Genome instability is related to disease development and carcinogenesis. DNA lesions are caused by genotoxic compounds but also by the dysregulation of fundamental processes like transcription, DNA replication and mitosis. Recent evidence indicates that impaired expression of RNA-binding proteins results in mitotic aberrations and the formation of transcription-associated RNA-DNA hybrids (R-loops), events strongly associated with DNA injury. We identify the splicing regulator SLU7 as a key mediator of genome stability. SLU7 knockdown results in R-loops formation, DNA damage, cell-cycle arrest and severe mitotic derangements with loss of sister chromatid cohesion (SCC). We define a molecular pathway through which SLU7 keeps in check the generation of truncated forms of the splicing factor SRSF3 (SRp20) (SRSF3-TR). Behaving as dominant negative, or by gain-of-function, SRSF3-TR impair the correct splicing and expression of the splicing regulator SRSF1 (ASF/SF2) and the crucial SCC protein sororin. This unique function of SLU7 was found in cancer cells of different tissue origin and also in the normal mouse liver, demonstrating a conserved and fundamental role of SLU7 in the preservation of genome integrity. Therefore, the dowregulation of SLU7 and the alterations of this pathway that we observe in the cirrhotic liver could be involved in the process of hepatocarcinogenesis.

Animal source foods (ASF) such as dairy, eggs, fish and meat are an important source of high-quality nutrients. Lack of ASF in diets can result in developmental disorders including stunting, anemia, poor cognitive and motor development. ASF are more effective in preventing stunting than other foods and promoting ASF consumption in low- and middle-income countries could help improve health, particularly among pregnant women and young children. Production and consumption of ASF are, however, also associated with potential food safety risks. Strengthening of food control systems, informed by quantitative assessments of the disease burden associated with ASF is necessary to meet global nutrition goals. We present the human disease burden associated with 13 pathogens (bacteria and parasites) in ASF, based on an analysis of global burden of foodborne disease (FBD) estimates of the WHO Foodborne Disease Burden Epidemiology Reference Group (FERG). The FBD burden of these pathogens was combined with estimates of the proportion of disease transmitted by eight main groups of ASF. Uncertainty in all estimates was accounted for by Monte Carlo simulation. In 2010, the global burden of ASF was 168 (95% uncertainty interval (UI 137-219) Disability Adjusted Life Years (DALYs) per 100,000 population, which is approximately 35% of the estimated total burden of FBD. Main pathogens contributing to this burden included non-typhoidal Salmonella enterica, Taenia solium, and Campylobacter spp. The proportion of FBD burden associated with ASF varied considerably between subregions and between countries within subregions. Likewise, the contribution of different pathogens and ASF groups varied strongly between subregions. Pathogens with a localized distribution included T. solium and fishborne trematodes. Pathogens with a global distribution included non-typhoidal S. enterica, Campylobacter spp., Toxoplasma gondii, and Mycobacterium bovis. Control methods exist for many hazards associated with ASF, and their implementation is linked to economic development and effective food safety systems.

A viral haemorrhagic syndrome was induced in 14 pigs by inoculation with an African swine fever (ASF) virus strain of moderate virulence, to determine changes in megakaryocyte (MK) numbers and morphology and thus to assess the role of these cells in the thrombocytopenia characteristic of subacute ASF. The strain tested induced changes in the proportion of different types of MK (typical nucleated MKs, apoptotic MKs and immature MKs); it also caused subcellular lesions over the first 7 days post-inoculation (dpi). At 7 dpi, severe thrombocytopenia was observed. There was a statistically significant increase in apoptotic MK numbers. The MKs showed three stages in the course of the disease: a compensatory stage, represented by cytoplasmic projections, a hypermaturity stage, represented by apoptotic MKs, and a regenerative stage, represented by clusters of immature MKs. These changes, especially the presence of numerous apoptotic MKs, may explain the early and transitory thrombocytopenia detected in subacute ASF. The large number of apoptotic MKs observed may be associated with the accelerated maturation of these cells, resulting from the action of cytokines, or peripheral platelet consumption, or both.

Four and a half years of African Swine Fever (ASF) in population of free-ranging wild boars and domestic pigs revealed a number of novel insights into the disease epidemiology. Until No- vember 20th, 2018, in total 3048 cases in wild boars and 213 outbreaks in domestic pigs have been confirmed. In spite of low contagiosity as well as low rate of ASF spread in wild boars the disease has an enormous socio-economical impact on the production of pigs in Poland. One of the most important aspects which directly influences the dynamics of ASF spread is the unpredictable hu- man activity. Another important factor responsible for continuous ASF spread is fast recovery of wild boar population in spite of efforts taken by hunters. Assuming our scientific opinion ASF seems to be present in wildlife for the incoming few or several years. Therefore, extraordinary measures should be prepared and undertaken to limit the risk of the occurrence of future out- breaks in domestic pigs. One of the most crucial issues is implementation of strict biosecurity measures in all domestic pigs holdings.

Abstract: African swine fever (ASF), a disease of obligatory declaration to the World Organization for Animal Health (OIE), has contributed to poverty and underdevelopment of affected areas. The presence of ASF has been historically neglected in Africa, contributing to its uncontrolled expansion and favouring its spread to continental Europe on at least three occasions, the last one in 2007 through the Republic of Georgia. Since then, African swine fever virus (ASFV) has spread to neighbouring countries, reaching the European Union in 2014, China in the summer of 2018 and spreading through Southeast Asia becoming a global problem. Lack of available vaccines against ASF makes its control even more difficult, representing today the number one threat for the swine industry worldwide and negatively affecting the global commerce equilibrium.

Main body: In this review, we intend to put in perspective the reality of ASF vaccination today, taking into account that investment into ASF vaccine development has been traditionally unattractive, overall since ASF-free areas with large swine industries applied a non-vaccination policy for diseases listed by the OIE. The dramatic situation suffered in Asia and the increasing threat that ASF represents for wealthy countries with large swine industries, has dramatically changed the perspective that both private and public bodies have about ASF vaccinology, although this is controversial. The feasibility of modifying the ASFV genome has led to safe and efficacious experimental recombinant live attenuated viruses (LAVs). The main challenge today will be confirming the safety and efficacy of these technologies in the field, accelerating transfer to the industry for official registration and commercialization. The complexity of ASFV, together with the lack of knowledge about the mechanisms involved in protection and the specific antigens involved in it, requires further investment in research and development. Although far from the efficacy achieved by LAVs, subunit vaccines are the optimal choice for the future. If the world can wait for them or not is a contentious issue.

Conclusion: Despite their inherent disadvantages, LAVs will be the first technology to reach the market, while subunit vaccines will need much further research to become a successful commercial reality.

Keywords: African swine fever (ASF); African swine fever virus (ASFV); Antibodies; Biosafety; Cytotoxic CD8+ T-cells (CTLs); Live attenuated virus (LAV); Protection; Subunit vaccines.

African swine fever (ASF) is a complex, highly lethal, notifiable disease of swine. ASF is wide-spread in sub-Saharan Africa and East European countries and there is presently a great risk of spread to neighboring countries. Since there is no vaccine for ASF virus (ASFV), control is based on rapid and early detection of the disease via surveillance. This approach requires collecting blood samples from large number of animals. Laborious and expensive of itself, this process also presents an additional risk because ASFV is present at high concentrations in the blood. The objective of this study was to initiate studies into the potential use of oral fluid as an alternative to serum for ASF diagnosis, for latter studying its possible use in surveillance and control programs. To this end, oral fluid samples collected at different times post infection from eight pigs experimentally inoculated with an attenuated ASFV were assayed using modified protocols of the two validated serological techniques, the enzyme-immune-liked assay (ELISA) and immunoperoxidase technique (IPT). Antibodies against ASFV were detected in oral fluid samples of all animals from early post infection through the end of the experiment by ELISA and IPT. These results confirmed the presence of ASFV antibodies in swine oral fluids samples, the possibility of an oral fluid-based approach in ASF diagnosis and, potentially in ASF surveillance.

African swine fever (ASF) is a swine disease caused by a large, structurally complex, double-stranded DNA virus, African swine fever virus (ASFV). In domestic pigs, acute infection by highly virulent ASF viruses causes hemorrhagic fever and death. Previous work has suggested that ASFV pathogenesis is primarily mediated by host cytokines produced by infected monocytes and macrophages. To better understand molecular mechanisms mediating virus pathogenesis and immune evasion, we used transcriptome analysis to identify gene expression changes after ASFV infection in ex vivo swine macrophages. Our results suggest that the cytokines of TNF family including FASLG, LTA, LTB, TNF, TNFSF4, TNFSF10, TNFSF13B and TNFSF18 are the major causative cytokine factors in ASF pathogenesis via inducing apoptosis. Other up-regulated proinflammatory cytokines (IL17F and interferons) and down-regulated anti-inflammatory cytokine (IL10) may also significantly contribute to ASF pathogenesis and cause excessive tissue inflammatory responses. The differential expression of genes also indicates that ASFV could evade both the innate and adaptive immune responses by (i) inhibiting MHC Class II antigen processing and presentation, (ii) avoiding CD8+ T effector cells and neutrophil extracellular traps via decreasing expression of neutrophil/CD8+ T effector cell-recruiting chemokines, (iii) suppressing M1 activation of macrophages, (iv) inducing immune suppressive cytokines, and (v) inhibiting the processes of macrophage autophagy and apoptosis. These results provide novel information to further investigate and better understand the mechanism of pathogenesis and immune evasion of this devastating swine disease.

African Swine Fever (ASF) is a viral disease that affects animals of the Suidae family, and soft ticks from the genus Ornithodoros can also be infected by the ASF virus (ASFV). The disease was first described in Africa at the beginning of the twentieth century as an acute disease characterized by high mortality and fatal hemorrhages. ASF has caused outbreaks in numerous countries and it continues to be devastating nowadays for the porcine sector in those countries affected, and a massive threat for those free of the disease. ASF can follow clinical courses from peracute to chronic in domestic pigs (Sus scrofa) depending on a variety of factors, including the immune status of the animals and the virulence of the ASFV strain. The key features of the pathogenesis of the disease in domestic swine are a) a severe lymphoid depletion including lymphopenia and a state of immunodeficiency, and b) hemorrhages. However, African wild swine like bushpigs (Potamochoerus larvatus), red river hogs (Potamochoerus porcus), and warthogs (Phacochoerus africanus) can be infected by ASFV showing no clinical signs of disease and acting as natural reservoir hosts. In this article we review the key features of the gross and microscopic pathology together with a description of the pathogenesis of ASFV infection in domestic pigs following the different clinical courses. The pathogenesis of ASF in wild and domestic swine is also described, what can provide important information for the design of control strategies, such as vaccines.

Keywords: African swine fever; pathogenesis; pathology; swine; virus.

African swine fever virus (ASFV) is spreading throughout Eurasia and there is no vaccine nor treatment available, so the control is based on the implementation of strict sanitary measures. These measures include depopulation of infected and in-contact animals and export restrictions, which can lead to important economic losses, making currently African swine fever (ASF) the greatest threat to the global swine industry. ASF has been endemic on the island of Sardinia since 1978, the longest persistence of anywhere in Eurasia. In Sardinia, eradication programs have failed, in large part due to the lack of farm professionalism, the high density of wild boar and the presence of non-registered domestic pigs (free-ranging pigs). In order to clarify how the virus is transmitted from domestic to wild swine, we examined the interaction between free-ranging pigs and wild boar in an ASF-endemic area of Sardinia. To this end, a field study was carried out on direct and indirect interactions, using monitoring by camera trapping in different areas and risk points. Critical time windows (CTWs) for the virus to survive in the environment (long window) and remain infectious (short window) were estimated, and based on these, the number of indirect interactions were determined. Free-ranging pigs indirectly interacted often with wild boar (long window = 6.47 interactions/day, short window = 1.31 interactions/day) and these interactions (long window) were mainly at water sources. They also directly interacted 0.37 times per day, especially between 14:00 and 21:00 h, which is much higher than for other interspecific interactions observed in Mediterranean scenarios. The highly frequent interactions at this interspecific interface may help explain the more than four-decade-long endemicity of ASF on the island. Supporting that free-ranging pigs can act as a bridge to transmit ASFV between wild boar and registered domestic pigs. This study contributes broadly to improving the knowledge on the estimation of frequencies of direct and indirect interactions between wild and free-ranging domestic swine. As well as supporting the importance of the analysis of interspecific interactions in shared infectious diseases, especially for guiding disease management. Finally, this work illustrates the power of the camera-trapping method for analyzing interspecific interfaces.

The spread of African swine fever virus (ASFV) threatens to reach further parts of Europe. In countries with a large swine production, an outbreak of ASF may result in devastating economic consequences for the swine industry. Simulation models can assist decision makers setting up contingency plans. This creates a need for estimation of parameters. This study presents a new analysis of a previously published study. A full likelihood framework is presented including the impact of model assumptions on the estimated transmission parameters. As animals were only tested every other day, an interpretation was introduced to cover the weighted infectiousness on unobserved days for the individual animals (WIU). Based on our model and the set of assumptions, the within- and between-pen transmission parameters were estimated to β w = 1·05 (95% CI 0·62-1·72), β b = 0·46 (95% CI 0·17-1·00), respectively, and the WIU = 1·00 (95% CI 0-1). Furthermore, we simulated the spread of ASFV within a pig house using a modified SEIR-model to establish the time from infection of one animal until ASFV is detected in the herd. Based on a chosen detection limit of 2·55% equivalent to 10 dead pigs out of 360, the disease would be detected 13-19 days after introduction.

In 2007 African swine fever (ASF) entered Georgia and in the same year the disease entered the Russian Federation. From 2007 to 2012 ASF spread throughout the southern region of the Russian Federation. At the same time several cases of ASF were detected in the central and northern regions of the Russian Federation, forming a northern cluster of outbreaks in 2011. This northern cluster is of concern because of its proximity to mainland Europe. The aim of this study was to use details of recorded ASF outbreaks and human and swine population details to estimate the spatial distribution of ASF risk in the southern region of the European part of the Russian Federation. Our model of ASF risk was comprised of two components. The first was an estimate of ASF suitability scores calculated using maximum entropy methods. The second was an estimate of ASF risk as a function of Euclidean distance from index cases. An exponential distribution fitted to a frequency histogram of the Euclidean distance between consecutive ASF cases had a mean value of 156 km, a distance greater than the surveillance zone radius of 100-150 km stated in the ASF control regulations for the Russian Federation. We show that the spatial and temporal risk of ASF expansion is related to the suitability of the area of potential expansion, which is in turn a function of socio-economic and geographic variables. We propose that the methodology presented in this paper provides a useful tool to optimize surveillance for ASF in affected areas.

Serine/arginine-rich splicing factor 1 (SRSF1), previously designated SF2/ASF, belongs to a family of SR proteins that regulate constitutive and alternative splicing. SRSF1 expression is increased in tumors from several tissues and elicits changes in key target genes involved in tumor genesis. Several protein kinases phosphorylate SRSF1, which regulates its localization and function. It is previously reported that protein kinase A (PKA) phosphorylates SRSF1, but the importance of this modification is not well characterized. Here, we show that PKA phosphorylates SRSF1 on serine 119 in vitro. Phosphorylation of SRSF1 on this site enhanced the RNA binding capacity of SRSF1 in vivo and reduced the protein's capacity to activate splicing of the Minx transcript in vitro. We also confirm an interaction between SRSF1 and PKA Cα1 and demonstrate that this interaction is not dependent on serine 119 phosphorylation but requires active PKA Cα1. We conclude that PKA phosphorylation of SRSF1 at serine 119 regulates SFRS1-dependent RNA binding and processing but not its interaction with PKA.

Two indirect, sandwich ELISAs are described for use in African swine fever (ASF) diagnosis. One assay uses polyclonal serum raised in rabbits and guinea pigs against the cytoplasmic soluble ASF virus protein and the second, a combination of monoclonal antibody raised against the VP73 protein and rabbit polyclonal serum. Both assays have been shown to detect antigen of representative field strains of phylogenetically distinct groupings of ASF virus but the ELISA, which utilises polyclonal antisera was slightly more sensitive than that using the monoclonal antibody.

Classical approaches to African swine fever virus (ASFV) vaccine development have not been successful; inactivated virus does not provide protection and use of live attenuated viruses generated by passage in tissue culture had a poor safety profile. Current African swine fever (ASF) vaccine research focuses on the development of modified live viruses by targeted gene deletion or subunit vaccines. The latter approach would be differentiation of vaccinated from infected animals (DIVA)-compliant, but information on which viral proteins to include in a subunit vaccine is lacking. Our previous work used DNA-prime/vaccinia-virus boost to screen 40 ASFV genes for immunogenicity, however this immunization regime did not protect animals after challenge. Here we describe the induction of both antigen and ASFV-specific antibody and cellular immune responses by different viral-vectored pools of antigens selected based on their immunogenicity in pigs. Immunization with one of these pools, comprising eight viral-vectored ASFV genes, protected 100% of pigs from fatal disease after challenge with a normally lethal dose of virulent ASFV. This data provide the basis for the further development of a subunit vaccine against this devastating disease.

Keywords: African swine fever virus; adenovirus; modified vaccinia Ankara (MVA); pathology; vaccine; viral-vector.

Following short immunization protocols, naturally attenuated African swine fever virus (ASFV) isolate OURT88/3 and deletion mutant BeninΔMGF have previously been shown to induce high percentage of protection in domestic pigs against challenge with virulent virus. Results obtained in the present study showed that a single intramuscular immunization of domestic pigs with OURT88/3 or BeninΔMGF followed by a challenge with virulent Benin 97/1 isolate at day 130 post-immunisation did not trigger the necessary mechanisms to generate immunological memory able to induce long-term protection against disease. All pigs developed acute forms of ASF. IFNγ producing cells peaked at day 24 post-immunisation, declining thereafter. Surprisingly, levels of T regulatory cells (Tregs) and IL-10 were elevated at the end of the experiment suggesting that regulatory components of the immune system may inhibit effective protection.Importance. Duration of immunity for any vaccine candidate is crucial. In the case of African swine fever virus vaccine candidates, this issue has received little attention. Attenuated viruses have been proven protective following short immunization protocols in which pigs were challenged a few weeks after the first immunization. Here, duration of immunity and immune responses induced over a duration of 130 days were studied during pre-challenge and after challenge of pigs immunised with the naturally attenuated isolate OURT88/3 and an attenuated gene-deleted isolate BeninΔMGF. After a single intramuscular immunization of domestic pigs with the OURT88/3 isolate o BeninΔMGF virus, animals were not protected against challenge with virulent Benin 97/1 ASFV genotype I isolate at day 130 post-immunization. Levels of T regulatory cells and IL-10 were elevated at the end of the experiment, suggesting that regulatory components of the immune system may inhibit effective protection.

Antibody neutralization of African swine fever (ASF) virus measured by a plaque reduction assay presents frequent difficulties because of the absence or delay in plaque formation by many strains, especially low-passage viruses. To overcome this problem, a new ASF virus neutralization test has been developed. The new test consists of a conventional plaque reduction assay in which the viral plaques are detected by expression of marker genes. For the development of this neutralization assay 4 mutant viruses were generated by homologous recombination, containing beta-galactosidase or beta-glucuronidase reporter genes inserted into the thymidine kinase locus of the viral genome. These recombinant viruses have the following advantages with respect to parental viruses: (1) the neutralization assay takes less than a third of the time needed using non-recombinant viruses; (2) the small plaques can be detected more accurately by color contrast; and (3) the neutralization-resistant virus clones can be recovered easily post-plaque counting. Additionally, these recombinant viruses permit differentiation by chromogenic staining of individual infected pig macrophages, the natural host cell for ASF virus, facilitating neutralization assays in these primary cultures as described in cell lines.

African swine fever virus (ASFV) is a macrophage-tropic virus responsible for ASF, a transboundary disease that threatens swine production world-wide. Since there are no vaccines available to control ASF after an outbreak, obtaining an understanding of the virus-host interaction is important for developing new intervention strategies. In this study, a whole transcriptomic RNA-Seq method was used to characterize differentially expressed genes in pigs infected with a low pathogenic ASFV isolate, OUR T88/3 (OURT), or the highly pathogenic Georgia 2007/1 (GRG). After infection, pigs infected with OURT showed no or few clinical signs; whereas, GRG produced clinical signs consistent with acute ASF. RNA-Seq detected the expression of ASFV genes from the whole blood of the GRG, but not the OURT pigs, consistent with the pathotypes of these strains and the replication of GRG in circulating monocytes. Even though GRG and OURT possess different pathogenic properties, there was significant overlap in the most upregulated host genes. A small number of differentially expressed microRNAs were also detected in GRG and OURT pigs. These data confirm previous studies describing the response of macrophages and lymphocytes to ASFV infection, as well as reveal unique gene pathways upregulated in response to infection with GRG.

The soft tick Ornithodoros puertoricensis Fox has been found on the Caribbean island of Hispaniola (Haiti and the Dominican Republic) where African swine fever (ASF) was endemic from 1978 to 1984. To evaluate the vector potential of O. puertoricensis for African swine fever virus (ASFV), second-instar nymphs were experimentally infected by feeding on a viremic pig that was infected with the Dominican Republic isolate (DR-II) of ASFV. Subsequent infection rates and mean virus titers for individually triturated ticks were: second-instar nymph (95.4%, 10(4.38 +/- 0.85)), third-instar nymph (48.9%, 10(4.59 +/- 0.61)), male (46.7%, 10(4.36 +/- 0.61)), and female (35.3%, 10(4.38 +/- 1.09)). Infected ticks transmitted ASFV to susceptible pigs by bite 23, 85, 126, 160, 182, and 239 d after the infective blood meal. These findings show that ASFV is passed transstadially among O. puertoricensis and that O. puertoricensis can be an efficient vector of African swine fever virus.

BACKGROUND

Alternative splicing factor (ASF)-regulated alternative splicing of calcium/calmodulin-dependent protein kinase IIδ (CaMKIIδ) plays an important role in pathologic cardiac remodeling. ASF can be phosphorylated by dual-specificity tyrosine phosphorylation-regulated kinase 1A (Dyrk1A). This study aimed to investigate the possible involvement of the Dyrk1A-ASF-CaMKIIδ signaling pathway in the progression of myocardial infarction (MI)-induced heart failure (HF).

RESULTS

MI in rats was induced by means of left anterior descending coronary artery ligation. Seven weeks after MI, the increase in left ventricular internal diameter at end-diastole (LVIDd), and the decrease in both ejection fraction (EF) and fractional shortening (FS) indicated that MI rats had developed HF. Quantitative real time reverse-transcription polymerase chain reaction indicated the dysregulation of CaMKIIδ alternative splicing, ie, up-regulation of CaMKIIδA and CaMKIIδC and down-regulation of CaMKIIδB in the hearts of HF rats. Electrophoresis and immunostaining revealed that HF activated the phosphorylation of ASF and affected its subcellular localization. Western blot analysis demonstrated a significant elevation in the activity and expression of Dyrk1A in HF rats. Inversely, treatment of MI-induced HF rats with Dyrk1A inhibitor, either harmine or EGCG, improved the symptoms of HF, reversed the molecular changes of Dyrk1A and ASF, and regulated alternative splicing of CaMKIIδ in HF rats.

CONCLUSIONS

Enhanced activation of Dyrk1A-ASF-CaMKIIδ signaling pathway may underlie the mechanisms of HF after MI, and Dyrk1A inhibition may contribute to inactivation of this pathway and thereby retard the progression of MI-induced HF.

An outbreak of African swine fever (ASF) was first detected in December 1989 in the southern region of Malawi. During 1990 the outbreak reached epidemic proportions: by August 1990, over 31,000 pigs (45%) from a population of 70,000 in the affected areas had died or been slaughtered. In affected villages this accounted for 83% of the pigs present. The outbreak probably originated in the central region of Malawi, where ASF is enzootic. Virus isolates from the southern and central region outbreaks in 1989-1990 were indistinguishable using DNA restriction fragment pattern analysis. The rapid spread of the disease and the difficulty experienced in halting this spread are discussed. Important factors included the type of pig husbandry (mainly scavenging without penning) and the fact that veterinary field staff lacked the mobility to ensure the observance of restrictions. New initiatives will be required--in particular, raising public awareness and developing community participation--if ASF is to be controlled in the future.

Observations in witnessed Sudden Unexpected Death in Epilepsy (SUDEP) suggest that a fatal breakdown of the central autonomic control could play a major role in SUDEP. A previous MR study found volume losses in the mesencephalon in focal epilepsy that were more severe and extended into the lower brainstem in two patients who later died of SUDEP. The aims of this study were to demonstrate an association (1) between brainstem volume loss and impaired autonomic control (reduced heart rate variability [HRV]); (2) between brainstem damage and time to SUDEP in patients who later died of SUDEP. Two populations were studied: (1) Autonomic system function population (ASF, 18 patients with focal epilepsy, 11 controls) with HRV measurements and standardized 3 T MR exams. (2) SUDEP population (26 SUDEP epilepsy patients) with clinical MRI 1-10 years before SUDEP. Deformation-based morphometry of the brainstem was used to generate profile similarity maps from the resulting Jacobian determinant maps that were further characterized by graph analysis to identify regions with excessive expansion indicating significant volume loss or atrophy. The total number of regions with excessive expansion in ASF was negatively correlated with HRV (r = -.37, p = .03), excessive volume loss in periaqueductal gray/medulla oblongata autonomic nuclei explained most of the HRV associated variation (r/r2 = -.82/.67, p < .001). The total number of regions with excessive expansion in SUDEP was negatively correlated with time to SUDEP (r = -.39, p = .03), excessive volume loss in the raphe/medulla oblongata at the obex level explained most of the variation of the time between MRI to SUDEP (r/r2 = -.60/.35,p = .001). Epilepsy is associated with brainstem atrophy that impairs autonomic control and can increase the risk for SUDEP if it expands into the mesencephalon.

African swine fever remains the greatest limitation to the development of the pig industry in Africa, and parts of Asia and Europe. It is especially important in West and Central African countries where the disease has become endemic. Biosecurity is the implementation of a set of measures that reduce the risk of infection through segregation, cleaning and disinfection. Using a 122-sow piggery unit, a financial model and costing were used to estimate the economic benefits of effective biosecurity against African swine fever. The outcomes suggest that pig production is a profitable venture that can generate a profit of approximately US$109,637.40 per annum and that an outbreak of African swine fever (ASF) has the potential to cause losses of up to US$910,836.70 in a single year. The implementation of biosecurity and its effective monitoring can prevent losses owing to ASF and is calculated to give a benefit-cost ratio of 29. A full implementation of biosecurity will result in a 9.70% reduction in total annual profit, but is justified in view of the substantial costs incurred in the event of an ASF outbreak. Biosecurity implementation is robust and capable of withstanding changes in input costs including moderate feed price increases, higher management costs and marginal reductions in total outputs. It is concluded that biosecurity is a key to successful pig production in an endemic situation.

A study was undertaken between September 2014 and December 2014 to assess the perceptions of smallholder pig value chain actors of the risks and practices associated with the spread of African swine fever (ASF) disease within the pig value chains. Data was collected from 136 value chain actors and 36 key informants through 17 group discussions and two key informant interview (KII) sessions respectively using Participatory Rural Appraisal (PRA) tools. Results from this study revealed that according to value chain actors and stakeholders, the transporting, slaughtering, and collecting/bulking nodes represent the highest risk, followed by the inputs and services (feeds and drugs) supply nodes. The processing, whole sale and consumption nodes represented the lowest risk. Value chain actors are aware of the disease and its consequences to the pig industry, however biosecurity measures are poorly implemented at all nodes. As for the causes, value chain actors pointed to several factors, such as inadequate knowledge of mechanisms for the spread of the disease, poor enforcement of regulations on disease control, and low capacities of actors to implement biosecurity measures, amongst others. Although traders, butchers and veterinary practitioners accepted that they played an important role in the spread of the virus, they did not perceive themselves as key actors in the control of the disease; instead, they believed that only farmers should adopt biosecurity measures on their farms because they keep the pigs for a longer period. Most of the recommendations given by the value chain actors for controlling and preventing ASF disease were short term, and targeted mainly pig producers. These recommendations included: the establishment of live pig collection centres so that traders and brokers do not have to directly access pig farms, capacity building of value chain actors on application of biosecurity, enactment and enforcement of by-laws on live pig movements and establishment of operational outbreak reporting mechanism at district level. Long term recommendations included the development of a vaccine, as well as pen-side diagnostic tests. This study suggests that interventions to control ASF disease through application of biosecurity measures should target all value chain nodes, while putting more emphasis on post-farm nodes especially the trading.

African swine fever (ASF) is a devastating disease, which is causing huge economic losses in China. Therefore, it is urgent to provide a rapid, highly specific and sensitive diagnostic method for the detection of African swine fever virus (ASFV), the ASF infectious agent. In this study, a novel quantitative real-time polymerase chain reaction (qPCR) assay with lyophilized powder reagents (LPR), targeting the major structural protein p72 gene, was established for the detection of ASFV. This assay had many advantages, such as saving time and money, good sensitivity and repeatability. The sensitivity of this assay was 100 copies/μl of ASFV plasmid templates, and the assay showed 10-fold greater sensitivity than a qPCR assay recommended by OIE. Furthermore, specificity analysis showed that the qPCR with the LPR for ASFV had no cross-reactivity with other important swine pathogens. In clinical diagnoses of 218 blood samples of domestic pigs in China, the positive rate of the diagnosis of ASFV by qPCR with the LPR and commercial kit reached 80.73% (176/218) and 76.61% (167/218), respectively. The coincidence rate between the two assays is 92.20% (201/218), and kappa value is 0.768 (P < 0.0001) by SPSS analysis. The overall agreement between the two assays was 95.87% (209/218). Further Pearson correlation and linear regression analysis showed a significant correlation between the two assays with an R² value of 0.9438. The entire procedure, from specimen processing to result reporting, can be completed within 2 hours. Our results demonstrated the qPCR-LPR assay is a good laboratory diagnostic tool for sensitive and efficient detection of ASFV. This article is protected by copyright. All rights reserved.