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Laboratory-scale inactivation of African swine fever virus and swine vesicular disease virus in pig slurry.

Two methods were evaluated for the inactivation of African swine fever (ASV) and swine vesicular disease (SVD) viruses in pig slurry: chemical treatment and heat treatment. The addition of NaOH or Ca(OH)2 at different concentration/time combinations at 4 degrees C and 22 degrees C was examined, as was virus stability at different temperature/time combinations. ASF virus (ASFV) was less resistant to both methods than SVD virus (SVDV). In slurry from one source, ASFV was inactivated at 65 degrees C within 1 min, whereas SVDV required at least 2 min at 65 degrees C. However, it was found that thermal inactivation depended on the characteristics of the slurry used. Addition of 1% (w/v) of NaOH or Ca(OH)2 caused the inactivation of ASFV within 150 s at 4 degrees C; 0.5% (w/v) NaOH or Ca(OH)2 required 30 min for inactivation. NaOH or Ca(OH)2 (1% (w/v)) was not effective against SVDV at 22 degrees C after 30 min, and 1.5% (w/v) NaOH or Ca(OH)2 caused inactivation of SVDV at both 4 degrees C and 22 degrees C. At higher chemical concentrations or temperatures, ASFV and SVDV inactivation was faster in slurry than in buffered medium.

African Swine Fever Virus↗

Comparison of precipitin antibodies and virus-neutralizing antibodies to infectious bursal disease virus.

Three hundred twenty-two serum samples from commercial pullets and multiplier breeders were analyzed for agar-gel precipitin (AGP) antibodies and virus-neutralizing (VN) antibodies to infectious bursal disease virus. Two hundred thirty-four of these sera were AGP-positive, and 88 were AGP-negative. The geometric mean of the reciprocal of the VN titers for the AGP-positive sera was 208.7, and 232 (99.1%) had a VN titer of 1:16 or greater. In contrast, the geometric mean of the reciprocal of the VN titers for the AGP-negative sera was 6.1, but 53 (60.2%) had a VN titer ranging from 1:4 to 1:256. When the AGP test was compared with the VN test, the sensitivity and specificity, respectively, of the AGP test were 81.5% and 100%.

Animals↗

Purification, crystallization and X-ray analysis of swine vesicular disease virus.

Swine vesicular disease virus (SVDV) is the etiological agent of swine vesicular disease, a highly contagious disease in pigs, and is related to coxsackie B virus. Crystalline arrays of SVDV can be observed in the cytoplasm of cells 4.5 h after inoculation to porcine kidney cells (IBRS-2 cells). Crystals of the JX/78 strain of SVDV were obtained from virus in two wells of crystallization conditions and present preliminary X-ray data to 3.6 A resolution.

Crystallization↗

A phase II study on the postsurgical management of Stage II malignant melanoma with a Newcastle disease virus oncolysate.

A Newcastle disease virus lysate of malignant melanoma cells was examined for its possible value in delaying the progression of malignant melanoma with palpable regional node disease (Stage II) to disseminated melanoma (Stage III). This Phase II study was carried out in a group of 32 patients following therapeutic lymphadenectomy. The patients were not prospectively randomized. In each patient, the viral oncolysate was administered subcutaneously at regular intervals over 3 years. The cumulated progressions to disseminated disease at 1, 2 and 3 years were 6%, 8% and 12% of the study group, respectively. These experienced losses were considerably lower than in the control group and in similar control groups described by other investigators. The results suggest that an oncolysate prepared with Newcastle disease virus is a helpful adjunct to surgery in the management of Stage II malignant melanoma.

Adolescent↗

Tardive dyskinetic syndrome in rats infected with Borna disease virus.

Tardive Dyskinesia (TD) is a hyperkinetic movement disorder caused by chronic treatment of psychiatric patients with dopamine (DA) receptor blocking drugs (Stacy & Jankovic 1991). Although TD is one of the most important and frequently encountered iatrogenic disorders in clinical medicine, its pathophysiology is poorly understood. We have observed a hyperkinetic movement disorder in rats experimentally infected with a neurotropic RNA virus, Borna disease virus, that may provide important insights into the pathophysiology of TD. Like TD patients, infected rats show prominent orofacial dyskinesias. In keeping with the dopamine (Goetz & Klawans 1982) and anatomic (Fibiger & Lloyd 1984) hypotheses of TD, the Borna disease rat model shows enhanced behavioural sensitivity to DA agonists and selective striatal cell damage. There is also evidence of DA deafferentation and heterogeneous reduction of D2 binding in the caudate-putamen, particularly from sites implicated in oral behaviour. These observations on a virus-induced movement disorder offer novel approaches to TD pathogenesis.

Animals↗

Immunofluorescent detection of double-stranded RNA in cells infected with reovirus, infectious pancreatic necrosis virus, and infectious bursal disease virus.

Urea treatment of ethanol-fixed virus-infected cells exposed nucleic acid antigens for immunofluorescence. Three double-stranded (ds) RNA-containing viruses showed bright fluorescence using antibodies against dsRNA. Three single-stranded RNA-containing viruses showed less intense fluorescence with anti-dsRNA. Four out of five cell lines persistently infected with various RNA-containing viruses showed no dsRNA detectable by immunofluorescence.

Cells, Cultured↗

Borna disease virus in mice: host-specific differences in disease expression.

We developed a mouse model of Borna disease to facilitate immunopathogenesis research by adaptation of Borna disease virus to mice through serial passage in mouse brain tissue. Borna disease virus replication, antibody production, inflammation, and Borna disease expression in several different strains of mice were examined.

Animals↗

[Antigenic structure of the foot-and-mouth disease virus. II. Synthesis of protective peptides from the major immunogenic region of VP1 protein of foot-and-mouth disease virus type A22].

Earlier we found that the immune response and antiviral protection from FMDV can be achieved by immunization with uncoupled FMDV peptides. In a search of approaches to animal protection from FMDV A22 strain we prepared a series of peptides corresponding to the putative antigenic determinants. Synthetic 131-149 and 140-149 sequences afforded 50 to 80% protection, both in the free state and conjugated with keyhole limpet hemocyanin. We believe that the 140-149 segment is so far the smallest peptide capable of eliciting specific antiviral protection without conjugation with a high molecular carrier.

Animals↗

Effects of early infectious bursal disease virus infection on immunity to Newcastle disease in adult chickens.

Experimental infection with infectious bursal disease virus (IBDV) at hatching or at 3 weeks of age in White Leghorn chickens without maternally derived antibodies to IBDV resulted in a depression in the antibody response of chickens to Newcastle disease vaccination (NDV) at 4 weeks of age and increased the susceptibility of those birds to challenge with virulent NDV. Infection of non-IBDV immune chickens with IBDV at hatching, but not at 3 weeks of age, also depressed the antibody response of chickens vaccinated at 18, 30, or 42 weeks of age, but had no effect on the susceptibility of those birds to challenge with virulent NDV. Prior exposure to IBDV did not alter disease resistance afforded a bird by NDV vaccination at 18, 30, or 42 weeks of age. However, IBDV infection at hatching did render chickens that were not vaccinated against ND more susceptible to challenge with virulent NDV at 21, 33, or 45 weeks of age than unvaccinated birds which were not infected with IBDV or unvaccinated chickens infected with IBDV at 3 weeks of age.

Age Factors↗

Influence of Major Histocompatibility Complex (MHC) Diversity on Immune Modulation, Pathogenesis, and Control of Lumpy Skin Disease Virus.

INTRODUCTION: Lumpy Skin Disease Virus (LSDV), a member of the genus Capripoxvirus within the family Poxviridae, is an economically important transboundary viral pathogen affecting cattle and water buffalo. The disease causes severe production losses through decreased milk yield, infertility, hide damage, reduced growth performance, and occasional mortality. The rapid geographic spread of LSDV, together with its vectorborne transmission and emerging recombinant strains, has intensified the need for improved understanding of viral pathogenesis, host immune responses, and effective prevention strategies. In particular, the role of the bovine Major Histocompatibility Complex (BoLA/MHC) in regulating antiviral immunity, disease susceptibility, and vaccine responsiveness has gained increasing scientific attention. METHODS: This review summarises the published literature related to the epidemiology, transmission, structure, pathogenesis, diagnosis, prevention, and control of LSDV, with special emphasis on the immunological and molecular role of bovine MHC molecules. Relevant studies concerning BoLA-mediated antigen presentation, immunoinformaticsbased epitope prediction, vaccine development, antiviral drug repurposing, molecular docking, genomic surveillance, and diagnostic approaches, including PCR- and ELISAbased assays, were critically evaluated. Recent advances in computational biology, molecular virology, and host-pathogen interaction studies were also reviewed. RESULTS: The reviewed studies demonstrate that Lumpy Skin Disease Virus (LSDV) possesses a complex double-stranded DNA genome enabling immune modulation and efficient transmission through arthropod vectors such as mosquitoes, ticks, and biting flies. Disease progression involves systemic viral replication, vascular injury, dermal necrosis, and inflammatory skin lesions. Real-time PCR remains the most sensitive diagnostic method for early detection, while ELISA supports surveillance. Evidence highlights the central role of bovine Major Histocompatibility Complex (BoLA) molecules in antigen presentation and T-cell activation. Computational studies identified promising BoLA-binding epitopes and repurposed antiviral candidates, including ivermectin, theaflavin, canagliflozin, and tepotinib, for future therapeutic development. DISCUSSION: Current evidence indicates that effective LSDV control requires integration of molecular diagnostics, vector management, vaccination, and host immunogenetics. BoLAguided immunoinformatics provides promising opportunities for developing multi-epitope vaccines, although experimental validation remains essential. Similarly, repurposed antiviral candidates require comprehensive in vivo and pharmacological evaluation before clinical application. Future research should focus on elucidating viral immune-evasion mechanisms, validating predicted epitopes, and translating computational findings into practical vaccines and therapeutics for sustainable disease control. CONCLUSION: Lumpy Skin Disease continues to pose a major threat to global cattle health and livestock economies. Advances in molecular diagnostics, genomic surveillance, antiviral drug discovery, and BoLA-guided vaccine design provide promising opportunities for improved disease control. Understanding the interaction between LSDV and the bovine MHC system is essential for developing next-generation vaccines, immunotherapeutics, and precision disease-management strategies. Future research should prioritise experimental validation of predicted epitopes, large-scale vaccine trials, and mechanistic studies on host-virus immune interactions to establish effective and sustainable global control programs for LSDV.

BoLA↗

Molecular epidemiology of two US orbiviruses: bluetongue virus and epizootic hemorrhagic disease virus.

The degree of relatedness between 4 US serotypes (10, 11, 13 and 17) of bluetongue (BT) virus (BTV) were determined by both oligonucleotide fingerprint analyses of double-stranded (ds) RNA as well as tryptic peptide analyses of viral coded polypeptides. Similar studies were undertaken using different alternate isolates of particular serotypes as well as 2 serotypes (1 and 2) of epizootic hemorrhagic disease (EHD) virus (EHDV), a closely related serogroup of orbiviruses. The results indicate that all BT viruses are genetically related to each other and although EHDV-1 and EHDV-2 originated from a common gene pool, the 2 serogroups, EHDV and BTV, are not genetically interactive.

Bluetongue virus↗

Induction of apoptosis in a flounder gill cell line by lymphocystis disease virus infection.

Lymphocystis disease virus (LCDV), a large icosahedral DNA virus classified to the iridovirus family, is the causative agent of lymphocystis, a disease which occurs in marine and freshwater fish species and is characterized by formation of papilloma-like lesions on the surface of the skin. In vitro, LCDV infection causes flounder gill cells, an adherent cell line, to exhibit an obvious cytopathic effect (CPE). In order to test whether apoptosis is responsible for the observed CPE, cells infected with LCDV at a multiplicity of infection (m.o.i.) of 5 PFU per cell were examined at various time intervals for the appearance of apoptotic signs. Nuclear fragmentation, DNA laddering and caspase activation were observed in the infected cells at the time (i.e. 10 days post-infection) when an intensive CPE was observed. These findings demonstrate that LCDV is capable of inducing apoptosis in vitro, which is different from the result of LCDV infection in vivo, and consequently suggest an intricate LCDV-host interaction.

Animals↗

DNA configuration in the core of Marek's disease virus.

Marek's disease virus DNA appears to be wound around a central structure connecting the two inner poles of the capsid. Based on electron micrographs of Marek's disease virions, a diagram of spatial configuration of virus DNA is presented. This diagram may explain the pleomorphic character of the herpesvirus core observed with the electron microscope.

Animals↗

Human infections with Borna disease virus: seroprevalence in patients with chronic diseases and healthy individuals.

Borna disease virus (BDV) is as yet an unclassified infectious agent which causes a neurologic disease in horses and sheep and is transmissible to other animal species. Human sera were tested for BDV-specific antibodies by immunofluorescence and immunoprecipitation. The sera were collected from three thousand subjects in Europe, the USA, and Africa classified by clinical syndromes/infectious diseases, and from healthy controls. In all three continents, positive serum samples were detected which recognized the major BDV antigen of 38/40 KD present in the nuclei of infected cells. In contrast to 2% of seropositives among the normal population, significantly higher prevalences (13-14%) were present among patients with chronic progressive diseases of the brain and the immune system. In children, antibody frequencies were two to four times higher than in adults. The results suggest a latent infection with BDV in humans leading to low antigen expression in healthy subjects and frequent reactivation events in chronically ill patients.

Adult↗