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Bahan bu uun HSP

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Bahan bu uun HSP
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  The RNA genome of betanodaviruses is very simple and only encodes 3 genes (Okinaka andNakai, 2!"# Therefore, host factors play an important role in the virus life cycle, including viralentry, replication, virion assembly, and release# An important part of the virus$host interactionincludes viral hi%acking of host factors that support its o&n biological functions and disruption of gene e'pression and defenses of the host# or e'ample, increased e'pression of heat shockprotein )A* (+-)A*" modulates betanodavirus replication (.hen et al#, 2/"# +-)A* isone of the most abundant proteins in organisms, and is recogni0ed as a cellular stress proteinthat functions as a chaperone &hich contributes to the folding ofne&ly synthesi0ed proteins andthe refolding of denatured proteins (reedhar et al#, 21"# +ence, viral infection may hi%ack thefunction of chaperones to enhance the stability or assembly of viral proteins#n addition small +-s, such as crystallin, have higher e'pression in the brains and eyes of infected fish, locations &here betanodavirus accumulates during infection# This protein functionsas an anti$inflammatory and neuroprotective agent (.hen et al#, 2//"# 'amination of genee'pression by subtractive hybridi0ation in the kidney head of sea bass during betanodavirusinfection indicated that +sp) &as a critical component in the immune response to infection(-oisa$*eiro et al#, 2)"# urthermore, transcriptome ne't$generation se4uencing (N5" of grouper kidney (56" cells during betanodavirus infection indicated increased e'pression of t&ostress$related genes, +-), and +-7 (8u et al#, 2/2"# Taken together, these resultssuggest that +-s are important host factors in response to betanodavirus infection#.hemokines are another class of host factors related to betanodavirus infection# Thechemokines are a superfamily of small (79/: k;a" proinflammatory and chemoattractantcytokines that &ere srcinally characteri0ed by their ability to induce migration of leukocytes(+o&ard et al#, /)):"# To date, more than < chemokines and 2 chemokine receptors havebeen identified and the chemokines have been divided into 1 subfamilies according to thenumber and spacing of the first 2 conserved cysteine residues in the N$terminal region (.=.,.., .=3., and ." ( Allen et al#, 27"#These cysteine residues mediate chemokine function by binding to and interacting &ith 5$protein coupled receptors# .hemokine signaling has important roles in angiogenesis,hematopoiesis, embryologic development, and in many immune functions including dendriticcell maturation, * cell antibody class s&itching, and T cell activation and differentiation (scheet al#, 2<"#tivation and differentiation (sche et al#, 2<"# -revious research has identified chemokinesfrom several species of marine fish, including rainbo& trout (8aing et al#, 22> ?iens et al#,2:", giltehead seabream (.uesta et al#, 2/", @apanese flounder (6hattiya et al#, 27", and grouper (8in et al#, 2/2"# These chemokines have been characteri0ed and implicated inantiviral responses# or e'ample, fish N$ c can modulate cytokine and chemokine e'pressionand .=. chemokines (5rayfer and *elosevic, 2)> ou et al#, 2<> 5rayfer et al#, 2/"#.hemokine signaling is induced by a ligandBreceptor interaction, so host receptors are alsoimportant in determining their biological effects on homeostasis and immunity# A functional studyindicated that grouper chemokine receptor e'pression is important for the recruitment of immune cells in the early steps of the immune response to microbial infection (8in et al#, 2/2"#  This indicates that chemokine signaling is important in early antiviral defense (Mao Chen, et. al.,  2014) It has been known for some time that heat shock proteins respond to various stressors including infection,but recently studies have focused on their role in innate immunity [58]. Infection of mammals with certainviruses induces host anti-viral activity associated with sp!" protein synthesis [5#,$"]. I%&infection, and toa lesser e'tent the administration of poly I(), induced the greatest changes in sp!" e'pression in this study. *here was a general pattern of down-regulation of +'-, &ig-8, and sp!" at  day post-inection andthe pro-inammatory cytokines at later time points /days 5 and 081. *he signi2cance of theobserveddown-regulation is not clear but other studies have noted transient down-regulation of cytokine genes soonafter infection in rainbow trout [5$,$]. 3arly down-regulation could be due to the movementof cells intoor out of the lymphoid tissues or changes in transcription patterns following activation while  downregulation at later time points may be related to the onset of adaptive immunity. 4ourth, the pro-inammatorycytokines and the sp!" stress protein were induced to high levels by I% virus. ow-level e'pressionchanges of the pro-inammatory cytokines and sp!" observed after inection of the 6%7 constructs maybe due to the aduvant ualities of the plasmid vector backbone because they are not speci2c to theprotective pI%&w-9 vaccine (Purchell, et. al.,  2004) 3# ;o&n$regulated stress response featureseatures &ith similarity to stress response genes &ere do&nregulated after C and D virusinfection relative to the mock controls (ig# 3 A and *", such as the o'idative stress gene ;@$/(Table 2"# tress response features &ere also significantly differentially regulated bet&een the Dand C group (ig# 3", including both heat shock protein (+sp" 7 and +sp)$b (Table 2"# +sp) may be an essential host protein for replication of EE and other negative sense virusesF37G# +sp7 and +sp) are also kno&n to have antiapoptotic activity F3!G# +ere &e observed that the less virulent D virus infection resulted in a greater do&n$regulation of +sp7 and+sp) relative to the C virus# Cacken0ie et al# F33G observed do&nregulation of +sp7 and+sp) in response to infection &ith both virulent and attenuated +NE strains at 21 h p#i# but up$regulation of these genes at 72 h p#i# in fish infected &ith the virulent +NE strain# (Purchell, et. al.,  2011) hostH s cellular protein synthesis machinery by the virus for the production of nascent viral particles# The up$regulation of +- ) beta is also of potential interest since it is kno&n to play a role in the assembly and nuclear import of infl uen0a virus RNA polymerase subunits F<G# ?ork by .hase et al# (2!" has sho&n that inhibitors of +- ) could reduce influen0a virus replication in vitro, making them potential antiviral compounds F</G# (Leblanc, et. al.,  2010) or e'ample, ;u*eau and colleagues F//G reported that heat stressed Atlantic salmon that had artificially elevated levels of branchial and hepatic +-7 sho&ed an increased tolerance to a follo&ing osmotic challenge# ubse4uent &ork of Todgham et al# F/<G demonstrated that e'posure of tidepool sculpin to a /2 . heat shock resulted in a significant higher survival of the fish to a follo&ing osmotic or hypo'ic shock#The danger signals, on the other hand, are molecules &hich are released or e'posed throughin%ury, infection, inflammation or normal cell apoptosis but are not normally e'pressed on the cellsurface F2:G# These include molecules like the hostHs ;NA, RNA, heat shock proteins and other chaperons and oligomannose of pre$secreted glycoproteins# 8ike&ise, the surface  carbohydrates of apoptotic cells are kno&n to undergo a subtle change in the terminal sialic acidcontent identified by certain cell receptors F:G# The -RR can be soluble components like thecomplement protein .3, lectins and various other humoral innate components or they can bee'pressed as receptors on phagocytes and other cells of the immune system# There is evidencefor b/,3$glucan receptors on salmon macrophages F27G and on catfish neutrophils F2!G# Receptors &ith 8- binding activity have also been described in rainbo& trout and seabreammacrophages F2),3G# The Toll$like -RRs have received considerable attention in recent years#Toll &as first described in the fruit fly ;rosophilia melanogaster F3/G and Toll$like genes havesince been demonstrated in vertebrates and sho&n to be involved in the recognition of non$self F32,33G# -utative homologues of the T8R family have also been described in fish F31,3<G# (Magnadotir, 2006) n recent years, the highly conserved family of heat shock proteins (+-s" has receivede'tensive attention for their roles in response to stress# Cembers of different +- families aregrouped according tomolecular si0e and perform varying and different roles in the cell# The+-: is involved in protein stability and folding (.echetto et al#, 2", the +-7 family isnecessary for translocation and protein folding (=ing et al#, 2/3", and the +-) familyis involved in steroid receptor formation and protein folding (8iu et al#, 2/3a"# These +-families are important for immune function (?allin et al#, 22" and have been demonstrated tobe upregulated in fish during stress (=ing et al#, 2/3"# (Xing, et. al.,  2015) On the other hand, t+sp7 not only helped to reduce the proliferation inhibitions induced by the .- treatment, but also assisted antigens to enhance the vaccine$induced protection against treptococcus iniae (Xing, et. al.,  2015) +eme o'ygenase (+O$/" is a cytoprotective en0yme that plays a critical role in defending thebody against o'idant$induced in%ury during inflammatory processes# +eme o'ygenase (+O$/",also kno&n as heat$shock protein 32, plays a ma%or metabolic role in heme catabolism along&ith accessory proteins F/G# +O$/ en0ymatically degrades free heme to form biliverdin, releasingof .O and free iron# *y itself or its en0ymatic products, +O$/ has an important role in tissuehomeostasis e preventing suppressing o'idative stress and in maintaining cellular integrity# Accumulated evidences have demonstrated that +O$/ has potent anti$o'idative, anti$inflammatory, and anti$apoptotic properties (Yuan, et. al.,  2012) Three ma%or facets of hsp$immune system interactions &ill be considered &ith respect to theevolution of immunityI (i" the capacity of hsps to elicit T$cell response specific against antigenic  peptide they chaperone> (ii" the ability of hsp to modulate innate response that are independentof chaperoned peptides> and (iii" hsp surface e'pression .
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