Three Loxocaudinae species (Ostracoda, Podocopida) from South Korea.

For many ostracod groups in Korea, published records are missing or are very limited. Loxocaudinae is one such subfamily, with only one named species, Loxocaudaorientalis Schornikov, 2011 reported from Korea. Having fewer than 50 species, this subfamily can be considered a small ostracod group, with most of the species known only by their shell morphology. The diagnoses of genera are based on the shell characters that are often homoplastic, and soft body appendages that are difficult to observe, such as the mandibular exopodite. Because of this, the validity of the entire subfamily and some of its genera have been questioned. Here three Loxocaudinae species were collected from the marine macrobenthic assemblages from Korea. Two are new and belong to the genus Glacioloxoconcha Hartmann, 1990, previously known only from Antarctica: Glacioloxoconchajeongokensis sp. nov. and Glacioloxoconchajisepoensis sp. nov. Loxocaudaorientalis is briefly redescribed, with some of the populations having unusual morphological features. COI and 18S rRNA sequences of all three species are provided and the latter marker used to assess the position of the subfamily within the family Loxoconchidae and the superfamily Cytheroidea. The resulting tree shows that within the family Loxoconchidae, the genera Glacioloxoconcha and Loxocauda Schornikov, 1969 are the most closely related, with very shallow but well-supported branches. Polyphyletic and paraphyletic natures of several Cytheroidea families are discussed, inferred from the reconstructed phylogeny.

Circulating level of sPD-1 and PD-1 genetic variants are associated with hepatitis B infection and related liver disease progression.

BACKGROUND: Programmed cell death-1 (PD-1) variants and circulating level of soluble PD-1 are associated with susceptibility to malignant and infectious disease. This study aimed to examine the association of PD-1.5 and PD-1.9 variants, and plasma sPD-1 level with hepatitis B virus (HBV) infection and disease progression. METHODS: The study cohort consisted of adults infected with HBV (n=513) - stratified by clinical course, including chronic hepatitis B (CHB, n=173), liver cirrhosis (LC, n=134) and hepatocellular carcinoma (HCC, n=206) - and matched healthy controls (HC, n=196). The PD-1.5 (rs2227981 C/T) and PD-1.9 (rs2227982 C/T) genetic variants were genotyped by Sanger sequencing, and plasma sPD-1 levels were quantified by enzyme immunoassay. RESULTS: Plasma sPD-1 levels were significantly higher among patients infected with HBV. The highest plasma sPD-1 levels were observed in patients with CHB, followed by patients with LC and HCC. In addition, the plasma sPD-1 levels correlated positively with liver inflammation [aspartate transaminase (AST): rho=0.57, P<0.0001; alanine aminotransferase: rho=0.57, P<0.0001], and were positively correlated with liver fibrosis [AST to platelet ratio index score: rho=0.53, P<0.0001). The PD-1.9 TT genotype was less common in patients with CHB compared with patients with LC, HCC, and HCC+LC in both codominant and recessive models (P<0.01), and was found to be a risk factor for HCC predisposition {HCC vs non-HCC: odds ratio (OR) 2.0 [95% confidence interval (CI) 1.13-3.7], Padj=0.017}. The PD-1.5 CT genotype was associated with reduced risk of acquiring HCC [OR 0.6 (95% CI 0.4-0.9), Padj=0.031]. CONCLUSION: sPD-1 level was associated with liver inflammation and progression of liver fibrosis, and the PD-1.5 and PD-1.9 variants were associated with HBV infection and progression of liver disease.

Genetic variants of programmed cell death 1 are associated with HBV infection and liver disease progression.

The inhibitory effects of programmed cell death 1/programmed cell death ligand 1 (PD-1/PD-L1) modulates T-cell depletion. T-cell depletion is one of the key mechanisms of hepatitis B virus (HBV) persistence, in particular liver disease progression and the development of hepatocellular carcinoma (HCC). This case-control study aimed to understand the significance of PD-1 polymorphisms (PD-1.5 and PD-1.9) association with HBV infection risk and HBV-induced liver disease progression. Genotyping of PD-1.5 and PD-1.9 variants was performed by direct Sanger sequencing in 682 HBV-infected patients including chronic hepatitis (CHB, n = 193), liver cirrhosis (LC, n = 183), hepatocellular carcinoma (HCC, n = 306) and 283 healthy controls (HC). To analyze the association of PD-1 variants with liver disease progression, a binary logistic regression, adjusted for age and gender, was performed using different genetic models. The PD-1.9 T allele and PD-1.9 TT genotype are significantly associated with increased risk of LC, HCC, and LC + HCC. The frequencies of PD-1.5 TT genotype and PD-1.5 T allele are significantly higher in HCC compared to LC patients. The haplotype CT (PD-1.5 C and PD-1.9 T) was significantly associated with increased risk of LC, HCC, and LC + HCC. In addition, the TC (PD-1.5 T and PD-1.9 C) haplotype was associated with the risk of HCC compared to non-HCC. The PD-1.5 CC, PD-1.9 TT, genotype, and the CC (PD-1.5 C and PD-1.9) haplotype are associated with unfavorable laboratory parameters in chronic hepatitis B patients. PD-1.5 and PD1.9 are useful prognostic predictors for HBV infection risk and liver disease progression.