Porcine reproductive and respiratory syndrome: characteristic features of the infected fetus

Pregnant gilts were infected at 90 days of gestation with porcine reproductive and respiratory virus (PRRSV) isolate SD-23983. Fetuses recovered between 109 and 112 days of gestation were analyzed for the presence of PRRSV. The results showed that not all fetuses were infected, and that infected fetuses tended to be clustered within the uterine horns, suggesting that virus is spread from fetus to fetus. Even though affected litters exhibited different degrees of gross pathology, the presence of an anatomical abnormality was not an identifier of an infected fetus. Analysis of virus replication in individual tissues identified the thymus as the principal site of PRRSV replication. The results show that PRRSV infection in the developing fetus follows a unique course and that PRRSVinduced alterations may be the result of the effect of PRRSV on maternal tissues. These factors need to be taken into consideration when diagnosing PRRSV infection as the cause for aborted and stillborn fetuses.; Swine Day, 2005, Kansas State University, Manhattan, KS, 200

Animal Arterivirus Infections

No abstract

Genetic parameters and genomic regions associated with piglet response to vaccination for porcine reproductive and respiratory syndrome (PRRS) virus and co-infection with PRRS virus and porcine circovirus type 2b (PCV2b)

Citation: Dunkelberger, J. R., Serao, N. V. L., Kerrigan, M. A., Lunney, J. K., Rowland, R. R. R., & Dekkers, J. C. M. (2016). Genetic parameters and genomic regions associated with piglet response to vaccination for porcine reproductive and respiratory syndrome (PRRS) virus and co-infection with PRRS virus and porcine circovirus type 2b (PCV2b). Journal of Animal Science, 94, 52-53. doi:10.2527/msasas2016-112Objectives of this research were to estimate genetic parameters and to identify genomic regions associated with PRRS viral load (VL), PCV2b VL, and average daily gain (ADG) in nursery pigs vaccinated or non-vaccinated for PRRS virus (PRRSV), followed by co-infection with PRRSV and PCV2b. Data used included 396 commercial crossbred pigs from two PRRS Host Genetics Consortium trials, all from the same genetic supplier. Pigs were sent to Kansas State University after weaning and randomly sorted into two rooms. All pigs in one room were vaccinated for PRRS, and 28 d later, pigs in both rooms were co-infected with PRRSV and PCV2b, followed for 42 d, and genotyped using the 80K BeadChip. PRRS VL after vaccination and post co-infection and PCV2b VL were calculated as area under the curve of serum viremia from ?28 to 0, 0 to 21, and 0 to 42 d post co-infection, respectively. Genetic parameters were estimated by fitting multivariate animal models in ASReml4 with litter and pen (trial) as additional random effects. Trait-specific fixed effects of trial and weight and age at vaccination were also fitted. Genome-wide association (GWA) studies were performed by fitting SNPs as fixed effects one at a time in bivariate animal models for the non-vaccinated (Non-Vx) and vaccinated (Vx) groups for each trait. Heritability estimates following vaccination were 0.31, 0.07, and 0.10 for ADG Non-Vx, ADG Vx, and PRRS Vx, respectively. During the co-infection period, heritability estimates were slightly higher at 0.53, 0.57, 0.56, 0.20, 0.18, and 0.15 for ADG Non-Vx, ADG Vx, PRRS Non-Vx, PRRS Vx, PCV2b Non-Vx, and PCV2b Vx, respectively. Standard errors ranged from 0.14 to 0.22. A strong, positive genetic correlation (0.95 ± 1.01) was observed for PRRS VL post-vaccination with PRRS VL Non-Vx. Unique genomic regions were identified between Vx and Non-Vx pigs for each trait, the most significant of which was identified for PCV2b VL and located near the major histocompatibility complex, an important region for response to infection. The chromosome 4 region, which has been associated with VL following PRRSV-only infection, was associated with PRRS VL Non-Vx but not PRRS Vx or PRRS VL post-vaccination. Together, these results suggest that selection for improved performance under co-infection of PRRS and PCV2b is possible. Additionally, identification of unique genomic regions between Vx and Non-Vx pigs may enable selection of pigs with better response to vaccination. This research was supported by USDA-NIFA grants 2012–38420–19286 and 2013–68004–20362

Animal Arterivirus Infections

No abstract

Bovine leukemia virus non-productive infection of human mammary epithelial cells (MCF10A)

Bovine leukemia virus (BLV) is a retrovirus that causes lymphosarcoma in cattle. Some researchers suggestthat BLV could be related to breast cancer development, however, evidence that the virus can infect thehuman counterpart is lacking. For that reason, the objective of this study was to infect in vitro a humanmammary epithelial cell line (MCF10A) with BLV. The results suggest that the infection is non-productive,since only a fragment of the viral gene pol was detected in the cellular DNA. These results are consistentwith previous studies, where fragments of different BLV genes were found in human mammary tissue.Future studies should investigate whether this non-productive infection can be associated with human breastcancer.Fil: Martinez Cuesta, Lucia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tandil. Centro de Investigación Veterinaria de Tandil. Universidad Nacional del Centro de la Provincia de Buenos Aires. Centro de Investigación Veterinaria de Tandil. Provincia de Buenos Aires. Gobernación. Comision de Investigaciones Científicas. Centro de Investigación Veterinaria de Tandil; ArgentinaFil: Lendez, Pamela Anahí. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tandil. Centro de Investigación Veterinaria de Tandil. Universidad Nacional del Centro de la Provincia de Buenos Aires. Centro de Investigación Veterinaria de Tandil. Provincia de Buenos Aires. Gobernación. Comision de Investigaciones Científicas. Centro de Investigación Veterinaria de Tandil; ArgentinaFil: Sheahan, Maureen A.. Kansas State University; Estados UnidosFil: Rowland, Raymond R. R.. Kansas State University; Estados UnidosFil: Nieto Farías, María Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tandil. Centro de Investigación Veterinaria de Tandil. Universidad Nacional del Centro de la Provincia de Buenos Aires. Centro de Investigación Veterinaria de Tandil. Provincia de Buenos Aires. Gobernación. Comision de Investigaciones Científicas. Centro de Investigación Veterinaria de Tandil; ArgentinaFil: Dolcini, Guillermina Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tandil. Centro de Investigación Veterinaria de Tandil. Universidad Nacional del Centro de la Provincia de Buenos Aires. Centro de Investigación Veterinaria de Tandil. Provincia de Buenos Aires. Gobernación. Comision de Investigaciones Científicas. Centro de Investigación Veterinaria de Tandil; ArgentinaFil: Ceriani, Maria Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tandil. Centro de Investigación Veterinaria de Tandil. Universidad Nacional del Centro de la Provincia de Buenos Aires. Centro de Investigación Veterinaria de Tandil. Provincia de Buenos Aires. Gobernación. Comision de Investigaciones Científicas. Centro de Investigación Veterinaria de Tandil; Argentin

Reprogramming viral immune evasion for a rational design of next-generation vaccines for RNA viruses

Type I interferons (IFNs-α/β) are antiviral cytokines that constitute the innate immunity of hosts to fight against viral infections. Recent studies, however, have revealed the pleiotropic functions of IFNs, in addition to their antiviral activities, for the priming of activation and maturation of adaptive immunity. In turn, many viruses have developed various strategies to counteract the IFN response and to evade the host immune system for their benefits. The inefficient innate immunity and delayed adaptive response fail to clear of invading viruses and negatively affect the efficacy of vaccines. A better understanding of evasion strategies will provide opportunities to revert the viral IFN antagonism. Furthermore, IFN antagonism-deficient viruses can be generated by reverse genetics technology. Such viruses can potentially serve as next-generation vaccines that can induce effective and broad-spectrum responses for both innate and adaptive immunities for various pathogens. This review describes the recent advances in developing IFN antagonism-deficient viruses, their immune evasion and attenuated phenotypes in natural host animal species, and future potential as veterinary vaccines

Effect of Bovine leukemia virus on bovine mammary epithelial cells

Bovine leukemia virus (BLV) is a retrovirus that infects cattle and is associated with an increase in secondary infections. The objective of this study was to analyze the effect of BLV infection on cell viability, apoptosis and morphology of a bovine mammary epithelial cell line (MAC-T), as well as Toll like receptors (TLR) and cytokine mRNA expression. Our findings show that BLV infection causes late syncytium formation, a decrease in cell viability, downregulation of the anti-apoptotic gene Bcl-2, and an increase in TLR9 mRNA expression. Moreover, we analyzed how this stably infected cell line respond to the exposure to Staphylococcus aureus (S. aureus), a pathogen known to cause chronic mastitis. In the presence of S. aureus, MAC-T BLV cells had decreased viability and decreased Bcl-2 and TLR2 mRNA expression. The results suggest that mammary epithelial cells infected with BLV have altered the apoptotic and immune pathways, probably affecting their response to bacteria and favoring the development of mastitis.Fil: Martinez Cuesta, Lucia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tandil. Centro de Investigación Veterinaria de Tandil. Universidad Nacional del Centro de la Provincia de Buenos Aires. Centro de Investigación Veterinaria de Tandil. Provincia de Buenos Aires. Gobernación. Comision de Investigaciones Científicas. Centro de Investigación Veterinaria de Tandil; Argentina. Kansas State University. College of Veterinary Medicine. Department of Diagnostic Medicine and Pathobiology; Estados UnidosFil: Nieto Farías, María Victoria. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tandil. Centro de Investigación Veterinaria de Tandil. Universidad Nacional del Centro de la Provincia de Buenos Aires. Centro de Investigación Veterinaria de Tandil. Provincia de Buenos Aires. Gobernación. Comision de Investigaciones Científicas. Centro de Investigación Veterinaria de Tandil; ArgentinaFil: Lendez, Pamela Anahí. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tandil. Centro de Investigación Veterinaria de Tandil. Universidad Nacional del Centro de la Provincia de Buenos Aires. Centro de Investigación Veterinaria de Tandil. Provincia de Buenos Aires. Gobernación. Comision de Investigaciones Científicas. Centro de Investigación Veterinaria de Tandil; ArgentinaFil: Rowland, Raymond R. R.. Kansas State University. College of Veterinary Medicine. Department of Diagnostic Medicine and Pathobiology; Estados UnidosFil: Sheahan, Maureen A.. Kansas State University. College of Veterinary Medicine. Department of Diagnostic Medicine and Pathobiology; Estados UnidosFil: Cheuquepán Valenzuela, Felipe Andrés. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Instituto Nacional de Tecnología Agropecuaria. Centro Regional Buenos Aires Sur. Estación Experimental Agropecuaria Balcarce. Agencia de Extensión Rural Balcarce; ArgentinaFil: Marin, Maia Solange. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Instituto Nacional de Tecnología Agropecuaria. Centro Regional Buenos Aires Sur. Estación Experimental Agropecuaria Balcarce. Agencia de Extensión Rural Balcarce; ArgentinaFil: Dolcini, Guillermina Laura. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tandil. Centro de Investigación Veterinaria de Tandil. Universidad Nacional del Centro de la Provincia de Buenos Aires. Centro de Investigación Veterinaria de Tandil. Provincia de Buenos Aires. Gobernación. Comision de Investigaciones Científicas. Centro de Investigación Veterinaria de Tandil; ArgentinaFil: Ceriani, Maria Carolina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Tandil. Centro de Investigación Veterinaria de Tandil. Universidad Nacional del Centro de la Provincia de Buenos Aires. Centro de Investigación Veterinaria de Tandil. Provincia de Buenos Aires. Gobernación. Comision de Investigaciones Científicas. Centro de Investigación Veterinaria de Tandil; Argentin

Fecal Microbiota Transplantation Is Associated With Reduced Morbidity and Mortality in Porcine Circovirus Associated Disease

Porcine circovirus associated disease (PCVAD) is a term used to describe the multifactorial disease syndromes caused by porcine circovirus type 2 (PCV-2), which can be reproduced in an experimental setting through the co-infection of pigs with PCV-2 and porcine reproductive and respiratory syndrome virus (PRRSV). The resulting PCVAD-affected pigs represent a subpopulation within the co-infected group. In co-infection studies, the presence of increased microbiome diversity is linked to a reduction in clinical signs. In this study, fecal microbiota transplantation (FMT) was investigated as a means to prevent PCVAD in pigs co-infected with PRRSV and PCV-2d. The sources of the FMT material were high-parity sows with a documented history of high health status and robust litter characteristics. The analysis of the donated FMT material showed the absence of common pathogens along with the presence of diverse microbial phyla and families. One group of pigs (n = 10) was administered the FMT while a control group (n = 10) was administered a sterile mock-transplant. Over the 42-day postinfection period, the FMT group showed fewer PCVAD-affected pigs, as evidenced by a significant reduction in morbidity and mortality in transplanted pigs, along with increased antibody levels. Overall, this study provides evidence that FMT decreases the severity of clinical signs following co-infection with PRRSV and PCV-2 by reducing the prevalence of PCVAD

Detection of African Swine Fever Virus Antibodies in Serum and Oral Fluid Specimens Using a Recombinant Protein 30 (p30) Dual Matrix Indirect ELISA

In the absence of effective vaccine(s), control of African swine fever caused by African swine fever virus (ASFV) must be based on early, efficient, cost-effective detection and strict control and elimination strategies. For this purpose, we developed an indirect ELISA capable of detecting ASFV antibodies in either serum or oral fluid specimens. The recombinant protein used in the ELISA was selected by comparing the early serum antibody response of ASFV-infected pigs (NHV-p68 isolate) to three major recombinant polypeptides (p30, p54, p72) using a multiplex fluorescent microbead-based immunoassay (FMIA). Non-hazardous (non-infectious) antibody-positive serum for use as plate positive controls and for the calculation of sample-to-positive (S:P) ratios was produced by inoculating pigs with a replicon particle (RP) vaccine expressing the ASFV p30 gene. The optimized ELISA detected anti-p30 antibodies in serum and/or oral fluid samples from pigs inoculated with ASFV under experimental conditions beginning 8 to 12 days post inoculation. Tests on serum (n = 200) and oral fluid (n = 200) field samples from an ASFV-free population demonstrated that the assay was highly diagnostically specific. The convenience and diagnostic utility of oral fluid sampling combined with the flexibility to test either serum or oral fluid on the same platform suggests that this assay will be highly useful under the conditions for which OIE recommends ASFV antibody surveillance, i.e., in ASFV-endemic areas and for the detection of infections with ASFV isolates of low virulence

Harnessing longitudinal information to identify genetic variation in tolerance of pigs to Porcine Reproductive and Respiratory Syndrome virus infection

Background: High resistance (the ability of the host to reduce pathogen load) and tolerance (the ability to maintain high performance at a given pathogen load) are two desirable host traits for producing animals that are resilient to infections. For Porcine Reproductive and Respiratory Syndrome (PRRS), one of the most devastating swine diseases worldwide, studies have identified substantial genetic variation in resistance of pigs, but evidence for genetic variation in tolerance has so far been inconclusive. Resistance and tolerance are usually considered as static traits. In this study, we used longitudinal viremia measurements of PRRS virus infected pigs to define discrete stages of infection based on viremia profile characteristics. These were used to investigate host genetic effects on viral load (VL) and growth at different stages of infection, to quantify genetic variation in tolerance at these stages and throughout the entire 42-day observation period, and to assess whether the single nucleotide polymorphism (SNP) WUR10000125 (WUR) with known large effects on resistance confers significant differences in tolerance. Results: Genetic correlations between resistance and growth changed considerably over time. Individuals that expressed high genetic resistance early in infection tended to grow slower during that time-period, but were more likely to experience lower VL and recovery in growth by the later stage. The WUR genotype was most strongly associated with VL at early- to mid-stages of infection, and with growth at mid- to late-stages of infection. Both, single-stage and repeated measurements random regression models identified significant genetic variation in tolerance. The WUR SNP was significantly associated only with the overall tolerance slope fitted through all stages of infection, with the genetically more resistant AB pigs for the WUR SNP being also more tolerant to PRRS. Conclusions: The results suggest that genetic selection for improved tolerance of pigs to PRRS is possible in principle, but may be feasible only with genomic selection, requiring intense recording schemes that involve repeated measurements to reliably estimate genetic effects. In the absence of such records, consideration of the WUR genotype in current selection schemes appears to be a promising strategy to improve simultaneously resistance and tolerance of growing pigs to PRRS.</p