Rotavirus A (RVA) is an important pathogen for porcine health. In comparison to humans, RVA in domestic animals and especially in wildlife is under researched. Therefore, the aim of the present study was to investigate the prevalence, genetic diversity, molecular epidemiology and interspecies transmission of RVA in domestic pigs and wild boars. During the three consecutive RVA seasons (2018–2021) we collected 445 and 441 samples from domestic pigs and wild boars, respectively. Samples were tested by real-time RT-PCR, and RVA-positive samples were genotyped in VP7 and VP4 segments. Our results report an RVA prevalence of 49.9% in domestic pigs and 9.3% in wild boars. Outstanding RVA genetic diversity was observed in VP7 and VP4 segments, especially in domestic pigs exhibiting a striking 23 different RVA combinations (G5P[13] and G9P[23] prevailed). Interspecies transmission events were numerous between domestic pigs and wild boars, sharing G3, G5, G6, G9, G11 and P[13] genotypes. Furthermore, our data indicate that such transmission events involved even bovines (G6, P[11]) and, intriguingly, humans (G1P[8]). This study contributes to the basic knowledge that may be considered important for vaccine development and introduction, as a valuable and currently missing tool for efficient pig health management in the EU.

Rotaviruses (RV), especially Rotavirus A (RVA), are globally recognized as pathogens causing neonatal diarrhea, but they also affect intensive animal farming. However, the knowledge on their significance in wildlife is rather limited. The aim of the study was to unveil the prevalence, molecular epidemiology, and genetic diversity of RVA strains circulating in the red fox (Vulpes vulpes) population in Croatia. From 2018 to 2019, 370 fecal samples from fox carcasses hunted for rabies monitoring were collected. All samples were first tested using a VP2 real-time RT-PCR; in the subsequent course, positives were subjected to VP7 and VP4 genotyping. The results revealed an RVA prevalence of 14.9%, while the circulating RVA strains showed a remarkable genetic diversity in terms of 11 G and nine P genotypes, among which one G and three P were tentatively identified as novel. In total, eight genotype combinations were detected: G8P[14], G9P[3], G9P[23], G10P[11], G10P[3], G11P[13], G15P[21], and G?P[?]. The results suggest a complex background of previous interspecies transmission events, shedding new light on the potential influence of foxes in RVA epidemiology. Their role as potential reservoirs of broad range of RVA genotypes, usually considered typical solely of domestic animals and humans, cannot be dismissed.

The intricate interplay between somatic mutations and copy number alterations critically influences tumour evolution and patient prognosis. Traditional genomic studies often overlook this interplay by analysing these two biomarker types in isolation. Leveraging an innovative computational model capable of detecting allele-specific copy number alterations from clinical targeted panels without matched normal, we conducted a comprehensive analysis of over 500,000 mutations across 60,000 clinical samples spanning 39 cancer types. Our findings uncovered 11 genes and 6 hotspots exhibiting recurrent tumour-specific patterns of co-existing mutations and copy-number alterations across 17 tumours. By stratifying more than 24,000 patients based on these composite genotypes across multiple oncogenes and tumour suppressor genes, we identified 66 groups with distinct prognostic significance, 25% more than using a standard mutation-centric stratification. Notably, 7 groups displayed a heightened propensity for metastasis, while 16 were associated with site-specific patterns of metastatic dissemination. This augmented insight into genomic drivers enhances our understanding of cancer progression and metastasis, holding the potential to significantly foster biomarker discovery. Statement of significance By leveraging large datasets and new computational modelling, this study demonstrates the critical interplay between somatic mutations and copy number alterations in driving patient prognosis, tumour progression and metastatic tropism. This work implies a shift towards a more integrative and comprehensive approach in clinical sequencing, with significant implications for biomarker discovery and target identification.