Taken together, these data highlighted the potentials of lncRNA as targets for antiviral therapy and provided some novel knowledge of the mechanisms underlying the host interaction with PRV-II. To improve the innate and adaptive immune responses elicited by a killed/inactivated swine influenza virus antigen (KAg)-loaded chitosan nanoparticles (CS NPs-KAg), we used the adjuvant, poly(IC). The formulated CS NPs-KAg and CS NPs-poly(IC) had a net surface charge of +30.7 mV and +25.1 mV, respectively. The CS NPs-KAg was coadministered with CS NPs-poly(IC) (chitosan nanovaccine) as intranasal mist. Vaccinations enhanced homologous (H1N2-OH10) and heterologous (H1N1-OH7) hemagglutination inhibition (HI) titers in both vaccinated and virus-challenged animals compared to the control soluble poly(IC) vaccinated pigs. In addition, the chitosan nanovaccine induced the proliferation of antigen-specific IFNγ secreting T-helper/memory and γδ T cells compared to control poly(IC) group; and an increased Th1 (IFNγ, IL-6 and IL-2) and Th2 (IL-10 and IL-13) cytokines mRNA expression in the tracheobronchial lymph nodes compared to lymphoid tissues obtained from pigs given commercial influenza vaccine. The virus load in nasal passages and microscopic lung lesions were partially reduced by both chitosan nanovaccine and commercial vaccine. The HA gene homology between the vaccine and challenge viruses indicated that the chitosan nanovaccine induced a cross-protective immune response. In conclusion, coadministration of CS NPs-poly(IC) with CS NPs-KAg augmented the cross-reactive specific HI titers and the cell-mediated immune responses in pigs.  https://www.selleckchem.com/products/chir-98014.html  Reticuloendotheliosis virus (REV) infection of multiple avian species can lead to a number of diseases such as runting syndrome, immunosuppression and oncogenesis, causing major economic losses. MicroRNAs play important roles in post-transcriptional regulation, effectively inhibiting protein synthesis, and participating in many biological processes in cells, including proliferation, differentiation, apoptosis, lipometabolism, virus infection and replication, and tumorigenesis. Based on our previous high-throughput sequencing results, we explore the regulatory mechanisms of microRNA-155(miR-155) in chicken embryo fibroblasts (CEFs) in response to REV infection. Our results revealed expression of miR-155 in CEFs after REV infection upregulated in a time- and dose-dependent manner, indicating miR-155 plays a role in REV infection in CEFs indeed. After transfected with miR-155-mimic and miR-155-inhibitor, we found overexpression of miR-155 targeted caspase-6 and FOXO3a to inhibit apoptosis and accelerate cell cycle, thus improving viability of REV-infected CEFs. This result also verified the protective role of miR-155 in the viability of CEFs in the presence of REV. Knockdown of miR-155 also supported these above conclusions. Our findings uncover a new mechanism of REV pathogenesis in CEFs, and also provide a theoretical basis for uncovering new effective treatment and prevention methods for RE based on miR-155. African swine fever virus can be transmitted through direct contact with infected animals and their excretions, or indirect contact with contaminated fomites. Risk assessment of the disease spreading requires quantitative knowledge about time and conditions needed for its inactivation in various material of pig origin. In this study we aimed to assess ASFV stability in naturally contaminated tissues during storage in selected environmental conditions. Virus half-life (T ½) and decimal reduction rate (D-value) were determined for temperatures relevant for freezing, chilling and ambient storage. A nonlinear regression model was developed to predict T ½ for temperatures between -20 °C and +23 °C. The half-life of the infectious ASFV in tissues ranged from 31.95 days at -20 °C to 0.38 days at +23 °C, with estimated D-values between 106.12-1.27 days, respectively. In order to assess the influence of environmental conditions on the rate of ASFV inactivation in decomposing tissue, viral half-life was evaluated at +4 °C and +23 °C in tissues stored within various matrices, mimicking possible natural conditions. Water, soil and leaf litter presence induced significantly faster ASFV inactivation. Straw, hay and grain provided stable conditions and prolonged virus viability for a considerable amount of time. In contrast to viable virus reduction over time, no change in ASFV DNA concentration was detected by real-time PCR. Based on estimated half-life values, the investigated tissues are predicted to remain infectious for 353-713 days at -20 °C, 35-136 days at +4 °C, and from 9 to 17 days at +23 °C. These data provide valuable information for the ASF preventive measures improvement. We aimed to identify the dynamics of the within-herd prevalence of Mycoplasma (M.) bovis intramammary infection (IMI) in four dairy herds, estimate prevalence of M. bovis in colostrum and clinical mastitis cases and compare M. bovis strains from calves' respiratory and cow clinical mastitis samples. Within a six-month study period, cow composite milk samples (CMS) were collected three times during routine milk recording, first milking colostrum samples from all calving cows and udder quarter milk samples from clinical mastitis cases. Calf respiratory samples were collected from calves with respiratory disease. Pooled milk samples were analysed for M. bovis with the Mastitis 4B polymerase chain reaction (PCR) test kit (DNA Diagnostic A/S). Prevalence estimates were calculated with Bayesian framework in R statistical programme. cg-MLST was used for M. bovis genotyping. In Herd I and II first testing M. bovis IMI within-herd prevalence (95 % credibility interval (CI)) was 4.7 % (2.9; 6.8) and 3.4 % (2.3; 4.6), changing to 1.0 % (0.1; 1.7) and 0.8 % (0.1; 1.4) in Herd I and 0.4 % (0.0; 0.7) in Herd II at the next samplings. In Herd III and IV first testing M. bovis IMI within-herd prevalence was 12.3 % (9.7; 15.2) and 7.8 % (6.2; 9.5), changing to 4.6 % (3.0; 6.4) and 3.2 % (1.9; 4.8) in Herd III and to 2.8 % (1.9; 3.8) and 4.9 % (3.6; 6.4) in Herd IV at the next samplings. The estimated prevalence of M. bovis in colostrum ranged between 1.7 % (0.2; 2.8) and 4.7 % (2.7; 7.1) and in clinical mastitis cases between 3.7 % (1.7; 6.4) and 11.0 % (7.5; 15.2) in the study herds. M. bovis strains isolated from cows and calves clustered within herds indicating possible transmission of M. bovis between dairy cows and calves. Prevalence of M. bovis in colostrum and clinical mastitis cases as well as the within-herd prevalence of M. bovis IMI was low in endemically infected dairy herds.