Foot-and-Mouth Disease Virus: Comparison
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Foot-and-mouth disease (FMD) is an acute and highly contagious disease affecting the cloven-hoofed animals, such as pigs and cattle. The pathogen that causes FMD is known as FMD virus (FMDV), a single-stranded positive-sense RNA virus that is classified into the genus Aphthovirus in the family Picornaviridae.口蹄疫（FMD）是一种急性和高度传染性疾病，会影响到诸如猪和牛之类的蹄类动物。导致FMD的病原体称为FMD病毒（FMDV），这是一种单链正义RNA病毒，在Picornaviridae家族中被归类为Aphthovirus属。

  • foot-and-mouth disease virus
  • immune escape
  • innate immune response
  • Interferon
  • protein interaction
  • viral protein

Note：All the information in this draft can be edited by authors. And the entry will be online only after authors edit and submit it.

1. Introduction

Foot-and-mouth disease (FMD) is an acute and highly contagious disease affecting thecloven-hoofed animals, such as pigs and cattle. The pathogen that causes FMD is known as FMD virus(FMDV), a single-stranded positive-sense RNA virus that is classified into the genus Aphthovirus inthe family Picornaviridae [1][2]. The pathogen causes vesicular disease of mouth and feet in susceptibleanimals [3]. The high mutation rate of the genome of FMDV and the rapid proliferation has led to therapid evolution of the virus and the formation of seven main serotypes [4][5][6]. The antigenic diversityamong the serotypes poses challenges to the research of efficient and cross-protective vaccines [8].The genome of FMDV contains an open reading frame (ORF) that encodes a polyprotein precursor,and it is cleaved into four structural proteins and 10 non-structural proteins by viral autoproteases andhost protease [7](Figure 1).Upon infection of the host, a virus will face the attack from the host’s immune response. In thelong-term battle with the host immune response, the virus has evolved and developed a series ofimmune escape mechanisms to overcome the killing and inhibition from the host immune system.The mechanism of virus immune escape can be divided into three categories: (1) enable the virus toavoid the recognition of humoral immune response; (2) interfere with the function of cellular immuneresponse; (3) interfere with the host’s immune response to the virus [8]. All these strategies would beexploited by the virus for replication and spreading to other hosts.As a highly contagious and fast-spreading virus, FMDV has multiple ways to evade the killing bythe immune system [9], which makes it difficult for controlling the virus. Viral capsid protein VP1 and leading protein Lpro can inhibit the production of interferon (IFN) and innate immune responseby interacting with soluble resistance-related calcium-binding protein (sorcin) or host transcriptionfactor ADNP [10][11]. Recently, new mechanisms and functions of FMDV proteins inhibiting innateimmunity have been discovered. DDX56 (a kind of RNA helicase), participate in RNA metabolism andribosome synthesis is reported to involve in this new mechanism. The interaction between FMDV3A and DDX56 suppresses the host innate immunity by reducing the phosphorylation of IRF3 [12].In addition, nucleotide-binding oligomerization domain 2 (NOD2), a member of the nucleotide-bindingoligomerization domain-like receptor (NLR) family [13], activates the NF-κB and IFN-βsignalingpathways during FMDV infection and inhibits the replication of FMDV in infected cells [14]. FMDV 2B,2C, and 3Cproinhibit the expression of NOD2 protein, which antagonizes the antiviral response [14].Reportedly, multiple structural and non-structural proteins of FMDV escape the killing of the hostimmune system. This review summrized the molecular mechanisms of immune evasion caused byFMDV proteins. The present study aimed to fill the gaps of knowledge on FMDV immune evasionmechanism, providing the basis for the prevention and control strategies for FMDV.

Figure 1.Schematic of the genome and polypeptide processing of FMDV [2][7]. The FMDV genomecontains an ORF of about 7 kbp, indicated by the shaded rectangle. Each region within the ORFrectangle represents a single protein. The flank of ORF is a long 5′untranslated region (5′-UTR) and ashort 3′-UTR. 3B covalently binds to the 5′-end.

2. Prospects and Future Directions

FMDV is a highly contagious virus that infects almost all cloven-hoofed animals, showingvesicles on the foot and mouth, skin erosion on the mucous membranes, fever, weight loss, pacing,and salivation, severely threatening the development of animal husbandry. However, in additionto causing acute infections and diseases, FMDV can be asymptomatic carriers in some cases, whichmight lead to another outbreak of FMD, making prevention and control challenging and costly. Highinfectivity, wide geographical distribution, wide host range, short-term immunity without serotypecross-protection, multiple modes of transmission, and persistent infection render the control and eradication of this disease rather difficult. Therefore, study the molecular mechanism underlyingFMDV evading immunity is imperative for the control of an epidemic situation.The immune system includes innate immunity and acquired immunity, which is a major protectivesystem against the invasion of pathogenic microorganisms, surveillance, and removal of foreign bodies.FMDV suppresses the function of the immune system at the initial stage of infection, such that thevirus can proliferate rapidly in the respiratory system and spread to its natural infection site [15].In terms of evading the humoral immune system, each serotype of FMDV is prone to antigenicvariation, which makes the virus escape from the neutralizing antibodies [16]. In the aspect ofinhibiting cellular immune response, FMDV infection can cause the decrease of host lymphocytes andis accompanied by severe viremia, which will eventually lead to the destruction of T cells and FMDVinfection inhibits the function of dendritic cells and weakens the ability of dendritic cells to processthem into antigens [143,144]. Previous studies have shown that, MHC class I molecule expression onthe surface of cells was suppressed at 30 min after FMDV infection, indicating that the cells infectedwith FMDV will immediately lose the ability to present MHC-I-related viral peptides to T lymphocytes.This mechanism would facilitate the virus escape from the host’s cytotoxic immune response. Limitingthe killing effect mediated by NK cells is also an important mechanism for FMDV to evade the cellularimmune response. Some studies have shown that the responsiveness of porcine NK cells decreasessignificantly 2–3 days after FMDV infection, and then returns to normal [17]. Strikingly, NK cellsisolated from infected pigs could not secrete IFN-γ [18]. The research on FMDV interference withimmune effect and suppression of innate immunity has been widely studied. Some proteins of FMDV(Lpro,2B, 3A, 3B, 3C) can directly or indirectly act on retinoic acid-induced gene I-like receptor (RLR) toinhibit innate immunity [19][20][21][22][23]. FMDV VP0, VP3, 3A, and 3B reduce the expression of junctionprotein VISA at the transcriptional or protein level [23][24][25]. FMDV Lpro, VP0, VP1, 2B, and 3A candirectly or indirectly target IRF3 to inhibit interferon production [21][23][26]. VP3 and 3C proteinsinhibit JAK-STAT signaling pathway, thus inhibiting ISGs production [27][28]. FMDV proteins Lproand 3C inhibit the synthesis of antiviral molecules by cutting related factors of host transcriptionand translation [11][29][30][31][32] . In addition, it is interesting that Lproprotein can not only induceapoptosis, but also inhibit host cell apoptosis and promote virus replication, which is achieved byblocking the translation ofα-IFN and inhibiting PKR synthesis [33]. FMDV protein VP2 and 2C canpromote virus replication by regulating autophagy [34][35]. These mechanisms provide opportunitiesfor rapid transcription and translation of FMDV.In the previous studies on FMDV, HEK293 cells have been widely used inin vitroexperimentsbecause of its highly transfected efficiency. However, HEK293 cells are not FMDV susceptible cells andthere are species differences between HEK293 cells and FMDV susceptible cells. Therefore, the use ofHEK293 cells for FMDV-related research has some limitations.FMDV是一种具有高度传染性的病毒，几乎感染了所有偶蹄类动物，在脚和嘴上显示出囊泡，在粘膜上出现皮肤侵蚀，发烧，体重减轻，起搏和流涎，严重威胁着畜牧业的发展。但是，FMDV除了引起急性感染和疾病外，在某些情况下还可能是无症状的携带者，这可能会导致口蹄疫的再次爆发，使预防和控制工作面临挑战且成本高昂。高传染性，广泛的地理分布，广泛的寄主范围，没有血清型交叉保护的短期免疫，多种传播方式和持续感染使控制和根除这种疾病相当困难。因此，研究控制FMDV逃避免疫力的分子机制对于控制流行病势在必行。免疫系统包括先天免疫力和获得性免疫力，这是抵抗病原微生物入侵，监视和清除异物的主要保护系统。在感染初期抑制免疫系统的功能，从而使病毒可以在呼吸系统中迅速增殖并传播到其自然感染部位[ 15 ]。就逃避体液免疫系统而言，FMDV的每种血清型都容易发生抗原变异，使病毒从中和抗体中逃脱[ 16 ]。在抑制细胞免疫反应方面，FMDV感染可引起宿主淋巴细胞减少，并伴有严重病毒血症，最终将导致T细胞的破坏，FMDV感染会抑制树突状细胞的功能，削弱树突状细胞的加工能力。抗原[143,144]。先前的研究表明，FMDV感染后30分钟，细胞表面的MHC I类分子表达被抑制，这表明被FMDV感染的细胞将立即失去向T淋巴细胞呈递M​​HC-I相关病毒肽的能力。将有助于病毒从宿主的细胞毒性免疫反应中逃脱。限制NK细胞介导的杀伤作用也是FMDV逃避细胞免疫应答的重要机制。[ 17 ]。令人惊讶的是，从感染猪中分离出的NK细胞不能分泌IFN-γ [ 18 ]。FMDV干扰免疫效果和抑制先天免疫的研究已广泛开展。FMDV（Lpro，2B，3A，3B，3C）的某些蛋白质可以直接或间接作用于视黄酸诱导的基因I样受体（RLR），以抑制先天性免疫[ 19 ] [ 20 ] [ 21 ] [ 22 ] [ 23 ]。FMDV VP0，VP3、3A和3B在转录或蛋白质水平上降低连接蛋白VISA的表达[ 23 ] [24 ] [ 25 ]。FMDV Lpro，VP0，VP1、2B和3A可以直接或间接靶向IRF3以抑制干扰素产生 [ 21 ] [ 23 ] [ 26 ]。VP3和3C蛋白抑制JAK-STAT信号传导途径，从而抑制ISG的产生 [ 27 ] [ 28 ]。FMDV蛋白Lproand 3C通过切割宿主转录和翻译的相关因子来抑制抗病毒分子的合成 [ 11 ] [ 29 ] [ 30 ] [ 31 ] [ 32]。此外，有趣的是，Lpro蛋白不仅可以诱导细胞凋亡，而且可以抑制宿主细胞凋亡并促进病毒复制，这是通过阻断α-IFN的翻译并抑制PKR合成来实现的[ 33 ]。FMDV蛋白VP2和2C可以通过调节自噬来促进病毒复制[ 34 ] [ 35 ]。这些机制为FMDV的快速转录和翻译提供了机会。在以前的FMDV研究中，HEK293细胞因其高转染效率而被广泛用于体外实验。但是，HEK293细胞不是FMDV易感细胞，并且HEK293细胞和FMDV易感细胞之间存在物种差异。因此，将HEK293细胞用于FMDV相关研究有一定的局限性。

3. Conclusions3.结论

In summary, FMDV has evolved a variety of ways to evade the immune response in the long-termcombat with the host immune system. Although there are many breakthroughs in the research on theimmune escape of FMDV, many mechanisms underlying the FMDV-affected host immunity have notyet been elucidated, and the interaction between FMDV protein and host protein need to be exploredfurther. In addition to the interaction between the virus and host protein, exploring the mechanismof synergistic inhibition of immune response by multiple viral proteins is of great significance forthe development of specific drugs and new vaccines. Previous studies mainly focused on the effectof FMDV with respect to innate immunity. However, there are a few studies on acquired immunity,and these need to be supplemented further. Also, persistent infection of FMDV needs to be investigatedintensively in the future. 总之，FMDV已经进化出多种方法来逃避与宿主免疫系统的长期战斗中的免疫反应。尽管FMDV的免疫逃逸研究取得了许多突破，但仍阐明了受FMDV影响的宿主免疫的许多机制，还需要进一步探讨FMDV蛋白与宿主蛋白之间的相互作用。除了病毒与宿主蛋白之间的相互作用外，探索多种病毒蛋白协同抑制免疫反应的机制对于开发特定药物和新疫苗也具有重要意义。先前的研究主要集中于FMDV对先天免疫的影响。但是，关于获得性免疫的研究很少，有待进一步补充。也， 

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