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Background: Advances in American mink (Neogale vison) genomics have identified candidate genes linked to disease resistance, including RNF165, which is involved in immune response and virus–host interactions. Objectives: This study aimed to characterize genetic variation within the RNF165 (Ring Finger Protein 165) gene in farmed and wild mink to identify polymorphisms potentially associated with resistance to Aleutian mink disease virus (AMDV). Methods: Two groups of mink were analyzed: farmed animals from Latvia (n = 50) and wild animals (n = 20) from Poland. The presence of viral DNA was verified by PCR amplification targeting the VP2 and NS1 viral protein genes. To assess polymorphism within RNF165, primers spanning eight exons were designed, optimized, and applied in PCR amplification. PCR products were sequenced and subjected to bioinformatic analysis. Results: Two single nucleotide polymorphisms were identified: a synonymous substitution at c.G141A and a missense mutation c.G596A (p.R199K). Both variants were present in farmed and wild populations; however, the G allele at position c.141 was nearly twice as frequent in farmed mink compared to wild mink (p < 0.05). In silico functional prediction (SNAP2) indicated that the p.R199K mutation may moderately affect RNF165 protein function. Conclusions: Owing to its high conservation and role in immune regulation, RNF165 may serve as a promising candidate gene for molecular selection in breeding programs aimed at enhancing resistance to Aleutian mink disease (AMD).

Aleutian disease (AD) is a devastating infectious disease in American mink ( Neogale vison ) industry caused by Aleutian mink disease virus (AMDV). Two crucial steps toward controlling infectious diseases in farm animals are: (i) assessment of the infection risk factors to minimize the likelihood of infection and (ii) selection of animals with superior immune responses against pathogens to build tolerant farms. This study aimed to investigate AD risk factors and evaluate a novel “ImmunAD” approach for genetic improvement of AD tolerance. Phenotypic records and pedigree information of 1,366 and 24,633 animals were included in this study. The risk of animal’s age, sex, color type, and year of sampling on AMDV infection was assessed using a logistic regression model and counter immune-electrophoresis (CIEP) test results. ImmunAD phenotype was calculated based on AMDVG enzyme-linked immunosorbent assay (ELISA) and CIEP test results, and breeding values for ImmunAD were estimated using an animal model. Animals were classified into high-coordinated (HCIR), average-coordinated (ACIR), and low-coordinated immune responders (LCIR) using ImmunAD’s breeding values, and the impact of selection of HCIR on live grade of pelt quality (PQ), harvest weight (HW), and harvest length (HL) breeding values were evaluated. Age of > 1 year, male sex, and year of sampling were identified as significant risk factors of AD (p < 0.05). A moderate-to-high heritability (0.55±0.07) was estimated for ImmunAD, while a higher heritability was observed among the CIEP-positive animals (0.76±0.06). Significantly higher breeding values were observed for PQ and HL among HCIR than those for LCIR and ACIR (p < 0.05). Our findings indicate the critical role of male breeders in AD distribution within mink farms. Regular screening of AD in male breeders before pairing them with females during breeding seasons can help disease control. ImmunAD strategy can be applied to genetic improvement of AD tolerance, with favorable impacts on some growth and production traits. Higher genetic gains can be achieved in populations with higher AD seroprevalences.

Mink enteritis virus (MEV) NS1 is a multidomain and multifunctional protein containing origin binding, helicase, and transactivation domains. In particular, parvoviral NS1 proteins are transactivators of the viral capsid protein promoter although the manner by which they exert these transactivation effects remained unclear. In this study, the region of the transactivation domain of the NS1 C-terminal was found located at aa 557 ~ 668 and any deletion within this region reduced the transactivation activity. A dominant negative mutation of the 63 aa deletion in the C-terminal of NS1 protein resulted in loss of ability to activate P38 and VP2-5′UTR in a dual-luciferase reporter assay system, a VP2 protein expression system, and within the whole MEV genome, independent of downstream genes. Additionally, a full-length MEV clone deficient in its NS1 C-terminal failed to rescue the virus, possibly due to the loss of integrity of DNA sequences interacting with NS1 protein, and expression of VP2 was also inhibited even when normal NS1 protein was supplied in trans.

Estimating the abundance or density of populations is fundamental to the conservation and management of species, and as landscapes become more fragmented, maintaining landscape connectivity has become one of the most important challenges for biodiversity conservation. Yet these two issues have never been formally integrated together in a model that simultaneously models abundance while accounting for connectivity of a landscape. We demonstrate an application of using capture–recapture to develop a model of animal density using a least-cost path model for individual encounter probability that accounts for non-Euclidean connectivity in a highly structured network. We utilized scat detection dogs (Canis lupus familiaris) as a means of collecting non-invasive genetic samples of American mink (Neovison vison) individuals and used spatial capture–recapture models (SCR) to gain inferences about mink population density and connectivity. Density of mink was not constant across the landscape, but rather increased with increasing distance from city, town, or village centers, and mink activity was associated with water. The SCR model allowed us to estimate the density and spatial distribution of individuals across a 388 km2 area. The model was used to investigate patterns of space usage and to evaluate covariate effects on encounter probabilities, including differences between sexes. This study provides an application of capture–recapture models based on ecological distance, allowing us to directly estimate landscape connectivity. This approach should be widely applicable to provide simultaneous direct estimates of density, space usage, and landscape connectivity for many species.

Background Mink self-biting behaviour causes skin damage, reducing fur quality and restricting the development of the mink farming industry. The aim of this study was to investigate the genetic mechanisms underlying self-biting behaviour in minks from a genomic perspective. Using weighted gene coexpression network analysis (WGCNA), we identified functional gene modules and then explored their associations with phenotype, thereby identifying key genes influencing this behaviour. Methods The daily behaviours of minks were analysed through behavioural observation. Gene expression profiles of hippocampi from self-biting and healthy minks (8 males and 10 females in each group) were constructed using transcriptome sequencing. Results The results revealed significant differences in self-biting, feeding, playing, and lying behaviour between self-biting and healthy minks ( P  < 0.01). Notably, grooming was significantly correlated with self-biting behaviour ( P  < 0.05), and slow pace, lying, playing, shaking, and feeding behaviours were strongly correlated with self-biting behaviour ( P  < 0.01). Differentially expressed genes between self-biting and healthy minks were identified and analysed via WGCNA; then, the correlation coefficient method was used to identify 50 and 20 single genes that may affect mink self-biting in females and males, respectively. Database annotation identified a single gene in the female group, corresponding to Hspa2. Conclusion This gene is associated with neurological disorders. The Hspa2 gene showed functionally enriched expression under cold and heat stress. Therefore, we speculate that such stress induces abnormal changes in the Hspa2 gene in mink hippocampal tissue, leading to nerve stimulation and neurological disorders, including self-biting behaviour, in mink.

SARS-CoV-2 infection outbreaks in minks have serious implications associated with animal health and welfare, and public health. In two naturally infected mink farms (A and B) located in Greece, we investigated the outbreaks and assessed parameters associated with virus transmission, immunity, pathology, and environmental contamination. Symptoms ranged from anorexia and mild depression to respiratory signs of varying intensity. Although the farms were at different breeding stages, mortality was similarly high (8.4% and 10.0%). The viral strains belonged to lineages B.1.1.218 and B.1.1.305, possessing the mink-specific S-Y453F substitution. Lung histopathology identified necrosis of smooth muscle and connective tissue elements of vascular walls, and vasculitis as the main early key events of the acute SARS-CoV-2-induced broncho-interstitial pneumonia. Molecular investigation in two dead minks indicated a consistently higher (0.3–1.3 log 10 RNA copies/g) viral load in organs of the male mink compared to the female. In farm A, the infected farmers were responsible for the significant initial infection of 229 out of 1,000 handled minks, suggesting a very efficient human-to-mink transmission. Subsequent infections across the sheds wherein animals were being housed occurred due to airborne transmission. Based on a R 0 of 2.90 and a growth rate equal to 0.293, the generation time was estimated to be 3.6 days, indicative of the massive SARS-CoV-2 dispersal among minks. After the end of the outbreaks, a similar percentage of animals were immune in the two farms (93.0% and 93.3%), preventing further virus transmission whereas, viral RNA was detected in samples collected from shed surfaces and air. Consequently, strict biosecurity is imperative during the occurrence of clinical signs. Environmental viral load monitoring, in conjunction with NGS should be adopted in mink farm surveillance. The minimum proportion of minks that need to be immunized to avoid outbreaks in farms was calculated at 65.5%, which is important for future vaccination campaigns.

The European mink Mustela lutreola is one of the most threatened carnivores in Europe, having suffered dramatic range contractions and severe population fragmentation. Accurate knowledge of its genetic diversity is crucial for conservation planning, yet earlier studies based on partial mitochondrial markers offered limited resolution and often underestimated haplotype richness. In this study, complete mitochondrial genomes from four extant populations (Russia, n = 11; Romania, n = 16; Germany, n = 24; France–Spain, n = 15) were analysed using a suite of non-parametric and asymptotic estimators (Fisher’s α, ACE, Jackknife1, Bootstrap, Chao1-based iNEXT) together with negative binomial modelling. A total of 41 haplotypes were detected, but extrapolated estimates indicated substantially higher richness, particularly in populations dominated by singletons. Rarefaction and extrapolation analyses revealed that sample sizes of 70–130 individuals per population are needed to approach complete haplotype detection. The France–Spain and Romania populations harboured the highest predicted richness, whereas Germany and Russia, both represented by ex situ stocks, showed lower diversity. These results refine earlier assumptions of extreme homogeneity in the Western population and demonstrate that significant mitochondrial variation persists at the continental scale. The study provides quantitative benchmarks for sampling design and genetic management, supporting preservation of evolutionary potential in this critically endangered species.

Background Copy number variations (CNVs) represent a major source of genetic diversity and contribute to the phenotypic variation of economically important traits in livestock species. In this study, we report the first genome-wide CNV analysis of American mink using whole-genome sequence data from 100 individuals. The analyses were performed by three complementary software programs including CNVpytor, DELLY and Manta. Results A total of 164,733 CNVs (144,517 deletions and 20,216 duplications) were identified representing 5378 CNV regions (CNVR) after merging overlapping CNVs, covering 47.3 Mb (1.9%) of the mink autosomal genome. Gene Ontology and KEGG pathway enrichment analyses of 1391 genes that overlapped CNVR revealed potential role of CNVs in a wide range of biological, molecular and cellular functions, e.g., pathways related to growth (regulation of actin cytoskeleton, and cAMP signaling pathways), behavior (axon guidance, circadian entrainment, and glutamatergic synapse), lipid metabolism (phospholipid binding, sphingolipid metabolism and regulation of lipolysis in adipocytes), and immune response (Wnt signaling, Fc receptor signaling, and GTPase regulator activity pathways). Furthermore, several CNVR-harbored genes associated with fur characteristics and development ( MYO5A , RAB27B , FGF12 , SLC7A11 , EXOC2 ), and immune system processes ( SWAP70 , FYN , ORAI1 , TRPM2 , and FOXO3 ). Conclusions This study presents the first genome-wide CNV map of American mink. We identified 5378 CNVR in the mink genome and investigated genes that overlapped with CNVR. The results suggest potential links with mink behaviour as well as their possible impact on fur quality and immune response. Overall, the results provide new resources for mink genome analysis, serving as a guideline for future investigations in which genomic structural variations are present.

Of all known airborne diseases in the twenty-first century, coronavirus disease 19 (COVID-19) has the highest infection and death rate. Over the past few decades, animal origin viral diseases, notably those of bats-linked, have increased many folds in humans with cross-species transmissions noted and the ongoing COVID-19 pandemic has emphasized the importance of understanding the evolution of natural hosts in response to viral pathogens. Cross-species transmissions are possible due to the possession of the angiotensin-converting enzyme 2 (ACE2) receptor in animals. ACE2 recognition by SARS-CoV-2 is a critical determinant of the host range, interspecies transmission, and viral pathogenesis. Thus, the phenomenon of breaking the cross-species barrier is mainly associated with mutations in the receptor-binding domain (RBD) of the spike (S) protein that interacts with ACE2. In this review, we raise the issue of cross-species transmission based on sequence alignment of S protein. Based on previous reports and our observations, we can conclude that the occurrence of one of two mutations D614G or Y453F is sufficient for infection of minks by SARS-CoV-2 from humans. Unfortunately, D614G is observed in the world’s most common line of virus B.1.1.7 and the latest SARS-CoV-2 variants B.1.617.1, B.1.617.2, and B.1.617.3 too.

The economic efficiency of mink production is greatly influenced by reproductive performance. Therefore, the objective of this study was to estimate phenotypic and genetic parameters for reproduction traits including total number of kits born (TB), number of live kits at birth (LB), number of live kits at weaning (LW), survival rate at birth (SB), survival rate at weaning (SW), gestation length (GL), average kit weight per litter at birth (AWB), average kit weight per litter at week 3 (AW3), and average kit weight per litter at weaning (AWW) in American mink. Data included records of 3,046 litters collected by the Canadian Centre for Fur Animal Research at Dalhousie Faculty of Agriculture between 2002 and 2016. Significance (P < 0.05) of fixed effects (year, number of matings, color type, age of dam, origin of dam, sex ratio, and number of live kits) and random effects of permanent environment were determined using univariate repeatability models. A significant effect of permanent environment was only found for survival rate traits (P < 0.05). Subsequently, genetic and phenotypic parameters for all traits were estimated by fitting a set of bivariate models using ASREML 4.0. Heritabilities (± SE) were estimated to be 0.07 ± 0.03 for TB, 0.07 ± 0.02 for LB, 0.09 ± 0.04 for LW, 0.13 ± 0.03 for SB, 0.10 ± 0.02 for SW, 0.29 ± 0.03 for GL, 0.28 ± 0.05 for AWB, 0.19 ± 0.04 for AW3, and 0.10 ± 0.04 for AWW. Moderate positive genetic correlation was observed between AWB with SB (0.66 ± 0.10) and SW (0.61 ± 0.13). Furthermore, genetic correlations of LB with SW and AWB were 0.55 ± 0.16 and 0.53 ± 0.18, respectively. On the other hand, negative and moderate genetic correlations were observed between GL and survival rates at birth (-0.43 ± 0.14) and at weaning (-0.37 ± 0.15). These results indicated that selection for higher litter weights at birth can effectively improve survival rate and number of live kits in mink farms. It was suggested to incorporate litter weight traits as a selection criterion to increase maternal ability in mink breeding programs. Unfavorable genetic trends were observed for the studied traits indicating that phenotypic selection with low selection intensity had not been an efficient method to improve them over the last 10 yr. It was recommended to use genetic or genomic evaluation methods for mink selection.