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Porcine reproductive and respiratory syndrome virus (PRRSV) is one of the most important pathogens in pig production worldwide and responsible for enormous production and economic losses. PRRSV infection in gestating gilts and sows induces important reproductive failure. Additionally, respiratory distress is observed in infected piglets and fattening pigs, resulting in growth retardation and increased mortality. Importantly, PRRSV infection interferes with immunity in the respiratory tract, making PRRSV-infected pigs more susceptible to opportunistic secondary pathogens. Despite the availability of commercial PRRSV vaccines for more than three decades, control of the disease remains a frustrating and challenging task. This paper provides a comprehensive overview of PRRSV, covering its history, economic and scientific importance, and description of the viral structure and genetic diversity. It explores the virus’s pathogenesis, including cell tropism, viral entry, replication, stages of infection and epidemiology. It reviews the porcine innate and adaptative immune responses to comprehend the modulation mechanisms employed by PRRS for immune evasion.

Vaccination against Porcine Reproductive and Respiratory Syndrome virus (PRRSv) is widely used to control clinical disease, but the effectiveness appears in some cases to be suboptimal. Field reports have stated the presence of routinely PRRSv-vaccinated but ELISA seronegative sows: the ELISA non-responders. The real extent of this phenomenon (prevalence–origin–consequences) was not yet investigated. In this study, the prevalence of ELISA non-responders was assessed by measuring PRRSv-specific antibodies in 1400 sows, originating from 70 PRRSv-vaccinating sow herds, using IDEXX ELISA (ELISA 1) and CIVTEST E/S ELISA (ELISA 2). Neutralizing antibodies (NAbs) were quantified in a virus neutralization assay. Univariable logistic regression was used to identify herd risk factors for the presence of ELISA non-responders. The global prevalence of non-responders varied from 3.5% (ELISA 1) to 4.1% (ELISA 2), the herd-level prevalence was 40% and the within-herd prevalence ranged from 5% to 20% (ELISA 1) and from 5% to 30% (ELISA 2). The ELISA non-responders had significantly lower NAbs than the ELISA responders. Herds using the combination of one modified live vaccine and one killed vaccine had a significantly reduced risk of having ELISA non-responders. A first assessment of the prevalence and possible consequences of ELISA non-responders has been provided by this study. The clinical importance, origin and underlying immunological mechanisms warrant further research.

African swine fever (ASF) is a highly fatal viral disease in pigs, with mortality rates that can reach 100%. The causative agent, African swine fever virus (ASFV), primarily targets cells of the mononuclear phagocytic system (MPS), particularly monocyte-derived macrophages (MDMs). Despite the severity of the disease, there are currently no effective antiviral treatments available in Europe. A significant barrier to therapeutic development is the limited understanding of how ASFV interacts with its primary target cells. A deeper understanding of the morphological changes induced by ASFV in infected cells is crucial to this effort. To address this knowledge gap, we used conventional and confocal immunofluorescence microscopy, as well as transmission electron microscopy, to investigate ASFV-infected primary MDMs. Our analysis revealed that ASFV infection leads to the formation of large cellular protrusions, which are characterized by vesicle-shaped cellular segments (CSs) at their tips. These protrusions contain all major cytoskeletal components, showing characteristics similar to those of tunneling nanotubes (TNTs). In 84.93% of the cases, the nucleus remained in the cell body (CB) near the viral factory. In the remaining cases, the nucleus was found within these CSs, whereas the viral factory was present in the CB. Additionally, 57.6% of the cells were in contact with the CS and distant cells, suggesting a potential mechanism for ASFV transmission. These findings suggest that ASFV induces cellular segmentation linked by TNT-like structures. Further research is needed to better understand the biogenesis and functional significance of these segmented cells, which could inform future strategies for combating ASFV.

Porcine reproductive and respiratory syndrome virus (PRRSV) and African swine fever virus (ASFV) cause serious economic losses to the swine industry worldwide. Both viruses show a tropism for macrophages, based on the use of specific entry mediators (e.g., Siglec-1 and CD163). Identifying additional mediators of viral entry is essential for advancing antiviral and vaccine development. In this context, monoclonal antibodies (mAbs) are valuable tools. This study employed a library of 166 mAbs targeting porcine alveolar macrophages (PAMs) to identify candidates capable of blocking early infection stages, including viral binding, internalization, and fusion. Immunofluorescence analysis revealed 74 mAbs with cytoplasmic staining and 70 mAbs with membrane staining. Fifteen reacted with blood monocytes as determined by flow cytometry. mAb blocking assays were performed at 4 °C and 37 °C to analyze the ability of mAbs to block PRRSV and/or ASFV infections in PAMs. The mAb 28C10 significantly blocked PRRSV (96% at 4 °C and 80% at 37 °C) and ASFV (64% at 4 °C and 81% at 37 °C) infections. The mAb 28G10B6 significantly blocked PRRSV (86% at 4 °C and 74% at 37 °C) and partially blocked ASFV (35% at 4 °C and 64% at 37 °C) infections. mAb 26B8F5-I only partially blocked PRRSV infection (65% at 4 °C and 46% at 37 °C). Western blotting and mass spectrometry identified the corresponding proteins as Siglec-1 (28C10; 250 kDa), MYH9 (28G10B6; 260 kDa), and ANXA1 (26B8F5-I; 37 kDa). Our findings are indicative that Siglec-1, MYH9, and ANXA1 play a role in PRRSV/ASFV entry into macrophages.

Porcine reproductive and respiratory syndrome virus (PRRSV) is the causative agent of one of the most widespread and economically devastating diseases in the swine industry. Typing circulating PRRSV strains by means of sequencing is crucial for developing adequate control strategies. Most genetic studies only target the highly variable open reading frame (ORF) 5, for which an extensive database is available. In this study, we performed whole-genome sequencing (WGS) on a collection of 124 PRRSV-1 positive serum samples that were collected over a 5-year period (2015–2019) in Belgium. Our results show that (nearly) complete PRRSV genomes can be obtained directly from serum samples with a high success rate. Analysis of the coding regions confirmed the exceptionally high genetic diversity, even among Belgian PRRSV-1 strains. To gain more insight into the added value of WGS, we performed phylogenetic cluster analyses on separate ORF datasets as well as on a single, concatenated dataset (CDS) containing all ORFs. A comparison between the CDS and ORF clustering schemes revealed numerous discrepancies. To explain these differences, we performed a large-scale recombination analysis, which allowed us to identify a large number of potential recombination events that were scattered across the genome. As PRRSV does not contain typical recombination hot-spots, typing PRRSV strains based on a single ORF is not recommended. Although the typing accuracy can be improved by including multiple regions, our results show that the full genetic diversity among PRRSV strains can only be captured by analysing (nearly) complete genomes. Finally, we also identified several vaccine-derived recombinant strains, which once more raises the question of the safety of these vaccines.

African swine fever virus (ASFV) is a substantial threat to pig populations worldwide, contributing to economic disruption and food security challenges. Its spread is attributed to the oronasal transmission route, particularly in animals with acute ASF. Our study addresses the understudied role of nasal mucosa in ASFV infection, using a nasal explant model. The explants remained viable and revealed a discernible ASFV infection in nasal septum and turbinates post-inoculation. Interestingly, more infected cells were found in the turbinates despite its thinner structure. Further analyses showed (i) a higher replication of genotype II strain BEL18 than genotype I strain E70 in the epithelial cell layer, (ii) a preference of ASFV infection for the lamina propria and a tropism of ASFV for various susceptible cell types in different areas in the nasal mucosa, including epithelial cells, macrophages, and endothelial cells. Using porcine respiratory epithelial cells (PoRECs), isolated from nasal tissue, we found a difference in infection mechanism between the two genotypes, with genotype I favoring the basolateral surface and genotype II preferring the apical surface. Moreover, disruption of intercellular junctions enhanced infection for genotype I. This study demonstrated that ASFV may use the respiratory mucosa for entry using different cell types for replication with a genotype difference in their infection of respiratory epithelial cells.

Vaccination against the porcine reproductive and respiratory syndrome virus (PRRSv) is widely used to prevent production losses in the swine industry. In this study, piglets born from both PRRSv-vaccinated ELISA-seropositive sows (E+ piglets) and PRRSv-vaccinated ELISA-seronegative sows (E− piglets) were followed-up pre-vaccination, 3 weeks post-vaccination (wpv) and 8 wpv in two Belgian farrow-to-finish herds. The aim of the study was to analyze the presence of PRRSv-specific maternally-derived antibodies (MDAs) and the PRRSv vaccine response in both groups of piglets. The E− piglets lacked the presence of PRRSv-specific MDAs (0% seropositive), while these were present in the E+ piglets (97% seropositive). Due to this, the E− piglets showed a strong initial vaccine response (72–80% seroconversion) and vaccine viremia (65–75% PCR positive) at 3 wpv. In contrast, the E+ piglets showed only limited initial vaccine responses (25–61% with increased ELISA values) and vaccine viremia (30–31% PCR positive) at 3 wpv. By 8 wpv, the proportion of seropositive E− piglets (78–100%) and seropositive E+ piglets (55–90%) increased in both herds. However, a difference in vaccine viremia duration was observed between both herds at 8 wpv, with a decrease in the proportion of PCR positive piglets in herd 1 (E−: 47%; E+: 25%) and an increase in the proportion of PCR positive piglets in herd 2 (E−: 85%; E+: 92%). This study identified clear differences in the presence of PRRSv-specific maternally-derived antibodies and PRRSv vaccine responses between E− and E+ piglets. Further research is warranted to elicit the biological relevance of these observed differences.

African Swine Fever Virus (ASFV), resulting in strain-dependent vascular pathology, leading to hemorrhagic fever, is an important pathogen in swine. The pathogenesis of ASFV is determined by the array and spatial distribution of susceptible cells within the host. In this study, the replication characteristics of ASFV genotype I E70 (G1-E70) and ASFV genotype II Belgium 2018/1 (G2-B18) in the environment of small veins were investigated in an established vein explant model. Immunofluorescence staining analysis revealed that perivenous macrophages (CD163+ cells) were widely distributed in the explant, with most of them (approximately 2–10 cells/0.03 mm2) being present close to the vein (within a radius of 0–348 µm). Upon inoculation with G1-E70 and G2-B18, we observed an increase in the quantity of cells testing positive for viral antigens over time. G1-E70 replicated more efficiently than G2-B18 in the vein explants (7.6-fold for the ear explant at 72 hpi). The majority of ASFV+ cells were CD163+, indicating that macrophages are the primary target cells. Additional identification of cells infected with ASFV revealed the presence of vimentin+, CD14+, and VWF+ cells, demonstrating the cellular diversity and complexity associated with ASFV infection. By the use of this new vein explant model, the susceptibility of vascular and perivascular cells to an ASFV infection was identified. With this model, it will be possible now to conduct more functional analyses to get better insights into the pathogenesis of ASFV-induced hemorrhages.

Animal leptospirosis, exempt in rodents, manifests as peculiar biology where the animal can function, simultaneously or not, as a susceptible host or reservoir. In the first case, clinical symptoms are likely. In the second case, infection is subclinical and manifestations are mild or absent. Mild clinical symptoms encompass reproductive failure in production animals for host-adapted Leptospira sp. serovars. This work presents a study on Leptospira sp. infection in a mixed-species (bovine and swine) farm with documented reproductive disorders in the cattle unit. A long calving interval (above 450 days) was the hallmark observed in cows. Some cows (2/26 tested) presented a high titre of antibodies against Leptospira sp. serogroup Sejroe, but the overall within-herd prevalence was low (11.5% and 7.7% for cut-off titres of 1:30 and 1:100, respectively). The in-herd prevalence of leptospirosis in the sow unit (determined for 113/140 animals) was high when using a lowered cut-off threshold (32.7% vs. 1.8% for cut-off titre of 1:30 and 1:100, respectively). In this unit, the most prevalent serogroup was Autumnalis. The final diagnostic confirmation of Leptospira sp. maintenance within the farm was obtained through detection by PCR of Leptospira sp. DNA in an aborted swine litter. Despite the fact that a common causative infective agent was diagnosed in both species, the direct link between the two animal units was not found. Factors such as drinking from the same water source and the use of manure prepared with the swine slurry might raise suspicion of a possible cross-contamination between the two units. In conclusion, this work suggests that leptospirosis be included in the differential diagnosis of reproductive disorders and spontaneous abortions in production animals and provides data that justify the use of a lowered threshold cut-off for herd diagnosis.

Background Border disease virus (BDV) is a pestivirus responsible for significant economic losses in sheep industry. The present study was conducted between 2015 and 2016 to determine the flock seroprevalence of the disease in Algeria and to identify associated risk factors. 56 flocks from nine departments were visited and 689 blood samples were collected from adult sheep between 6 and 24 months of age ( n  = 576) and from lambs younger than 6 months ( n  = 113). All samples were tested by RT-PCR as well as by Ag-ELISA, to detect Persistently Infected (PI) animals. Serum samples from adults were tested by Ab-ELISA (Enzyme Linked Immuno-Sorbent Assay), to detect specific antibodies against pestivirus and 197 of them were further characterized by VNT (virus neutralization test) for the detection of neutralizing antibodies specific for BDV and for Bovine virus diarrhea virus (BVDV-1 and BVDV-2). Results No PI animals were found among the 689 sheep tested. 144/197 sera were positive in VNT for BDV, and 2 sera were strongly positive BVDV-2. Fifty-five flocks (98%) had at least one seropositive animal and the apparent within-flock seroprevalence was estimated to be 60.17% (95% C.I.: 52.96–66.96). The true seroprevalence based on estimated sensitivity and specificity of the Ab-ELISA was 68.20% (95% C.I.; 60.2–76.3). Several risk factors were identified as linked to BDV such as climate, landscape, flock management and presence of other ruminant species in the farm. Conclusion These high seroprevalence rates suggest that BDV is widespread and is probably endemic all over the country. Further studies are needed to detect and isolate the virus strains circulating in the country and understand the distribution and impact of pestiviruses in the Algerian livestock.