Infectious bursal disease (IBD) is one of the most important immunosuppressive diseases of young chickens, causing considerable economic losses to the poultry industry. More than 30 years ago, an antigenic variant (av) pathotype of the IBD virus (IBDV) was reported to originate in, and subsequently spread among, poultry farms in the USA. Recently, a novel avIBDV lineage was identified in China and was shown to exhibit clear differences in its pathogenicity as well as molecular characteristics compared with the previously isolated variant strains. In this study, we conducted a passive surveillance of chicken carcasses submitted to our research division from June-December 2019, and detected the IBDV strains by reverse transcription PCR. Five avIBDV strains were isolated, and their pathogenicity was determined by necropsy and molecular analysis. Additionally, a coinfection field case involving an avIBDV strain and a very virulent IBDV (vvIBDV) strain was identified. Multiple sequence alignment and phylogenetic analysis of partial viral protein 1 (VP1) and hypervariable region (hv) VP2 genes revealed that those strains originated from two different avIBDV lineages. The co-occurrence of two subgroups of avIBDVs in South Korea confirms for the first time the evolution of antigenic variant IBDV strains, and highlights the urgency for the development of new strategies for IBDV intervention in South Korea. RESEARCH HIGHLIGHTS:. Five avIBDV strains were identified in South Korea by passive surveillance test in 2019.. A coinfection between two IBDV strains from different genogroups was reported in a field case.. By phylogenetic analysis, Korean avIBDVs belonged to two distinct lineages of antigenic variant genogroup.

Infectious bursal disease (IBD), caused by IBD virus (IBDV), threatens the health of the poultry industry. Recently, a subtype of genogroup (G) 2 IBDV named G2d has brought a new threat to the poultry industry. To determine the current status of IBDV prevalence in South Korea, active IBDV surveillance on 167 randomly selected broiler farms in South Korea from August 2020 to July 2021 was conducted. The bursas of Fabricius from five chickens from each farm were independently pooled and screened for IBDV using virus-specific RT-PCR. As a result, 86 farms were found to be infected with the G2d variant, 13 farms with G2b, and 2 farms with G3. Current prevalence estimation of IBDV infection in South Korea was determined as 17.8% at the animal level using pooled sampling methods. G2d IBDV was predominant compared to other genogroups, with a potentially high-risk G2d infection area in southwestern South Korea. The impact of IBDV infection on poultry productivity or Escherichia coli infection susceptibility was also confirmed. A comparative pathogenicity test indicated that G2d IBDV caused severe and persistent damage to infected chickens compared with G2b. This study highlights the importance of implementation of regular surveillance programs and poses challenges for the comprehensive prevention of IBDV infections.

Sesamin, the most abundant lignan in sesame seed oil, has many biological activities. However, the underlying molecular mechanisms behind the regulatory effects of sesamin on endothelial nitric oxide synthase (eNOS) activity and nitric oxide (NO) generation in endothelial cells (ECs) remain unclear. Sesamin induced the intracellular level of NO and eNOS phosphorylation in ECs in a concentration- and time-dependent manner. Additionally, sesamin induced levels of intracellular calcium, leading to the phosphorylation of calmodulin-dependent protein kinase II (CaMKII) at Thr286, calcium/calmodulin-dependent protein kinase kinase beta (CaMKKβ) at Ser511, protein kinase A (PKA) at Thr197, Akt at Ser473, and AMP-activated protein kinase (AMPK) at Thr172. In particular, blocking of the transient receptor potential vanilloid type 1 (TRPV1) channel by capsazepine (TRPV1 antagonist), as well as TRPV1 knockdown via TRPV1 silencing RNA, abrogated sesamin-induced PKA, Akt, AMPK, CaMKII, CaMKKβ, and eNOS phosphorylation and NO level in ECs. Furthermore, sesamin inhibited TNF-α-induced NF-κB translocation, intercellular adhesion molecule-1 expression, and monocyte adhesion. Sesamin triggered eNOS activity and NO production via activation of TRPV1-calcium signaling, which involved the phosphorylation of PKA, CaMKII, CaMKKβ, Akt, and AMPK. Sesamin may be useful for treating or preventing the endothelial dysfunction correlated with cardiovascular diseases.

Betulinic acid (BA) is a natural pentacyclic triterpenoid with protective effects against inflammation, metabolic diseases, and cardiovascular diseases. We have previously shown that BA prevents endothelial dysfunction by increasing nitric oxide (NO) synthesis through activating endothelial nitric oxide synthase (eNOS) in human endothelial cells. However, the effect of BA on eNOS expression remains unclear. Thus, the aim of our study was to investigate the intracellular pathways associated with the effect of BA to regulate eNOS expression in human endothelial cells. BA significantly increased eNOS expression in a time- and concentration-dependent manner. Additionally, BA upregulated the expression of the transcription factor KLF2, which is known to regulate eNOS expression. KLF2 silencing in human endothelial cells attenuated the ability of BA to upregulate eNOS. BA also increased levels of intracellular Ca2+, activating CaMKKβ, CaMKIIα, and AMPK. Inhibition of the TRPC calcium channel abolished BA-mediated effects on intracellular Ca2+ levels. Moreover, BA increased the phosphorylation levels of ERK5, HDAC5, and MEF2C. Pretreatment of cells with compound C (AMPK inhibitor), LMK235 (HDAC5 inhibitor), and XMD8-92 (ERK5 inhibitor) attenuated the BA-induced eNOS expression. Collectively, these findings suggest that BA induces eNOS expression by activating the HDAC5/ERK5/KLF2 pathway in endothelial cells. The data presented here provide strong evidence supporting the use of BA to prevent endothelial dysfunction and treat vascular diseases, such as atherosclerosis.

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