here, we ectopically expressed either Tat or its TatC22G mutant devoid of transactivation activity in the RPMI 8866 lymphoblastoid B cell line and performed a genome-wide analysis of host gene expression. Stable expression of both Tat and TatC22G led to substantial modifications of the host transcriptome, including pronounced changes in antiviral response and cell cycle pathways. We did not find any strong action of Tat on cell proliferation, but during prolonged culturing, Tat-expressing cells were displaced by non-expressing cells, indicating that Tat expression slightly inhibited cell growth. We also found an increased frequency of chromosome aberrations in cells expressing Tat. Thus, Tat can modify gene expression in cultured B cells, leading to subtle modifications in cellular growth and chromosome instability, which could promote lymphomagenesis over time.

SARS-CoV-2 can infiltrate the lower respiratory tract, resulting in severe respiratory failure and a high death rate. Normally, the airway and alveolar epithelium can be rapidly reconstituted by multipotent stem cells after episodes of infection. Here, we analyzed published RNA-seq datasets and demonstrated that cells of four different lung epithelial stem cell types express SARS-CoV-2 entry factors, including Ace2. Thus, stem cells can be infected by SARS-CoV-2, which can lead to defects in regeneration capacity and account for the severity of SARS-CoV-2 infection and its consequences.

Among land plants, genome sizes vary remarkably by > 2,200-fold. This variation depends on the loss and gain of non-coding DNA sequences, forming different heterochromatin complexes during interphase. In plants with a giant genome, the major part of chromatin stays condensed in interphase, forming a dense meshwork of heterochromatin threads, called interphase chromonemata. Using super-resolution light and electron microscopy, we studied the ultrastructure of chromonemata during and after replication in root meristem nuclei of Nigella damascena L. During S-phase, heterochromatin undergoes transient decompaction locally at the active sites of DNA synthesis, and due to the heterochromatin abundance, chromonema replication is accompanied by a robust chromonema meshwork disassembly, which led to the general reorganization of the nucleus morphology visible even by conventional light microscopy. After replication, the heterochromatin condenses again, restoring the chromonema structure. Thus, we showed that heterochromatin replication in interphase nuclei of giant-genome plants induces a global chromonema decondensation and reorganization.

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Pneumonia is an acute respiratory disease of varying aetiology, which drew much attention during the COVID-19 pandemic. Among many thoroughly studied aspects of pneumonia, lipid metabolism has been addressed insufficiently. Here, we report on abnormal lipid metabolism of both COVID-19- and non-COVID-19-associated pneumonias in human lungs. Morphometric analysis revealed extracellular and intracellular lipid depositions, most notably within vessels adjacent to inflamed regions, where they apparently interfere with the blood flow. Lipids were visualized on Sudan III- and Oil Red O-stained cryosections and on OsO4-contrasted semi-thin and ultrathin sections. Chromato-mass spectrometry revealed that unsaturated fatty acid content was elevated at inflammation sites compared with the intact sites of the same lung. The genes involved in lipid metabolism were downregulated in pneumonia, as shown by qPCR and in silico RNAseq analysis. Thus, pneumonias are associated with marked lipid abnormalities, and therefore lipid metabolism can be considered a target for new therapeutic strategies.