Abstract
Nervous necrosis virus (NNV), genus Betanodavirus, the etiological agent of the viral encephalopathy and retinopathy (VER), presents a genome with two positive-sense single-stranded RNA segments. Striped jack nervous necrosis virus (SJNNV) and red-spotted grouper nervous necrosis virus (RGNNV), together with reassortants RGNNV/SJNNV, are the betanodaviruses predominantly isolated in Southern Europe. An RGNNV/SJNNV reassortant isolated from Senegalese sole (wt160) causes high mortalities in this fish species. This virus presents differences in the sequence of the 3’ non-coding region (NCR) of both segments compared to RGNNV and SJNNV reference strains. Previously, it has been reported that the reversion of two of these differences (nucleotides 1408 and 1412) in the RNA2 3’NCR to the SJNNV-type (recombinant r1408-1412) resulted in a decrease in sole mortality. In the present study, we have applied an OpenArray® to analyse the involvement of sole immune response in the virulence of several recombinants: the r1408-1412 and two recombinants, developed in the present study, harbouring mutations at positions 3073 and 3093 of RNA1 3’NCR to revert them to RGNNV-type. According to the correlation values and to the number of expressed genes, the infection with the RNA2-mutant provoked the most different immune response compared to the immune response triggered after the infection with the rest of the viruses, and the exclusive and high upregulation of genes related to the complement system. The infection with the RNA1-mutants also provoked a decrease in mortality and their replication was delayed at least 24 h compared to the wt160 replication, which could provoke the lag observed in the immune response. Furthermore, the infection with the RNA1-mutants provoked the exclusive expression of pkr and the downregulation of il17rc.
Highlights
Viral nervous necrosis (VNN), called viral encephalopathy and retinopathy (VER), is a viral disease affecting a high number of fish species of great interest in aquaculture, such as sea bass (Dicentrarchus labrax), Senegalese sole (Solea senegalensis) and gilthead seabream (Sparus aurata) [1]
According to a variable region in the RNA2 segment, NNV has been classified into four species: striped jack nervous necrosis virus (SJNNV), tiger puffer nervous necrosis virus (TPNNV), red-spotted grouper nervous necrosis virus (RGNNV), and barfin flounder
The infection with the RNA2-mutant provoked the most different immune response compared to the one elicited by the wild type virus, highlighting the exclusive and high upregulation of genes related to the complement system
Summary
Viral nervous necrosis (VNN), called viral encephalopathy and retinopathy (VER), is a viral disease affecting a high number of fish species of great interest in aquaculture, such as sea bass (Dicentrarchus labrax), Senegalese sole (Solea senegalensis) and gilthead seabream (Sparus aurata) [1]. The etiological agent of this disease is the nervous necrosis virus (NNV), which belongs to the Nodaviridae family, Betanodavirus genus. NNV is a naked virus and presents bisegmented positive-sense single-stranded RNA. According to a variable region in the RNA2 segment (named T4), NNV has been classified into four species: striped jack nervous necrosis virus (SJNNV), tiger puffer nervous necrosis virus (TPNNV), red-spotted grouper nervous necrosis virus (RGNNV), and barfin flounder. Pathogens 2021, 10, x Pathogens 2021, 10, 1388 nervous necrosis virus (TPNNV), red-spotted grouper nervous necrosis virus (RGNNV), and barfin flounder nervous necrosis virus (BFNNV) [2]. NThoifsReNffeAc2t ownitthhehovsitruplreontceeinhsa, sorbetoena adtitfrfiebruetnetdiael iitmhemr utoneanreimsppoanisreed[9i]n.teraction of RNA2 with host proteins, or to a differential immuOnne trheespootnhseer [h9a]n. Tghaluess,eOslovleei,raneatmael.d[4S] preSpsoIArtuedsct1h6e0.i0s3ola(htieorneaofftearrewast1so6r0t)a, nwt firthomaSgeenneogmalesecosomlep,onsaemd eodf SRpGSNsINAVu-stcy1p6e0.R03N(Ah1eraenadfteSrJNwNt1V6-0t)y,pwe iRthNAa 2gesengommeenctsom(RpGoNseNdVo/fSJRNGNNVN).VT-htyispreeaRsNsoArt1andt pSrJoNvoNkVe-styhpigehRmNoArt2alisteygimn ethnits f(iRshGsNpNecVie/sSaJnNdNeVxh).ibTithsisdirfefearsesnocretasnint pthroev3o’ kneosn-hciogdhminogrrteagliitoynin(NthCiRs )fioshf bsoptehciseesgamnednetsxhwibhietns dcoifmfepreanrecdestoinththeere3f’enroen-cceosdtrinaginrseogfioenac(hNsCpRec)ioefs b[4o,t8h]. sReeggmaerdnitnsgwRhNenAc1o, mfopuarrdediffteoretnhtepreofseitrieonncsewsterraeinosbosefrevaecdh, swpheecriesas[4f,i8v]e. dRiefgfearrednicnegs RwNerAe1f,oufonudr idniftfheereRnNt Apo2s[i8ti]o. nTswwoeorfetohbesdeirfvfeerde,nwcehseorebasserfivveed dinifftheree3n’cNesCwR eorfethfoeuRnNdAin tahree lRoNcaAte2d[a8t].pTowsitoioonfst1h4e0d8iaffnedre1n4c1e2s, osbitseedrvineda isntetmhe-lo3o’NpCstRruocftuthree (R3’NSLA), warheiclhociasteesdaset nptoiaslitfioornrsep14li0c8ataionnd[19]4.1T2h, esiirterdevienrsaiosntetmo -SlJoNopNVst-rtuycpteurneu(c3le’SicLa),ciwdshircehsuislteedssiennctaia.l7f0o%r rdeepclriecaastieoinn[9so].leThmeoirrtraelviteyrscioomn ptoarSeJdNtNoVth-teypweilndutcylepiec avciriduss.rTeshuislteedffeinctcoan. 7t0h%e vdierucrleeanscee ihnassobleeemn oartttrailbituytecdomeipthaerredtotoanthime wpailidretdypinetevriarcutsio. nThoifsReNffeAc2t ownitthhehovsitruplreontceeinhsa, sorbetoena adtitfrfiebruetnetdiael iitmhemr utoneanreimsppoanisreed[9i]n.teraction of RNA2 with host proteins, or to a differential immuOnne trheespootnhseer [h9a]n. d, the effect on virulence of the above-described differences in the RNAO1 nhathsenootthbeerehnadnedt,etrhmeienfefdec. tTohnerveifrourlee,nicnetohfethpereasbenovt es-tuddesyc,rwibeedhadvifefeerxeanmceins eind tthhee RefNfeAct1ohfatswnoootfbteheensedcehtearnmgiense(dp.oTsihtieornef3o0re7,3ianntdhe30p9r3e)seonnt vstiruudlye,nwceebhyavtheeedxeavmeilnoepdmtehnet eofffetwctoofretwcoomobfitnhaenset vchiraunsgeessh(aprobsoituiorinng30p7o3ianntdm3u0t9a3t)ioonnsv, iwruhliecnhcembaykethtehde eRvNelAop1msiemntiloafr ttwo tohreerceofmerbenincaenRtGvNiruNsVesvhiraurbs.oFuurrinthgerpmoionrtem, inutoartdioenrst,owdhetiecrhmminaekethtehienRvoNlvAe1mseimntiolafrthtoe tfifbhiyssehhGriiemémfmemmreeuuzn-nncMeeearrReteaGssppeNotoNnnaslsV.ee[i1vinn0ir]bubheestat.aasFnnbuooerddetahanvveairirrpmuupsoslrivveeidi,rruiutnloleeonanrcncdeeaeltrtyootsosesoodtlhleeee,t,etithrmhmeem1i1n1u1e2n2tOehOgpepeeiennnnevAAoerrlxrvrapaeyrym®e®sedsdnieoetssnoiiggfannftetheededr bthyeGinéfmecetzio-Mn awtaithettahle. [r1e0c]ohmabsibneaennt vapirpulsieesdhtoarabnoaulryisnegthmeuitmatmiounnseatgethnee 3e’xNpCreRssoiofnRaNftAe1r tohreRinNfAec2t.ion with the recombinant viruses harbouring mutations at the 3’NCR of RNA1 or RNA2
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