Biology subjects

Evensen, O.

Publications and source records attributed to Evensen, O..

3 recordsLinked to original sources

bioRxiv2025

Investigating antiviral pathways in Atlantic salmon cells through interferon receptor knockouts via CRISPR-Cas9

In Atlantic salmon (Salmo salar), infectious salmon anemia virus (ISAV) and infectious pancreatic necrosis virus (IPNV) evade host immune response through complex antagonistic mechanisms. Type I interferons (IFNs) play a pivotal role in antiviral defense by signaling through heterodimeric receptors to activate the JAK-STAT pathway and drives the expression of interferon-stimulated genes (ISGs). In this study, CRISPR-Cas9 was used to knock out (KO) interferon receptor genes (crfb1a, crfb5a, il10rb, ifngr2a) and a combined group of candidate receptors (crfb1a, crfb5a, il10rb, ifngr2a, il10r2) to investigate their roles and their impact on downstream signaling cascades with RNA sequencing. Recombinant IFNa was used to induce an antiviral state before challenging cells with ISAV and IPNV. The knockouts significantly disrupt downstream antiviral signaling, with two knockouts, crfb1a and crfb5a, showing pronounced effects. During ISAV infection, the crfb1a KO group exhibited a marked reduction in the expression of critical signaling genes such as stat1b, stat2, stat6, and irf3 during ISAV infection, while irf7 was upregulated during IPNV infection. The crfb5a KO group exhibited reduced stat2 expression in ISAV infection and upregulated irf7 during IPNV infection. Despite these disruptions, ISGs such as Mx and isg15 maintained their expression levels across all knockout groups, suggesting potential alternative signaling pathways. Pathway analysis further revealed upregulation of cellular processes like actin regulation and phagosome activity, which may compensate for impaired immune signaling. These findings highlight the distinct roles of IFN receptor genes in mediating antiviral responses and underscore the complexity of IFN signaling in Atlantic salmon.

immunology↗

bioRxiv2024

Long-Term Colonization Dynamics of Probiotic Aliivibrio spp. in Atlantic Salmon (Salmo salar) Following Bath Administration

Ulcerative conditions present a major challenge in Norwegian salmon farming. Probiotic Aliivibrio species have previously been demonstrated to provide health benefits in both Atlantic salmon and lumpfish, although the underlying mechanisms and the host-bacteria interactions remain unclear. This study aimed to investigate whether these bacteria could colonize Atlantic salmon following bath administration, determine the tissue tropism, and assess the duration of colonization. We examined the host microbiota using culture-based methods, qPCR and immunohistochemistry techniques specifically designed to target the applied Aliivibrio strains. Our findings reveal that the probiotic bacteria can successfully colonize Atlantic salmon and persist for at least nine months post-administration. We identified the administered strains in the skin and underlying tissue with all three methods. The probiotics were also identified in the distal intestine and the visceral organs. Additionally, we isolated the probiotic Aliivibrio species from mixed cultures in ulcerated areas. While viable bacteria were recoverable from recently euthanized fish, tissue decay promoted bacterial recovery of the administered species across all experiments. Given prior evidence on ulcer reduction associated with these probiotics, competitive exclusion appears to be a plausible mechanism of action, though further investigation is warranted.

microbiology↗

bioRxiv2024

Structure of the T=13 capsid of infectious pancreatic necrosis virus (IPNV) - a salmonid birnavirus

Birnaviruses infect a broad range of vertebrate hosts, including fishes and birds, and cause substantial economic losses in the fishery and livestock industries. The infectious pancreatic necrosis virus (IPNV), an aquabirnavirus, specifically targets salmonids. While structures on T=1 subviral particles of the birnaviruses, including IPNV, have been studied, structural insights into the infectious T=13 particles have been limited to the infectious bursal disease virus (IBDV), an avibirnavirus. Determining the capsid structure of the T=13 particle of IPNV is crucial for advancing knowledge of its antigenicity, capsid assembly, and possible functional structures. Here, the capsid structure of the IPNV L5 strain has been determined at a resolution of 2.75 [A]. The overall structure resembles the T=13 IBDV structure, with notable differences in the surface loops on the P domain of the VP2 capsid protein, essential for antigenicity and virulence. Additionally, previously undescribed structural features have been identified, including the C-terminal regions of the VP2 subunits within the pentagonal assembly unit at each 5-fold axis, which interlock with adjacent VP2 subunits. This interlocking, together with class-averaged projections of triangular and pentagonal units, suggests that the pentagonal unit formation could be important for correct T=13 particle assembly, preventing the formation of T=1 subviral particles. Furthermore, positively charged residues in obstructed capsid pores at each 5-fold axis are speculated to facilitate intraparticle genome synthesis of IPNV. ImportanceAquabirnaviruses cause deadly infectious diseases in salmonid fish, posing significant challenges for both wild and farmed fish populations. The most prevalent aquabirnavirus worldwide is the infectious pancreatic necrosis virus, whose multifunctional capsid is critical to its infection, replication, and maturation. Previously, research has focused on the structure of the viruss non-infectious subviral capsid. In this study, however, the first structure of the large, infectious, and functional form of the capsid has been determined. This new capsid structure reveals functional motifs that were previously unclear in the non-infectious capsid. These motifs are believed to be essential for the viruss replication and particle assembly, making them promising targets for developing strategies to control virus proliferation.

biophysics↗