LitCovid-sentences  

PMC:7281546 / 27446-47211 JSONTXT 11 Projects

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Id Subject Object Predicate Lexical cue
T192 0-4 Sentence denotes 4.2.
T193 5-38 Sentence denotes Immune Evasion Mechanisms of PEDV
T194 39-158 Sentence denotes Induction of IFN-α/β is the most rapid and effective mechanism for hosts to initiate antiviral innate immune responses.
T195 159-215 Sentence denotes SARS-CoV, MHV and many other CoVs are sensitive to IFNs.
T196 216-372 Sentence denotes A great number of viral dsRNAs intermediates are generated during CoVs infection that contribute to IFN production, but these CoVs remain highly pathogenic.
T197 373-539 Sentence denotes As a matter of fact, CoVs have developed a set of elaborate mechanisms to evade or inhibit the host antiviral innate immune response during virus evolution [134,167].
T198 540-900 Sentence denotes The evasive strategies utilized by PEDV are classified into four major types: (1) inhibition of RLRs-mediated IFN production pathways, (2) inhibition of the activation of transcription factors responsible for IFN induction, (3) disruption of the signal cascades induced by IFN, and (4) hiding its viral RNA to avoid the exposure of viral RNA to immune sensors.
T199 901-1092 Sentence denotes In the past decade, accumulating evidence demonstrates that PEDV N protein, nsp1, PLP2, nsp5, nsp15, and nsp16 antagonize type I IFN or type III IFNs production [58,65,78,80,100,132,135,168].
T200 1093-1198 Sentence denotes This explains why only weak IFNs’ and cytokines’ expression is detected in PEDV-infected cells [169,170].
T201 1200-1206 Sentence denotes 4.2.1.
T202 1207-1221 Sentence denotes PEDV N Protein
T203 1222-1395 Sentence denotes N protein, as an abundantly produced structural protein within CoV-infected cells, has multiple functions, including virus replication, transcription, and assembly [56,134].
T204 1396-1550 Sentence denotes PEDV N protein has been identified as an IFN antagonist that blocks the expression of IFN-β and ISGs by suppression of the IRF3 and NF-κB activities [58].
T205 1551-1748 Sentence denotes PEDV N protein inhibits the activation of the IFN-β promoter induced by TBK1 and its upstream RIG-I, MDA-5, VISA, and TRAF3, while not affecting the activation of the IFN-β promoter driven by IRF3.
T206 1749-1939 Sentence denotes Further experiments confirm that N directly interacts with TBK1 to obstruct the association between TBK1 and IRF3, which inhibits TBK1-induced IRF3 phosphorylation and IFN-β production [58].
T207 1940-2036 Sentence denotes Moreover, the effect of PEDV N protein on type III IFN production has also been evaluated [168].
T208 2037-2279 Sentence denotes N protein inhibits polyinosinic-polycytidylic acid (poly(I:C))-induced IFN-λ3 production by blocking the nuclear translocation of NF-κB, but does not antagonize the type I or type II IFN expression induced by poly(I:C) in IPEC-J2 cells [168].
T209 2280-2418 Sentence denotes Recent studies show that SARS-CoV N protein inhibits type I IFN production through suppressing TRIM25-mediated RIG-I ubiquitination [171].
T210 2419-2502 Sentence denotes The MERS-CoV N protein also blocks IFN production by interacting with TRIM25 [171].
T211 2503-2735 Sentence denotes In addition, both MHV and SARS-CoV N proteins perturb the function of cellular protein activator of protein kinase R (PACT), which can bind to RIG-I and MDA5 to activate IFN production, and thus antagonize type-I IFN signaling [61].
T212 2736-2846 Sentence denotes These results indicate the important function of the CoVs N protein in modulating host innate immune response.
T213 2847-2916 Sentence denotes Whether PEDV N protein targets TRIM25 or PACT should be investigated.
T214 2917-3127 Sentence denotes Although several studies have been performed to understand the pathogenicity of PEDV, there remains limited information about the interaction between viral proteins and host cell factors during viral infection.
T215 3128-3197 Sentence denotes CoV N protein is a vital viral protein involved in virus replication.
T216 3198-3393 Sentence denotes Current researches have indicated that N protein interacts with many host proteins, such as hCypA [172], proteasome subunit p42 [173], Smad3 [174], hnRNP-A1 [175], and the chemokine CXCL16 [176].
T217 3394-3470 Sentence denotes In the host cells, a large number of host proteins reveal various functions.
T218 3471-3550 Sentence denotes However, for the virus, the genome only encodes several limited viral proteins.
T219 3551-3663 Sentence denotes Therefore, these viral proteins have to be multifunctional, which is pivotal to virus replication and existence.
T220 3665-3671 Sentence denotes 4.2.2.
T221 3672-3681 Sentence denotes PEDV nsp1
T222 3682-3842 Sentence denotes PEDV nsp1 is the N-terminal cleavage product from polyproteins pp1a and pp1a/b processed by nsp3 and nsp5 [177] and is about 110 amino acids in length [74,178].
T223 3843-3990 Sentence denotes Nsp1 of many α-CoV and β-CoV exhibits both functional conservation and mechanistic diversity in suppressing host gene expression and IFN signaling.
T224 3991-4150 Sentence denotes For SARS-CoV, nsp1 triggers the decay and cleavage of host mRNA and inhibits host protein translation, subsequently inhibiting type I IFN production [179,180].
T225 4151-4288 Sentence denotes SARS-CoV nsp1 also blocks the expression of IFN-inducible genes, by restraining the signal transduction during virus infection [181,182].
T226 4289-4379 Sentence denotes The TGEV nsp1 considerably suppresses host protein expression during viral infection [77].
T227 4380-4505 Sentence denotes Structural studies show that the core structure of PEDV nsp1 is highly similar to those of SARS-CoV nsp1 and TGEV nsp1 [183].
T228 4506-4734 Sentence denotes PEDV nsp1 inhibits host gene expression and three motifs (amino acids 67 to 71, 78 to 85, and 103 to 110) form a stable functional region for inhibition of host protein synthesis, differing considerably from SARS-CoV nsp1 [183].
T229 4735-4852 Sentence denotes PEDV nsp1 has been identified as an IFN antagonist, which constrains poly (I:C)-induced IFN-β promoter activity [65].
T230 4853-5012 Sentence denotes Nsp1 significantly inhibits the activation of IFN-β promoter triggered by IRF3, whereas it does not inhibit IRF3 phosphorylation and its nuclear translocation.
T231 5013-5167 Sentence denotes Nsp1 interrupts the association of IRF3 with CREB-binding protein (CBP), by promoting CBP degradation in the nucleus via the proteasome-dependent pathway.
T232 5168-5308 Sentence denotes CBP/p300, the transcription co-activator cAMP responsive element binding protein (CREB), forms a complex with the activated IRF3 in nucleus.
T233 5309-5548 Sentence denotes The IRF3-CBP/p300 complex binds to the positive regulatory domain (PRD) regions of the IFN-β promoter, to assemble the enhanceosome with NF-κB and other factors, which ultimately turn on the transcription of type I IFN genes [184,185,186].
T234 5549-5614 Sentence denotes Therefore, PEDV nsp1 blocks type I IFN production in the nucleus.
T235 5615-5747 Sentence denotes Activated NF-κB induces the production of type I IFNs and proinflammatory cytokines and is important for inhibiting viral infection.
T236 5748-5897 Sentence denotes PEDV nsp1 has been shown to interfere with the NF-κB activity [78] and is the most potent suppressor of proinflammatory cytokines at early infection.
T237 5898-6092 Sentence denotes It inhibits the phosphorylation and degradation of IκBα, and blocks p65 nuclear translocation, leading to the suppression of both IFN and the early production of pro-inflammatory cytokines [78].
T238 6093-6251 Sentence denotes Moreover, PEDV inhibits type III IFN production and nsp1, nsp3, nsp5, nsp8, nsp14, nsp15, nsp16, ORF3, E, M, and N are identified as type III IFN antagonists.
T239 6252-6318 Sentence denotes Among these antagonists, nsp1 is the most potent suppressor [130].
T240 6319-6459 Sentence denotes PEDV nsp1 blocks the nuclear translocation of IRF1 and decreases the amounts of peroxisomes and then suppresses IRF1-mediated type III IFNs.
T241 6460-6542 Sentence denotes The conserved residues of PEDV nsp1 protein are crucial for IFN suppression [130].
T242 6543-6688 Sentence denotes Multiple effects of nsp1 on modulating innate immune response during PEDV infection suggest the vital role of nsp1 in the PEDV replication cycle.
T243 6690-6696 Sentence denotes 4.2.3.
T244 6697-6701 Sentence denotes PLP2
T245 6702-7060 Sentence denotes The antiviral innate immune signaling pathways are regulated by several posttranslational modifications (PTMs), such as phosphorylation, ubiquitination, glycosylation, NEDDylation and SUMOylation [187], of which ubiquitination is a critical modification to modulate the stability and activity of PRRs and other components of innate immune signaling pathways.
T246 7061-7216 Sentence denotes During viral infection, a reciprocatory action (occurrence of ubiquitination and deubiquitination) helps maintain the homeostasis of host immune responses.
T247 7217-7327 Sentence denotes Hence, deubiquitinases (DUBs) are indispensable in the regulation of virus-induced type I IFN signaling [188].
T248 7328-7439 Sentence denotes Many host DUBs have been reported engaging in the regulation of innate immune signaling pathways [189,190,191].
T249 7440-7585 Sentence denotes In recent years, a variety of viral DUBs have been discovered to target key components of type I IFN pathway during various RNA virus infections.
T250 7586-7829 Sentence denotes For example, foot-and-mouth disease virus leader proteinase (FMDV Lbpro) [192], and porcine reproductive and respiratory syndrome virus nsp2 (PRRSV nsp2) possess ubiquitin-deconjugating activity to deubiquitinate key host components [193,194].
T251 7830-7942 Sentence denotes To counteract host antiviral response, CoVs likely take advantage of DUB activity to break host innate immunity.
T252 7943-8090 Sentence denotes Indeed, the PLPs of mouse hepatitis virus A59 (MHV-A59) [195], SARS [196], and human CoV NL63 have DUB activity and antagonize IFN induction [197].
T253 8091-8219 Sentence denotes PEDV PLP2 has been reported as having a deubiquitinase activity as well, and it can be co-immunoprecipitated by RIG-I and STING.
T254 8220-8389 Sentence denotes As mentioned above, FMDV Lbpro, MHV PLP2 and SARS PLPs all counteract host innate immune response through blocking the ubiquitination of the components of RLRs pathways.
T255 8390-8535 Sentence denotes Similarly, PEDV PLP2 removes the ubiquitinated conjugates from RIG-I and STING by its DUB activity, to negatively regulate type I IFN production.
T256 8536-8699 Sentence denotes PEDV PLP2 probably interacts with RIG-I and STING, which prevents the activation of RIG-I and STING by hindering the recruitment of downstream signaling molecules.
T257 8700-8820 Sentence denotes As expected, the interference with the ubiquitination of RIG-I and STING by PLP2 clearly benefits PEDV replication [80].
T258 8821-8881 Sentence denotes PEDV nsp3 contains two core domains of PLPs (PLPl and PLP2).
T259 8882-8985 Sentence denotes It is determined that PEDV PLP2, but not PLP1, inhibits the IFN-β promoter activation in HEK293T cells.
T260 8986-9057 Sentence denotes The DUB activity of PLP2 is highly dependent on its catalytic activity.
T261 9058-9239 Sentence denotes Three catalytically inactive mutants of PEDV PLP2 (C1729A, H1888A and D1901A) are defective in the deubiquitination of its targets and fail to impair virus-induced IFN-β production.
T262 9240-9420 Sentence denotes SARS-CoV PLP2 interacts with MDM2 (mouse double minute 2 homolog) to deubiquitinate and stabilize MDM2, approving the degradation of p53 and the suppression of IFN signaling [198].
T263 9421-9490 Sentence denotes PEDV infection degrades p53 by upregulation of MDM2 expression [198].
T264 9491-9616 Sentence denotes PEDV PLP2 may be responsible for targeting the p53 pathway and inhibiting p53-dependent apoptosis, leading to immune evasion.
T265 9617-9790 Sentence denotes A recent study determined that TGEV PL1 inhibits the IFN-β expression and interferes with the RIG-1- and STING-mediated signaling pathway through a viral DUB activity [195].
T266 9791-9906 Sentence denotes It suggests that different viral proteins are involved in the deubiquitination of host proteins for different CoVs.
T267 9907-10061 Sentence denotes However, these studies offer a probability to design a common therapeutic against different viral DUBs to reduce the replication and pathogenesis of CoVs.
T268 10062-10236 Sentence denotes Therefore, further studies are required to understand more about the substrate specificity of these viral DUBs and clarify the precise functions of CoV protease/DUB activity.
T269 10238-10244 Sentence denotes 4.2.4.
T270 10245-10254 Sentence denotes PEDV nsp5
T271 10255-10362 Sentence denotes Notably, 3Cpro is a critical IFN antagonistic protein identified in multiple different families of viruses.
T272 10363-10644 Sentence denotes The 3Cpro of picornaviruses, including FMDV [199], hepatitis A virus (HAV) [200], enteroviruses (EV71, EV-D68) and coxsackieviruses (CVB3, CV-A16, CV-A6) [201,202,203,204], antagonize innate immune signaling by targeting the critical components of the IFN pathways for proteolysis.
T273 10645-10797 Sentence denotes A newly emerged picornavirus, Seneca Valley virus (SVV), has also evolved an effective mechanism to escape host antiviral innate immune using its 3Cpro.
T274 10798-11010 Sentence denotes Moreover, 3Cpro cleaves the signaling components (MAVS, TRIF, and TANK) of type I IFN pathway and induces the degradation of the transcription factors IRF3 and IRF7 to constrain host antiviral response [205,206].
T275 11011-11103 Sentence denotes CoV nsp5 is called 3C-like protease (3CLpro), that resembles the 3Cpro of other RNA viruses.
T276 11104-11229 Sentence denotes For CoV, the polyprotein precursors (pp1a and pp1b) are mainly processed to generate mature nonstructural proteins by 3CLpro.
T277 11230-11417 Sentence denotes To date, the 3CLpro of CoVs, including PEDV and PDCoV, have been confirmed to antagonize type I IFN production by the cleavage of NF-κB essential modulator (NEMO) and STAT2 [100,207,208].
T278 11418-11500 Sentence denotes NEMO is essential for RNA virus-induced activation of NF-κB, IRF3, and IRF7 [209].
T279 11501-11611 Sentence denotes NEMO is required for MAVS-induced IKKα/β activation and is also crucial for the activation of TBK1/IKKε [149].
T280 11612-11706 Sentence denotes To establish successful infections, PEDV targets NEMO to subvert host innate immune responses.
T281 11707-11838 Sentence denotes PEDV nsp5 significantly inhibits Sendai virus (SeV)-induced IFN-β synthesis and the process depends on its protease activity [100].
T282 11839-11942 Sentence denotes Further experiments show that PEDV nsp5 inhibits RIG-I/MDA5 signaling and targets the upstream of TBK1.
T283 11943-12028 Sentence denotes The cleavage of NEMO by nsp5 is identified as responsible for this inhibitive effect.
T284 12029-12123 Sentence denotes The PEDV nsp5-mediated cleavage of NEMO efficiently blocks NEMO-mediated downstream signaling.
T285 12124-12198 Sentence denotes The cleavage site within NEMO that is grasped by nsp5 has been determined.
T286 12199-12366 Sentence denotes Of these reported immune evasion strategies employed by CoVs, the cleavage of innate immune adaptors is a particularly effective manner to disrupt antiviral responses.
T287 12367-12437 Sentence denotes Nsp5 is essential for the life cycle of PEDV and other CoVs [210,211].
T288 12438-12516 Sentence denotes It is a potential target for the development of anti-coronaviral therapeutics.
T289 12517-12689 Sentence denotes Although PEDV nsp5 does not target STAT2 mediated type Ⅰ IFN signaling pathway, PEDV nsp7 has been reported to inhibit the STAT1 and STAT2 induced activation of ISRE [212].
T290 12690-12854 Sentence denotes Nsp7 competes with Karyopherin α (KPNA1), which is an adaptor mediating nuclear translocation of ISGF3, in combination with STAT1, to block ISGF3 nuclear transport.
T291 12855-12948 Sentence denotes However, the expression and phosphorylation of STAT1 and STAT2 are not affected by PEDV nsp7.
T292 12949-13038 Sentence denotes In fact, PEDV infection degrades STAT1, leading to the inhibition of IFN signaling [170].
T293 13039-13116 Sentence denotes Therefore, other PEDV encoded proteins likely target IFNs mediated signaling.
T294 13118-13124 Sentence denotes 4.2.5.
T295 13125-13157 Sentence denotes Evasion of Viral RNA Recognition
T296 13158-13299 Sentence denotes CoVs belong to RNA viruses, which produce several RNA species, such as dsRNA intermediates and RNA with a 5′-triphosphate during replication.
T297 13300-13435 Sentence denotes These RNA intermediates are potent stimulators of PRRs and are associated with the organelles of viral RNA replication, DMVs [213,214].
T298 13436-13597 Sentence denotes DMVs formed from membranous rearrangements seem to sequester the replication intermediates using membrane-bound vesicles or invaginations to keep away from PRRs.
T299 13598-13715 Sentence denotes Therefore, the form of DMVs may be a strategy for PEDV to escape innate immune recognition in the cytosol (Figure 2).
T300 13716-13799 Sentence denotes However, whether DMVs alone are sufficient to shield RNA from PRRs remains unknown.
T301 13800-14017 Sentence denotes Besides, the replication organelles, the endoribonuclease activity and viral 5′ end RNA capping/protection mechanisms are also the critical ways of avoiding RNA recognition or protecting it from degradation [132,135].
T302 14018-14031 Sentence denotes 1) PEDV nsp15
T303 14032-14140 Sentence denotes CoV nsp15 has EndoU catalytic activity that was initially thought to play a vital role in virus replication.
T304 14141-14277 Sentence denotes However, the catalytic-defective EndoU of MHV shows only a subtle defect in viral replication compared to WT virus in fibroblasts [215].
T305 14278-14358 Sentence denotes Similar results are found for the nsp15 mutants of SARS-CoV and HCoV-229E [216].
T306 14359-14449 Sentence denotes These findings suggest that the EndoU activity of nsp15 is not required for RNA synthesis.
T307 14450-14541 Sentence denotes Recently, nsp15 has been demonstrated to act as a new IFN antagonist of CoVs [117,118,217].
T308 14542-14701 Sentence denotes Recent reports indicate that CoVs’ EndoU activity is essential for prevention of RNA recognition by MDA5, protein kinase R (PKR), and OAS/RNAse L system [118].
T309 14702-14798 Sentence denotes PKR and OAS/RNAse L recognize and destroy foreign RNA in the cytosol to defend viral infections.
T310 14799-14947 Sentence denotes To counteract the function of PKR and OAS/RNAse L, the virus hides or modifies its viral RNA, to avoid the exposure of viral RNA to these molecules.
T311 14948-15017 Sentence denotes In all CoVs, the EndoU catalytic domain in nsp15 is highly conserved.
T312 15018-15113 Sentence denotes PEDV EndoU activity has been indicated as having an antagonistic effect on IFN signaling [135].
T313 15114-15288 Sentence denotes The EndoU activity of PEDV nsp15 not only inhibits the type I IFN response in porcine macrophages, but also antagonizes the type III IFN response in porcine epithelial cells.
T314 15289-15437 Sentence denotes The replication of EndoU-mutant PEDV (icPEDV-EnUmt) is considerably impaired in porcine epithelial cells compared to the wild type PEDV (icPEDV-wt).
T315 15438-15593 Sentence denotes The icPEDV-EnUmt clearly induces early and robust type I and type III IFNs production, as well as ISGs’ expression compared with that induced by icPEDV-wt.
T316 15594-15683 Sentence denotes The EndoU-deficient PEDV infected animals also show reduced viral shedding and mortality.
T317 15684-15823 Sentence denotes These results indicate that the EndoU activity of PEDV nsp15 plays a vital role in evading host antiviral innate immunity (Figure 2) [135].
T318 15824-15837 Sentence denotes 2) PEDV nsp16
T319 15838-15889 Sentence denotes CoV nsp16 is a 2′-O-methyltransferase (2′-O-MTase).
T320 15890-16012 Sentence denotes To evade recognition by the host immune sensors, many CoVs encode methyltransferases involved in the capping of viral RNA.
T321 16013-16176 Sentence denotes This modification makes the viral RNA indistinguishable with host cell mRNA, which is important to avoid the recognition of viral RNA by MDA5 (Figure 2) [121,218].
T322 16177-16337 Sentence denotes Methylation of the two sites in the 5′ cap is catalyzed by three nsps, including nsp14 (the N-7-MTase), nsp16 (the 2′-O-MTase), and nsp10 [112,123,124,125,126].
T323 16338-16470 Sentence denotes For example, SARS-CoV nsp16 acts as a 2′-O-MTase to prevent innate immune recognition and promote viral proliferation [113,121,123].
T324 16471-16551 Sentence denotes PEDV nsp14 and nsp16 have been identified as the viral IFN antagonists [65,132].
T325 16552-16722 Sentence denotes The overexpression of nsp14 or nsp16 remarkably inhibits IFN-β production, but nsp16 appears to play a more important role in innate immunity regulation than nsp14 [132].
T326 16723-16848 Sentence denotes Nsp16 is a highly conserved methyltransferase which contains an invariant KDKE motif within the methyltransferase core [219].
T327 16849-16901 Sentence denotes This KDKE motif is required to mediate its activity.
T328 16902-17010 Sentence denotes Notably, the mutation of any of the KDKE active sit has been shown to abolish the 2′-O-MTase activity [123].
T329 17011-17179 Sentence denotes PEDV nsp16 KDKE motif plays a critical role in the inhibition of type I IFN production, suggesting the important role of the 2′-O-MTase in PEDV-mediated immune evasion.
T330 17180-17385 Sentence denotes PEDV nsp16 negatively regulates RLR-mediated signal pathway activation, and inhibits the expression of the IFN-stimulated IFIT family members (IFIT1, IFIT2, IFIT3), which in turn promotes PEDV replication.
T331 17386-17528 Sentence denotes Taken together, these results demonstrate that PEDV nsp16 negatively regulates cellular antiviral response to promote viral replication [132].
T332 17529-17708 Sentence denotes Screening inhibitors targeting the 2′-O-MTase of nsp16 might be a prominent strategy to inhibit CoV infections and develop antivirals for treatment of the diseases caused by CoVs.
T333 17709-17799 Sentence denotes Additionally, CoVs nsp14 also includes the 3′-to-5′ exoribonuclease (ExoN) activity [113].
T334 17800-17934 Sentence denotes A mutation of TGEV nsp14 ExoN generates lower levels of dsRNA than wildtype TGEV and thus triggers a reduced antiviral response [220].
T335 17935-18050 Sentence denotes Nsp14 ExoN activity is also critical for the resistance of host innate immune response in MHV-infected cells [221].
T336 18051-18192 Sentence denotes The role of nsp ExoN activity of PEDV in counteracting host antiviral response should be investigated to uncover more functions of PEDV nsps.
T337 18193-18373 Sentence denotes These data suggest that PEDV has evolved multiple evasive mechanisms to circumvent viral RNA recognition or prevent RNA degradation to establish a successful infection in the host.
T338 18375-18381 Sentence denotes 4.2.6.
T339 18382-18462 Sentence denotes PEDV Inhibits Heat Shock Protein 27 Expression to Impair Innate Immune Signaling
T340 18463-18702 Sentence denotes Heat shock protein 27 (HSP27) belongs to the small heat shock proteins family, which has been identified as a multifunctional protein involved in cytoskeletal stability, proinflammatory processes, and the inhibition of apoptosis [222,223].
T341 18703-18801 Sentence denotes Several HSPs have been reported to be implicated in PEDV infection in vitro and in vivo [224,225].
T342 18802-18985 Sentence denotes Indeed, the infection of many viruses up-regulates HSP27 expression by different mechanisms to delay cellular apoptosis, then supplies sufficient time for viral replication [226,227].
T343 18986-19111 Sentence denotes However, PEDV infection significantly induces the decreased expression of HSP27 in Vero cells [225] and MARC-145 cells [228].
T344 19112-19223 Sentence denotes HSP27 activates the phosphorylation of NF-κB, and thus promotes the mRNA expression of IFN-β in MARC-145 cells.
T345 19224-19357 Sentence denotes As HSP27 is an upstream regulator of antiviral immune signaling, overexpression of HSP27 significantly inhibits the PEDV replication.
T346 19358-19487 Sentence denotes PEDV has developed a strategy via mediating the suppression of HSP27 production to escape from host innate immune response [228].
T347 19488-19576 Sentence denotes HSP70, the most conserved HSP, is also important for the multiplication of several CoVs.
T348 19577-19686 Sentence denotes The recruitment of HSP70 is thought to be a viral survival strategy for several viruses in their hosts [229].
T349 19687-19765 Sentence denotes The relationship between HSP70 and PEDV should be exploited further in future.