Porcine bocavirus is a recently discovered virus that infects pigs and is classified within the Bocavirus genus (family Parvoviridae, subfamily Parvovirinae). The viral genome constitutes linear single-stranded DNA and has three open reading frames that encode four proteins: NS1, NP1, VP1, and VP2. There have been more than seven genotypes discovered to date. These genotypes have been classified into three groups based on VP1 sequence. Porcine bocavirus is much more prevalent in piglets that are co-infected with other pathogens than in healthy piglets. The virus can be detected using PCR, loop-mediated isothermal amplification, cell cultures, indirect immunofluorescence, and other molecular virology techniques. Porcine bocavirus has been detected in various samples, including stool, serum, lymph nodes, and tonsils. Because this virus was discovered only five years ago, there are still many unanswered questions that require further research. This review summarizes the current state of knowledge and primary research achievements regarding porcine bocavirus.

This study focused on the presence of antibiotic-resistant bacteria in a metro system as an example of a public transportation system. The molecular characteristics of Staphylococcus were investigated to discern which strains were isolated from metro stations in Shanghai. These were compared with strains isolated from hospital treatment rooms and parks. Airborne Staphylococcus samples in the metro were resistant to an average of 2.64 antibiotic types, and 58.0% of the strain samples were resistant to at least three antibiotics; this was a significantly higher rate than strains from the park, but was lower than those from hospitals. The presence of two antibiotic resistance genes of Staphylococcus strains, mecA (28.0%) and qac (40.0%), were also found at significantly higher levels in metro samples than park samples, but did not differ significantly from hospital samples. Furthermore, 22.0% of the metro Staphylococcus samples were found to be biofilm-positive. The high rate of antibiotic resistance found in Staphylococcus samples collected from metro stations, and the discovery of antibiotic-resistant genes, indicate that the closed indoor environment and crowded passengers may accelerate the spread of antibiotic resistant strains. More attention should be paid to the inspection and control of antibiotic resistant strains in public transportation systems.

SUMMARY: Host cellular receptors are key determinants of virus tropism and pathogenesis. Virus utilizes multiple receptors for attachment, entry, or specific host responses. However, other than ACE2, little is known about SARS-CoV-2 receptors. Furthermore, ACE2 cannot easily interpret the multi-organ tropisms of SARS-CoV-2 nor the clinical differences between SARS-CoV-2 and SARS-CoV. To identify host cell receptors involved in SARS-CoV-2 interactions, we performed genomic receptor profiling to screen almost all human membrane proteins, with SARS-CoV-2 capsid spike (S) protein as the target. Twelve receptors were identified, including ACE2. Most receptors bind at least two domains on S protein, the receptor-binding-domain (RBD) and the N-terminal-domain (NTD), suggesting both are critical for virus-host interaction. Ectopic expression of ASGR1 or KREMEN1 is sufficient to enable entry of SARS-CoV-2, but not SARS-CoV and MERS-CoV. Analyzing single-cell transcriptome profiles from COVID-19 patients revealed that virus susceptibility in airway epithelial ciliated and secretory cells and immune macrophages highly correlates with expression of ACE2, KREMEN1 and ASGR1 respectively, and A CE2/A S GR1/K R EMEN1 (ASK) together displayed a much better correlation than any individual receptor. Based on modeling of systemic SARS-CoV-2 host interactions through S receptors, we revealed ASK correlation with SARS-CoV-2 multi-organ tropism and provided potential explanations for various COVID-19 symptoms. Our study identified a panel of SARS-CoV-2 receptors with diverse binding properties, biological functions, and clinical correlations or implications, including ASGR1 and KREMEN1 as the alternative entry receptors, providing insights into critical interactions of SARS-CoV-2 with host, as well as a useful resource and potential drug targets for COVID-19 investigation.

SUMMARY: The global spread of SARS-CoV-2 is posing major public health challenges. One unique feature of SARS-CoV-2 spike protein is the insertion of multi-basic residues at the S1/S2 subunit cleavage site, the function of which remains uncertain. We found that the virus with intact spike (Sfull) preferentially enters cells via fusion at the plasma membrane, whereas a clone (Sdel) with deletion disrupting the multi-basic S1/S2 site instead utilizes a less efficient endosomal entry pathway. This idea was supported by the identification of a suite of endosomal entry factors specific to Sdel virus by a genome-wide CRISPR-Cas9 screen. A panel of host factors regulating the surface expression of ACE2 was identified for both viruses. Using a hamster model, animal-to-animal transmission with the Sdel virus was almost completely abrogated, unlike with Sfull. These findings highlight the critical role of the S1/S2 boundary of the SARS-CoV-2 spike protein in modulating virus entry and transmission.

Helicobacter pylori ( H. pylori ) is a key cause of chronic inflammation and gastric cancer, and Epstein-Barr virus (EBV) also contributes to gastric tumorigenesis. However, the role of EBV co-infection in H. pylori -related cancers remains unclear because of the lack of efficient ex vivo models. Organoids, which are derived from self-renewing stem cells, closely mimic in situ tissue structure and function, making them ideal for disease modeling. Here, we developed patient-derived normal gastric organoids (NGOs) and used high-accuracy microinjection to introduce EBV and H. pylori (NCTC11637 strain). We found that the co-infection of H. pylori and EBV induced a significant structural change and upregulated the expression of TFF1 , VIL1 , and Lgr5 to promote cell proliferation and tissue morphogenesis. Analysis of transmission electron microscopy revealed an increase of H. pylori internal location in NGOs after co-infection. Moreover, all tested H. pylori strains isolated from patients displayed similar toxicities when co-infected with EBV. These findings provide a fundamental basis for evaluating pathogen toxicity, predicting disease progression, and advancing the clinical treatment of gastric cancer. IMPORTANCE: Helicobacter pylori ( H. pylori ) infection is a major contributor to chronic inflammation and the development of gastric cancer. Furthermore, Epstein-Barr virus (EBV) has been shown to play a role in the oncogenic process of gastric cancer by promoting chronic inflammation and increasing tissue damage. However, the mechanism by which co-infection contributes to gastric carcinogenesis remains unclear. In this study, we used patient-derived gastric organoids as a model to establish EBV- H. pylori co-infection using microinjection technology and found that co-infection causes significant structural changes and promotes cell proliferation. This model will not only contribute to a better understanding of the pathogenesis of gastric cancer but will also be important for drug efficacy evaluation and the development of new therapeutic approaches.