The COVID-19 pandemic was officially announced in March 2020 and is still moving around the world. Virus strains, their pathogenicity and infectivity are changing, but the ability is fast to spread and harm people's health remained, despite the seasonality seasons and other circumstances. Most likely, humanity is doomed for a long time to coexistence with this emergent pathogen, since it is already circulating not only among the human population, but and among fauna, especially among wild animals in different regions of the planet. Thus, the range the virus has expanded, the material and conditions for its evolution are more than enough. The detection of SARS-CoV-2 in known infected fauna species is analyzed and possible spread and ongoing circulation of the virus in domestic and wild animals are discussed. One of the main focus of the article is the role of animal body temperature, its fluctuations and the presence of entry receptors in the susceptibility of different animal species to SARS-CoV-2 infection and virus spreading in possible new ecological niches. The possibility of long-term circulation of the pathogen among susceptible organisms is discussed.

Viral infection, particularly respiratory syncytial virus (RSV), causes inflammation in the bronchiolar airways (bronchial wall thickening, also known as bronchiolitis). This bronchial wall thickening is a common pathophysiological feature in RSV infection, but it causes more fatalities in infants than in children and adults. However, the molecular mechanism of RSV-induced bronchial wall thickening remains unknown, particularly in healthy adults. Using highly differentiated pseudostratified airway epithelium generated from primary human bronchial epithelial cells, we revealed RSV-infects primarily ciliated cells. The infected ciliated cells expanded substantially without compromising epithelial membrane integrity and ciliary functions and contributed to the increased height of the airway epithelium. Furthermore, we identified multiple factors, e.g., cytoskeletal (ARP2/3-complex-driven actin polymerization), immunological (IP10/CXCL10), and viral (NS2), contributing to RSV-induced uneven epithelium height increase in vitro. Thus, RSV-infected expanded cells contribute to a noncanonical inflammatory phenotype, which contributes to bronchial wall thickening in the airway, and is termed cytoskeletal inflammation.

Bacteriophages are viruses that exclusively infect bacteria which require local degradation of cell barriers. This degradation is accomplished by various lysins located mainly within the phage tail structure. In this paper we surveyed and analysed the genomes of 506 isolated bacteriophage and prophage infecting or harboured within the genomes of the medically important Enterococcus faecalis and faecium. We highlight and characterise the major features of the genomes of phage in the morphological groups podovirus, siphovirus and myovirus, and explore their categorisation according to the new ICTV classifications, with a focus on putative extracellular lysins chiefly within tail modules. Our analysis reveals a range of potential cell-wall targeting enzyme domains that are part of tail, tape measure or other predicted base structures of these phages or prophages. These largely fall into protein domains targeting pentapeptide or glycosidic linkages within peptidoglycan but also potentially the Extracellular Polysaccharide Antigen (EPA) and wall teichoic acids of these species (i.e., Pectinesterases and Phosphodiesterases). Notably, there is a great variety of domain architectures that reveal the diversity of evolutionary solutions to attack the Enterococcus cell wall. Despite this variety, most phage and prophage possess a putative endopeptidase (70%), reflecting the ubiquity of this cell surface barrier. We also identified a predicted lytic transglycosylase domain belonging to the glycosyl hydrolase (GH) family 23 and present exclusively within tape measure proteins. Our data also reveal distinct features of the genomes of podo-, sipho- and myo-type viruses that most likely relate to their size and complexity. Overall, we lay a foundation for expression of recombinant TAL proteins and engineering of enterococcal and other phage that will be invaluable for researchers in this field.

Cyanophages are known to influence the population dynamics and community structure of cyanobacteria and thus play an important role in biogeochemical cycles in aquatic ecosystems. In this study, a novel Synechococcus phage S-H9-2 infecting Synechococcus sp. WH 8102 was isolated from the coastal water of the Yellow Sea. Synechococcus phage S-H9-2 contains a 187,320 bp genome of double-stranded DNA with a G+C content of 40.3 %, 202 potential open reading frames (ORFs), and 15 tRNAs. Phylogenetic analysis and nucleotide-based intergenomic similarity suggest that Synechococcus phage S-H9-2 belongs to the Bristolvirus genus under the family Kyanoviridae. Homologs of the S-H9-2 open reading frame can be found in a variety of marine environments, as shown by the results of mapping the genome sequence of S-H9-2 to the Global Ocean Viromes 2.0 dataset. The presence of auxiliary metabolic genes (AMGs) related to photosynthesis, carbon metabolism, and phosphorus assimilation, as well as phylogenetic relationships based on complete genome sequences, reflect the mechanism of phage-host interaction and host-specific strategies for adaptation to environmental conditions. This study enriches the current genomic database of cyanophage and contributed to our understanding of the virus-host interactions and their adaption to the environment.

African swine fever (ASF) is a severe infectious disease that has a high global prevalence. The fatality rate of pigs infected with ASF virus (ASFV) is close to 100%; in the absence of a safe and reliable commercial vaccine, this poses a threat to the global pig industry and public health. To better understand the interaction of ASFV with its host, isobaric tags for relative and absolute quantitation combined with liquid chromatography-mass spectrometry was used to conduct quantitative proteomic analysis of bone marrow-derived macrophage cells infected with ASFV. Overall, 4579 proteins were identified; 286 of these were significantly upregulated and 69 were significantly downregulated after ASFV infection. Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, and protein-protein interaction network analyses were used to obtain insights into the dynamics and complexity of the ASFV-host interaction. In addition, immunoblotting revealed that the expression of PIK3AP1, RNF114, and FABP5 was upregulated and that of TRAM1 was downregulated after ASFV infection. Overexpression of PIK3AP1 and RNF114 significantly inhibited ASFV replication in vitro, but the suppressive effect of PIK3AP1 on ASFV replication was independent of the PI3K-Akt pathway. Further studies confirmed that ASFV MGF360-9L interacts with PIK3AP1 to reduce its protein expression level. Moreover, LY294002, an inhibitor of the PI3K-Akt pathway, inhibited ASFV replication, indicating the importance of the PI3K-Akt pathway in ASFV infection. This study identified the network of interactions between ASFV and host cells and provides a reference for the development of anti-ASFV strategies and for studying the potential mechanisms and pathogenesis of ASFV infection.