As one of emerging porcine viruses, atypical porcine pestivirus (APPV) was found in three continents since it emerged in 2015. It is now thought as the causative agent for congenital tremor type A‐II in piglets. At the end of 2017, two APPV strains were identified from piglets with congenital tremor in Guangxi and Yunnan, China. The genome of APPV GX04/2017 strain was so far determined to be 11,534 nucleotides (nt) in length and contains a single open reading frame (ORF) encoding a polyprotein comprising 3,635 amino acids. Comparative analysis of ORF, N^pro, E2, and NS3 gene sequences revealed that the APPV GX04/2017 strain shares nucleotide sequence identities of 82.8% to 92.8% with other APPV strains, while YN01/2017 strain is 79.4% to 97.4% homology to the others. Phylogenetic analysis showed that the APPV GX04/2017 and YN01/2017 are two novel APPV strains with the highest homology to each other, and relative high similarity to the APPV 000515 and JX‐JM01 strains in genome sequence. The current findings provide updated information about APPV epidemiology and divergence in China, which would certainly help to establish reliable diagnosis and surveillance programs for APPV.

Porcine reproductive and respiratory syndrome virus (PRRSV) is the cause of an economically important swine disease that has devastated the swine industry since the late 1980s. The aim of the present study was to investigate the interaction between reactive oxygen species (ROS) and NF-κB by PRRSV infection. We isolated the local strain of PRRSV from southwest China, designated YN-2011, then sequenced and analyzed the genome. YN-2011 was then used to evaluate the interaction of ROS and NF-κB. In PRRSV infected MARC-145 cells, there was a time-dependent increase in ROS and Maleic Dialdehyde (MDA). Accordingly, NF-κB activation was also increased as PRRSV infection progressed. Degradation of IκB mRNA was detected late in PRRSV infection, and overexpression of the dominant negative form of IκBα significantly suppressed NF-κB induced by PRRSV. The results indicate that the generation of ROS is involved in PRRSV replication and this progression is associated with the alteration in NF-κB activity induced by ROS. These results should extend our better understanding the interaction between PRRSV and host MARC-145 cells.

In this study, we isolated and identified bacteria from the feces of a diarrheal cynomolgus monkey. The results showed that the isolated strain was P. aeruginosa, named PA/CM-101101. Morphological observations indicated that when cultured on Luria–Bertani (LB) nutrient agar at 37 °C for 24 h, the strain formed smooth, slightly elevated colonies with neat and wavy edges. On acetamide agar at the same temperature and duration, the colonies appeared flat with irregular edges and a faint pink periphery, while the medium changed to rose-red; in LB broth at 37 °C for 24 h, the medium became turbid and yellowish-green. Gram staining revealed that it was negative and rod-shaped, without sporulation characteristics. The 16S rRNA gene sequence analysis showed that the sequence identity of the strain shared more than 98.4% similarity with 11 strains of P. aeruginosa from various sources in GenBank. The animal toxicity test showed that it had a strong pathogenic effect on mice. The results of drug sensitivity tests showed that strain PA/CM-101101 was sensitive to amikacin, azithromycin, cefoperazone, ceftazidime, ceftriaxone, ciprofloxacin, gentamicin, imipenem, levofloxacin, meropenem, norfloxacin, ofloxacin, and polymyxin B; however, it displayed resistance to ampicillin, cefadroxil, cefazolin, erythromycin, and vancomycin. The research findings provide valuable insights for diagnosis and treatment strategies for cynomolgus monkeys. It also provides a reference for molecular epidemiological studies. To our knowledge, this is the first time P. aeruginosa isolated from the diarrhea feces of cynomolgus monkey has been reported.

This study aims to establish a therapy strategy for canine leukopenia induced by canine parvovirus (CPV) infection through intravenous infusion of allogeneic bone marrow mesenchymal stem cells (BMMSCs) and to evaluate the therapeutic effect of BMMSCs on canine parvovirus. Forty healthy 2-month-old dogs were randomly divided into four groups including the BMMSC treatment group (A), conventional treatment group (B), CPV infection group (C), and a normal control group (D). Then the A, B, and C groups were orally infected with CPV (10^3.25 TCID₅₀/mL) at 1mL/kg, and the D group received the same dose of saline. After the onset of infection, Group A received mesenchymal stem cells (MSCs) and rehydration as the treatment; Group B was treated with anti-inflammatory therapeutics and rehydration; and Group C and D were injected with the same dose of physiological saline. The level of leukocytes rebounded significantly after the treatment with BMMSCs and returned to reference numbers on Day 3 after treatment, which was significantly higher than that in the conventional treatment group. The concentrations of IL-2 and IFN-α were gradually increased during the treatment, and the BMMSC treatment group exhibited significantly higher IL-2 and IFN-α concentrations than the conventional treatment group on Days 3 and 4. The expression of the virus in the blood gradually decreased during the treatment, and the BMMSC treatment group displayed a faster decrease than the conventional treatment group. These results showed the advantages of BMMSC treatment over conventional treatment. This study provides a new BMMSC treatment strategy for canine leukopenia induced by CPV infection and reveals the mechanism by which BMMSC increases leukocytes after CPV infection.