The Transmissible Gastroenteritis Virus (TGEV) causes severe diarrhea and other symptoms which end up in death in young piglets. We have studied the protective effects of the probiotic Lactobacillus plantarum strain N4(Lp) which metabolic products were added to the swine testis (ST) cells with three different orders using MTT cell proliferation assay and CPE analysis. Metabolic products led to dose-dependent rescue of viability of infected cells in a certain order: pre-treatment, post-infection, co-incubation. Pre-treatment of cells with probiotic metabolic products reduced viral proliferation up to 78% at non-cytotoxic concentration 1/4 dilution. The viral yields in pretreatment groups were reduced by over three log10 units. Quantitative real-time PCR revealed the optimal inhibition of TGEV RNA replication was 24 h apply pretreatment way that up to 71% of N gene. Analysised the composition of metabolic products by GC-MS revealed the major component is sugars. Then Exopolysaccharides (EPS) was extracted and showed inhibition effect that co-incubation with TGEV.

Cyanobacteria have a relatively high affinity for NH4 +, yet a NO3 –-rich environment is comparatively conducive to their proliferation. To date, little information is available on why NO3 –-N favors cyanobacterial biomass accumulation. This study investigated the dependence of biomass, nitrogen assimilation characteristics, and photophysiological performance of Microcystis aeruginosa on the forms of nitrogen supply, including NO3 –-N-only, NH4 +-N-only, and NO3 –-N + NH4 +-N. The results indicated that despite the retarded growth of M. aeruginosa, cells supplied with NO3 –-N-only maintained a simultaneous promotion in the growth rate, nitrogen assimilation efficiency, and photosynthetic capacity, resulting in high biomass production. Cells supplied with NH4 +-N-only and NO3 –-N + NH4 +-N were able to rapidly assimilate nitrogen during initial cell proliferation, showing a preferential use of NH4 +-N and the inhibition of NO3 – uptake by NH4 +. However, growth repression occurred as cultivation time was prolonged when NH4 +-N was excessively supplied, mainly due to PSII photodamage, intracellular redox imbalance, and increased electron energy accumulation. Thus, cells supplied with NH4 +-N-only had to reduce light energy capture, increase photoprotection, and consume excess electrons to mitigate the damage. These findings are critical for improving our understanding of the role of different nitrogen forms in the regulation of cyanobacterial photophysiological performance and growth.

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The H9N2 subtype influenza virus (IV) is a remarkable member of the influenza A viruses because it can infect not only chickens, ducks and pigs, but also humans. Pigs are susceptible to both human and avian influenza viruses and have been proposed to be intermediate hosts for the generation of pandemic influenza viruses through reassortment or adaptation to the mammalian host. To further understand the genetic characteristics and evolution, we investigated the source and molecular characteristics of the H9N2 subtype swine influenza virus (SIV), and observed its pathogenicity in BALB/c mice. The BALB/c mice were inoculated intranasally with 100 median mouse infectious dose of A/swine/HeBei/012/2008/(H9N2) viruses to observe the pathogenicity. The HA, NP, NA and M gene were cloned, sequenced and phylogenetically analyzed with related sequences available in GenBank. The infected mice presented with inactivity, weight loss and laboured respiration, while the pathological changes were characterized by diffuse alveolar damage in the lung. The nucleotide and deduced amino acid sequence of HA, NP, NA and M gene was similar with that of A/chicken/Hebei/4/2008(H9N2). The HA protein contained 6 glycosylation sites and the motif of HA cleavage site was PARSSR GLF, which is characteristic of low pathogenic IV. In the HA, NP, M and NA gene phylogenetic trees, the isolate clustered with A/chicken/Hebei/4/2008(H9N2). The isolate possibly came from A/chicken/Hebei/4/2008(H9N2) and was partially varied during its cross-species spread.

Introduction: Influenza is a severe respiratory viral infection that causes significant morbidity and mortality, due to annual epidemics and unpredictable pandemics. With the extensive use of neuraminidase inhibitor (NAI) drugs, the influenza B virus has carried different drug-resistant mutations. Thus, this study aimed to analyze the prevalence of drug-resistant mutations of the influenza B virus. Methodology: Near full-length sequences of the neuraminidase (NA) region of all influenza B viruses from January 1, 2006, to December 31, 2018, were downloaded from public databases GISAID and NCBI. Multiple sequence alignments were performed using Clustal Omega 1.2.4 software. Subsequently, phylogenetic trees were constructed by FastTree 2.1.11 and clustered by ClusterPickergui_1.2.3.JAR. Then, the major drug resistance sites and surrounding auxiliary sites were analyzed by Mega-X and Weblogo tools. Results: Among the amino acid sequences of NA from 2006 to 2018, only Clust04 in 2018 carried a D197N mutation of the NA active site, while other drug resistance sites were conserved without mutation. According to the Weblogo analysis, a large number of N198, S295, K373, and K375 mutations were found in the amino acid residues at the auxiliary sites surrounding D197, N294, and R374. Conclusions: We found the D197N mutation in Clust04 of the 2018 influenza B virus, with a large number of N198, S295, K373, and K375 mutations in the helper sites around N197, N294, and R374 from 2006 to 2018. NA inhibitors are currently the only kind of specific antiviral agent for the influenza B virus, although these mutations cause mild NAIs resistance.