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Swinepox virus (SWPV) is responsible for sporadic acute poxvirus infections in swine worldwide, causing a pathognomonic eruptive proliferative dermatitis. Beside direct and congenital transmission, the pig louse Haematopinus suis acts as a mechanical vector and favors virus infection through skin lesions. Infections are generally described in domestic pigs, while only a few cases have been reported in wild boars, in Austria and Germany. In September 2022, SWPV infection was suspected at post-mortem examination of a wild boar piglet with characteristic lesions in Liguria, Northwest Italy. The piglet was heavily parasitized by swine lice (H. suis). SWPV was then confirmed by histological and molecular analyses. Possible viral co-infections were also investigated (African swine fever virus, classical swine fever virus, parvovirus, circovirus, Aujeszky’s disease virus and hepatitis E virus). This article describes gross and histopathologic features of SWPV infection, differential diagnosis, and potential vector-borne transmission to domestic pigs, presenting a brief review of the literature on the topic. SWPV infection is reported in wild boars in Italy for the first time. The finding of SWPV in a wild boar in an area with a very limited pig population may suggest the existence of a “wildlife cycle” in the area. Further investigations are needed to understand the real risk of transmission of SWPV to domestic pigs as well as the role of other arthropod vectors.

In the preparation of transgenic murine ES cells it is important to verify the construct has a single insertion, because an ectopic neomycin phosphortransferase positive selection cassette (NEO) may cause a position effect. During a recent work, where a knockin SCA28 mouse was prepared, we developed two assays based on Real-Time PCR using both SYBR Green and specific minor groove binder (MGB) probes to evaluate the copies of NEO using the comparative delta-delta Ct method versus the Rpp30 reference gene. We compared the results from Southern blot, routinely used to quantify NEO copies, with the two Real-Time PCR assays. Twenty-two clones containing the single NEO copy showed values of 0.98 ± 0.24 (mean ± 2 S.D.), and were clearly distinguishable from clones with two or more NEO copies. This method was found to be useful, easy, sensitive and fast and could substitute for the widely used, but laborious Southern blot method.

Abstract 1080 Poster Board I-102 Feline Leukemia Virus, subgroup C, Receptor (FLVCR) was originally identified and cloned as a cell-surface protein receptor for feline leukaemic virus, subgroup C causing pure red blood cell aplasia in cats. Recent studies have demonstrated that FLVCR is a heme exporter essential for erythropoiesis. The heme efflux via FLVCR was shown to be essential for erythroid differentiation in K562 cells as well as in CD34+ precursors cells1. Moreover, Keel and co-authors have recently reported that Flvcr-null mice die in utero due to the failure of fetal erythropoiesis2. We have recently identified a novel FLVCR isoform, called FLVCRb, coding for a putative 7 transmembrane domain-containing protein. Both FLVCRb and the canonical FLVCR (described herein as FLVCRa) were expressed in all tissues: FLVCRa mRNA level was significantly higher than FLVCRb in liver, kidney, colon and duodenum, whereas the opposite was observed in heart and skeletal muscle. In bone marrow, spleen and brain, FLVCRa and FLVCRb mRNA levels were comparable. FLVCRa and FLVCRb display different sub-cellular distribution when over-expressed in vitro. As expected, FLVCRa is localized at the cell membrane while FLVCRb is expressed in intracellular compartment suggesting different functions of the two proteins in heme metabolism. To gain insights into the specific roles of the two isoforms, we have generated Flvcr mutant mice different from those previously reported2. Keel and co-author generated a mouse model in which both FLVCRa and FLVCRb were deleted. In our mouse model, FLVCRa has been specifically deleted and FLVCRb is still expressed (Flvcr-a-null mice). Flvcr-a heterozygous mice were grossly normal, fertile and indistinguishable from their wild-type littermates. When Flvcr-a +/- mice were intercrossed, no Flvcr-a homozygous knock-out newborns were obtained, and the analysis of the embryos from timed Flvcr-a +/- intercrosses showed that the Flvcr-a-/- genotype was lethal between E14.5-E16.5. Flvcr-a-null embryos showed multifocal and extended hemorrhages, visible in the limbs, head and throughout the body wall, as well as subcutaneous edema. Alcian blue-alizarin red staining demonstrated skeletal abnormalities in limbs and head similar to that observed in Diamond-Blakfan anemia (DBA) patients. Interestingly, flow cytometric analyses of E14.5 fetal liver cells double-stained for Ter119 (erythroid-specific antigen) and CD71 (transferrin receptor) show normal erythropoiesis in Flvcr-a-null embryos, opposite to the previously reported Flvcr-null mice2. Taken together, these data demonstrated that FLVCRb is sufficient to support fetal erythropoiesis, but not to prevent endothelial ruptures responsible for hemorrhages, thus suggesting that FLVCRa is needed for detoxifying heme excess at these sites. The involvement of the two isoforms in the pathogenesis of DBA is currently under investigation. Quigley JG, Yang Z, Worthington MT, Phillips JD, Sabo KM, Sabath DE, Berg CL, Sassa S, Wood BL, Abkowitz JL. Identification of a human heme exporter that is essential for erythropoiesis. Cell 2004;118:757-66. Keel SB, Doty RT, Yang Z, Quigley JG, Chen J, Knoblaugh S, Kingsley PD, De Domenico I, Vaughn MB, Kaplan J, Palis J, Abkowitz JL. A heme export protein is required for red blood cell differentiation and iron homeostasis. Science 2008;319:825-8. Disclosures No relevant conflicts of interest to declare.