P orcine reproductive and respiratory syndrome virus (PRRSV) is one of the most economically important viruses affecting the swine industry worldwide, resulting in significant economic losses each year (1-3). PRRSV is a small, enveloped, linear, single positive-stranded RNA virus and a member of the order Nidovirales, family Arteriviridae (4). Current vaccination strategies cannot effectively control PRRSV infection because of the high antigenic heterogeneity (5, 6), the replication in and destruction of lung alveolar macrophages (7-9), and the observed antibody-dependent enhancement of PRRSV (10, 11). Therefore, it is imperative to study PRRSV pathogenesis mechanisms so that more effective control measures can be developed.Heme oxygenase-1 (HO-1) is the rate-limiting enzyme of heme degradation, and it functions to catabolize free heme into biliverdin, carbon monoxide, and iron. HO-1 and its end products have antioxidant, anti-inflammatory, and antiviral properties, and it is known to be a pivotal cytoprotective enzyme (12). Upregulation of HO-1 expression suppresses replication of a number of viruses, including hepatitis C virus (HCV), HIV-1, hepatitis B virus (HBV), and influenza virus (13-17). Our previous work showed that PRRSV significantly downregulates HO-1

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The subcortical maternal complex (SCMC) is an oocyte‐to‐embryo‐specific maternal functional module. Some variants of SCMC genes that contribute to preimplantation embryonic arrest have been identified. However, more novel variants should be identified to broaden the genetic and phenotypic spectrum of SCMC genes and establish their roles in embryonic development. We identified 13 novel variants in the SCMC genes, TLE6, NLRP5, NLRP2, and PADI6, from 10 of a total of 50 infertile females with recurrent preimplantation embryonic arrest. Six variants in TLE6 were found in five patients with embryonic arrest, accompanied by direct cleavage and severe fragmentation at the cleavage stage. Three patients carried NLRP5 variants, and one patient each who carried NLRP2 and PADI6 variants had subsequent poor or failed fertilization and cleavage arrest with a relatively lower ratio of severely fragmented embryos. Our findings expand the genetic and phenotypic spectrum of SCMC genes associated with human embryogenesis and might help lay the foundation for the genetic diagnosis of female infertility.