Virion Production(病毒体生产)研究综述
Virion Production 病毒体生产 - We then focused on RhoV, a Rho GTPase with atypical terminal sequences and membrane association, and validated its proviral effects on ZIKV infection and virion production in SNB-19 cells. [1] The temporal expression of viral proteins was employed to identify potential candidate target proteins, especially those produced early in the replicative cycle before virion production. [2] We also found that there are a total of 19 signature single nucleotide polymorphisms (SNPs), of which 2 and 17 nonsynonymous mutation types were specific to rt269L and rt269I, respectively: Of these, most are HBeAg negative infections (preC-W28*, X-V5M and V131I), lowered HBV DNA or virion production (C-I97F/L, rtM204I/V) or preexisting nucleot(s)ide analog resistance (NAr) (rtN139K/H, rtM204I/V and rtI224V) or disease severity (preC-W28*, C-I97F/L, C-Q182K/*, preS2-F141L, S-L213I/S, V/L5M, T36P/S/A, V131I, rtN139K/H, rtM204I/V and rtI224V). [3] We recently identified a CD63-interacting protein to understand the role of CD63 in virion production of the human immunodeficiency virus type 1, and we have found that Rab3a forms a complex with CD63. [4] Ubiquitin and UBL posttranslational modifications, including FAT10, are utilized and dysregulated by viruses for achievement of effective infection and virion production. [5] However, late lytic gene expression and virion production were blocked after arsenic treatment. [6] Subsequent functional studies of the key members of the AP-1 family revealed that Fos, but not Jun, regulates ILTV infection through AP-1 since knockdown of Fos, but not Jun, by gene silencing significantly reduced ICP4 transcription and subsequent viral genome replication and virion production. [7] Interpretation Following administration of an LRA, quantification of MS RNA is more likely to reflect an increase in virion production and is therefore a better indicator of meaningful latency reversal. [8] The Open Reading Frame 45 (ORF45) of Kaposi sarcoma-associated herpesvirus (KSHV) is a gammaherpesvirus-specific, immediate-early, tegument protein required for efficient viral replication and virion production. [9] While takeover of the host replication and protein synthesis apparatus has long been considered an essential feature of infection, recent studies indicate that extensive reprogramming of host primary metabolism is a widespread phenomenon among prokaryotic viruses that is required to fulfill the biosynthetic needs of virion production. [10] Virion production was significantly diminished in the ORF20-deficient virus as observed by supernatant transfer assays. [11] Furthermore, in pulse-chase experiments, we demonstrated that the presence of dynasore only during the early phase of MCMV infection (4–14 hpi) is sufficient to prevent not only AC formation but also the synthesis of late-phase proteins and virion production. [12] We identify an antibacterial antibiotic, clofoctol, that is an activator of EBV lytic RNA and protein expression but that does not lead to virion production. [13] Here, a streamlined production system is described based on knowledge of the involvement of HBoV1 nonstructural (NS) proteins NS1, NS2, NS3, NS4, and NP1 in the process of virion production. [14] The short-term persistence period in Bm5 cells is characterized by low levels of viral replication and virion production as well as by the production of viral siRNAs. [15] coli by en passant recombineering before virion production in DF-1 cells. [16] During infection, their genomes are carried in capsids across the membranes of host cells to sites of virion production by exploiting cellular behaviour and resources to guide and achieve all aspects of delivery and the downstream virus manufacturing process. [17] Virus infection and cancer development share many similarities regarding metabolic reprogramming as both processes demand increased metabolic activity to produce biomass: cell proliferation in the case of cancer and virion production in the case of infection. [18] Although the PARP inhibitor decreased HTLV-1 infection through cell adhesion, it increased HTLV-1 infection through virion production and caused apoptosis of HTLV-1-infected cells. [19] Based on these results, we present a mechanistic model in which sfRNA sequesters ME31B to promote flavivirus replication and virion production to facilitate transmission by mosquitoes. [20] In this study, we showed by biological and molecular analyses that the linker region functions as an intramolecular modulator to tune Gag assembly, virion production, and viral infectivity. [21] Deciphering the modes of NS3-interacting host proteins functions in virion production will shed light on JEV pathogenic mechanisms and may also reveal new avenues for antiviral therapeutics. [22] Hepatitis delta virus (HDV) depends on the envelope proteins of hepatitis B virus (HBV) for virion production. [23] Isolated primary mouse IECs were subjected to AiV infection and virion production, inducing the mRNA expression of type I/type III IFNs and inflammatory cytokines. [24]然后，我们专注于 RhoV，一种具有非典型末端序列和膜结合的 Rho GTPase，并验证了它对 ZIKV 感染和 SNB-19 细胞中病毒粒子产生的前病毒作用。 [1] 病毒蛋白的时间表达用于鉴定潜在的候选靶蛋白，尤其是在病毒粒子产生之前的复制周期早期产生的那些。 [2] 我们还发现共有 19 种特征性单核苷酸多态性 (SNP)，其中 2 种和 17 种非同义突变类型分别对 rt269L 和 rt269I 具有特异性：其中，大多数是 HBeAg 阴性感染（preC-W28*，X -V5M 和 V131I)，降低 HBV DNA 或病毒粒子产生 (C-I97F/L, rtM204I/V) 或预先存在的核苷酸类似物抗性 (NAr) (rtN139K/H, rtM204I/V 和 rtI224V) 或疾病严重程度 ( preC-W28*、C-I97F/L、C-Q182K/*、preS2-F141L、S-L213I/S、V/L5M、T36P/S/A、V131I、rtN139K/H、rtM204I/V 和 rtI224V）。 [3] 我们最近鉴定了一种 CD63 相互作用蛋白，以了解 CD63 在人类免疫缺陷病毒 1 型病毒粒子产生中的作用，我们发现 Rab3a 与 CD63 形成复合物。 [4] 泛素和 UBL 翻译后修饰，包括 FAT10，被病毒利用和失调，以实现有效的感染和病毒粒子的产生。 [5] 然而，砷处理后，晚期裂解基因的表达和病毒粒子的产生被阻断。 [6] 随后对 AP-1 家族关键成员的功能研究表明，Fos 而不是 Jun 通过 AP-1 调节 ILTV 感染，因为 Fos 而不是 Jun 的敲低，通过基因沉默显着降低了 ICP4 转录和随后的病毒基因组复制和病毒粒子的产生。 [7] 解释 施用 LRA 后，MS RNA 的定量更可能反映病毒粒子产生的增加，因此是有意义的潜伏期逆转的更好指标。 [8] 卡波西肉瘤相关疱疹病毒 (KSHV) 的开放阅读框 45 (ORF45) 是一种 gammaherpesvirus 特异性、即早、被膜蛋白，是有效病毒复制和病毒粒子生产所必需的。 [9] 虽然接管宿主复制和蛋白质合成装置长期以来一直被认为是感染的基本特征，但最近的研究表明，宿主初级代谢的广泛重编程是原核病毒中普遍存在的现象，这是满足病毒体生产的生物合成需求所必需的。 [10] 如上清液转移分析所观察到的，ORF20 缺陷型病毒的病毒粒子产生显着减少。 [11] 此外，在脉冲追踪实验中，我们证明仅在 MCMV 感染的早期阶段（4-14 hpi）存在 dynasore 足以防止 AC 的形成，也足以防止晚期蛋白质的合成和病毒粒子的产生。 [12] 我们确定了一种抗菌抗生素，clofoctol，它是 EBV 裂解 RNA 和蛋白质表达的激活剂，但不会导致病毒粒子的产生。 [13] 在这里，基于 HBoV1 非结构 (NS) 蛋白 NS1、NS2、NS3、NS4 和 NP1 在病毒粒子生产过程中的参与知识，描述了一个简化的生产系统。 [14] Bm5 细胞中的短期持续期的特点是病毒复制和病毒粒子产生水平低以及病毒 siRNA 的产生。 [15] 在 DF-1 细胞中产生病毒粒子之前，通过 en passant 重组工程对大肠杆菌进行了研究。 [16] 在感染期间，通过利用细胞行为和资源来指导和实现递送和下游病毒制造过程的各个方面，它们的基因组通过宿主细胞的膜在衣壳中携带到病毒粒子产生的位点。 [17] 病毒感染和癌症发展在代谢重编程方面有许多相似之处，因为这两个过程都需要增加代谢活动来产生生物质：癌症情况下的细胞增殖和感染情况下的病毒粒子产生。 [18] 尽管 PARP 抑制剂通过细胞粘附减少了 HTLV-1 感染，但它通过病毒粒子的产生增加了 HTLV-1 感染并导致 HTLV-1 感染细胞的凋亡。 [19] 基于这些结果，我们提出了一个机制模型，其中 sfRNA 隔离 ME31B 以促进黄病毒复制和病毒粒子的产生，从而促进蚊子的传播。 [20] 在这项研究中，我们通过生物学和分子分析表明，接头区域作为分子内调节剂来调节 Gag 组装、病毒粒子产生和病毒感染性。 [21] 破译 NS3 相互作用的宿主蛋白在病毒粒子产生中的功能模式将阐明 JEV 的致病机制，并可能揭示抗病毒治疗的新途径。 [22] 丁型肝炎病毒 (HDV) 依赖于乙型肝炎病毒 (HBV) 的包膜蛋白来产生病毒粒子。 [23] 分离的原代小鼠 IEC 经受 AiV 感染和病毒粒子的产生，诱导 I 型/III 型 IFN 和炎性细胞因子的 mRNA 表达。 [24]
Infectiou Virion Production 传染性病毒粒子的产生
In addition, transcriptome analysis of viral and cellular genes in latent and lytic cells showed that unlike other infected cell lines, the latently infected cells expressed both latent and most, but not all, of the lytic genes required for infectious virion production. [1] Importantly, KSHV lytic replication and infectious virion production could be inhibited by both Kv1. [2] In this review, we discuss how the EBV infection program that leads to infectious virion production and co-infections, such as with malaria parasites, the human immunodeficiency virus (HIV) and the Kaposi sarcoma-associated herpesvirus (KSHV), modulate this immune control. [3] Interestingly, this mutation inhibited infectious virion production of ZIKV and yellow fever virus, but not West Nile virus. [4] Zinc salt treatment potently suppressed EV-D68 RNA replication, protein synthesis, and infectious virion production and inhibited cytopathic effects without producing significant cytotoxicity at virucidal concentrations (EC50=0. [5] Here, we show that knockout of PAF1 enhances DENV2 infectious virion production. [6] From 48 to 96 hpi, the expression of genes associated with virus replication and dissemination decreased, whereas the expression of genes related to infectious virion production and per os infectivity increased. [7] An additional chimera (PCV structural genes in the backbone of West Nile virus - WNV/PCV-prME) was also unable to infect vertebrate cells, but transfection with RNA from this virus resulted in detectable RNA replication and translation but no infectious virion production. [8] KSHV, like other herpesviruses, intermittently reactivates from latency and enters a lytic cycle in which numerous lytic mRNAs and proteins are produced, culminating in infectious virion production. [9] The addition of IFN-γ up to 36 hr after induction of viral lytic replication was effective in terms of the inhibition of infectious virion production, suggesting that its inhibitory effect is exerted at the early stages of KSHV life cycle. [10] The increase in HCV RNA levels, however, failed to augment intracellular infectious virion production, reflecting a lower rate of virion assembly. [11] The gold standard for testing antiviral activity is to quantify infectious virion production. [12]此外，潜伏和裂解细胞中病毒和细胞基因的转录组分析表明，与其他受感染的细胞系不同，潜伏感染的细胞表达感染性病毒粒子产生所需的潜伏和大多数（但不是全部）裂解基因。 [1] 重要的是，Kv1 都可以抑制 KSHV 裂解复制和感染性病毒粒子的产生。 [2] 在这篇综述中，我们讨论了导致传染性病毒粒子产生和合并感染的 EBV 感染程序如何调节这种免疫控制，例如疟疾寄生虫、人类免疫缺陷病毒 (HIV) 和卡波西肉瘤相关疱疹病毒 (KSHV) . [3] 有趣的是，这种突变抑制了 ZIKV 和黄热病病毒的传染性病毒粒子的产生，但不抑制西尼罗河病毒。 [4] 锌盐处理可有效抑制 EV-D68 RNA 复制、蛋白质合成和感染性病毒粒子的产生，并抑制细胞病变效应，而在杀病毒浓度下不会产生显着的细胞毒性 (EC50=0. [5] 在这里，我们表明敲除 PAF1 可增强 DENV2 感染性病毒粒子的产生。 [6] 从 48 到 96 hpi，与病毒复制和传播相关的基因表达下降，而与感染性病毒粒子产生和经口感染性相关的基因表达增加。 [7] 另一个嵌合体（西尼罗河病毒骨架中的 PCV 结构基因 - WNV/PCV-prME）也无法感染脊椎动物细胞，但用来自该病毒的 RNA 转染导致可检测到的 RNA 复制和翻译，但没有产生感染性病毒粒子。 [8] 与其他疱疹病毒一样，KSHV 会间歇性地从潜伏期重新激活并进入一个裂解周期，在该周期中产生大量裂解性 mRNA 和蛋白质，最终导致感染性病毒粒子的产生。 [9] 在诱导病毒裂解复制后最多 36 小时添加 IFN-γ 在抑制感染性病毒粒子产生方面是有效的，这表明其抑制作用在 KSHV 生命周期的早期阶段发挥作用。 [10] 然而，HCV RNA 水平的增加未能增加细胞内感染性病毒粒子的产生，这反映了病毒粒子组装率的降低。 [11] 测试抗病毒活性的金标准是量化传染性病毒粒子的产生。 [12]
1 Virion Production
HIV-1 virion production is driven by Gag and Gag-Pol (GP) proteins, with Gag forming the bulk of the capsid and driving budding while GP binds Gag to deliver the essential virion enzymes Protease, Reverse Transcriptase, and Integrase. [1] PPS was cytotoxic to certain HTLV-1-infected cells and significantly suppressed HTLV-1 virion production. [2] It does not affect HIV-1 virion production during the first round of infection. [3] Moreover, adenosine could inhibit activation-induced HIV-1 virion production and p24 expression. [4] We tested the ability of the human anti-PD-L1 mAb BMS-936559 and the human anti-PD-1 mAb nivolumab to increase HIV-1 virion production ex vivo from different peripheral blood mononuclear cell populations obtained from donors on suppressive antiretroviral therapy (ART). [5] CHIP transfection in HIV-1 reporter TZM-bl cells resulted in decreased Tat-dependent HIV-1 long-terminal repeat (LTR) promoter transactivation as well as HIV-1 virion production. [6]HIV-1 病毒粒子的产生由 Gag 和 Gag-Pol (GP) 蛋白驱动，Gag 形成衣壳的主体并驱动出芽，而 GP 结合 Gag 以传递必需的病毒粒子酶蛋白酶、逆转录酶和整合酶。 [1] PPS 对某些 HTLV-1 感染的细胞具有细胞毒性，并显着抑制 HTLV-1 病毒粒子的产生。 [2] 它不影响第一轮感染期间 HIV-1 病毒粒子的产生。 [3] 此外，腺苷可以抑制激活诱导的 HIV-1 病毒粒子的产生和 p24 的表达。 [4] 我们测试了人类抗 PD-L1 单克隆抗体 BMS-936559 和人类抗 PD-1 单克隆抗体 nivolumab 增加从接受抑制性抗逆转录病毒治疗的供体获得的不同外周血单核细胞群离体产生 HIV-1 病毒粒子的能力。艺术）。 [5] HIV-1 报告基因 TZM-bl 细胞中的 CHIP 转染导致 Tat 依赖性 HIV-1 长末端重复 (LTR) 启动子反式激活以及 HIV-1 病毒粒子产生减少。 [6]
Progeny Virion Production 后代病毒体生产
Kaposin-deficient latent iSLK cell lines displayed reduced viral genome copy number and often exhibited small LANA nuclear bodies; despite this, all were capable of progeny virion production. [1] Chimeric recombinant BoDV-1 expressing BoDV-2 N but not BoDV-1 N showed higher transcription and replication levels, whereas the propagation and infectious particle production of the chimeric virus were comparable to those of wild-type BoDV-1, suggesting that the level of viral replication in the nucleus is not directly involved in the progeny virion production of BoDVs. [2] Following reovirus infection, cells activate stress responses that repress canonical translation as a mechanism to limit progeny virion production. [3] Hepatitis B virus (HBV) core protein (HBc) serves pivotal roles in the viral life cycle, particularly serving as the basic unit for capsid assembly, and is closely associated with HBV genome replication and progeny virion production. [4]缺乏 Kaposin 的潜伏 iSLK 细胞系表现出病毒基因组拷贝数减少，并且经常表现出小的 LANA 核体；尽管如此，所有人都能够产生后代病毒粒子。 [1] 表达 BoDV-2 N 但不表达 BoDV-1 N 的嵌合重组 BoDV-1 表现出更高的转录和复制水平，而嵌合病毒的繁殖和感染性颗粒产生与野生型 BoDV-1 相当，表明水平病毒在细胞核中的复制不直接参与 BoDV 的子代病毒粒子产生。 [2] 呼肠孤病毒感染后，细胞会激活抑制典型翻译的应激反应，以此作为限制后代病毒粒子产生的机制。 [3] 乙型肝炎病毒 (HBV) 核心蛋白 (HBc) 在病毒生命周期中发挥着举足轻重的作用，尤其是作为衣壳组装的基本单位，与 HBV 基因组复制和后代病毒粒子的产生密切相关。 [4]
Kshv Virion Production
Together, these results indicated that ORF37’s proposed DNase activity is essential for viral genome processing and encapsidation and, hence, can be targeted for designing antiviral agents to block KSHV virion production. [1] Depletion of IFIT1, IFIT2 and IFIT3 (IFITs) increased infectious KSHV virion production 25-32-fold compared to that in control cells. [2] After screening a compound library that consisted of 1280 Food and Drug Administration (FDA)-approved drugs, 15 hit compounds that effectively inhibited KSHV virion production were identified, most of which have never been reported with anti-KSHV activities. [3]总之，这些结果表明，ORF37 提出的 DNase 活性对于病毒基因组加工和衣壳化至关重要，因此可以作为设计抗病毒剂以阻断 KSHV 病毒粒子产生的目标。 [1] 与对照细胞相比，IFIT1、IFIT2 和 IFIT3 (IFIT) 的消耗使感染性 KSHV 病毒粒子的产生增加了 25-32 倍。 [2] 在筛选由 1280 种食品和药物管理局 (FDA) 批准的药物组成的化合物库后，确定了 15 种有效抑制 KSHV 病毒粒子产生的热门化合物，其中大多数从未被报道具有抗 KSHV 活性。 [3]
Titer Virion Production
Interestingly, a second NS2 mutation (V439-D) identified by selection was essential for high titer virion production. [1] Interestingly, a second NS2 mutation (V439-D), identified by selection, was essential for high-titer virion production. [2]有趣的是，通过选择确定的第二个 NS2 突变 (V439-D) 对于高效价病毒粒子的生产至关重要。 [1] 有趣的是，通过选择鉴定的第二个 NS2 突变 (V439-D) 对于高效价病毒粒子的生产至关重要。 [2]
Extracellular Virion Production
Higher intracellular DENV RNA, DENV E protein, and intracellular virion were observed, whereas the extracellular virion production was comparably less than that of control. [1] In this study, inhibition the protein expression of the ESCRT components reduces the extracellular virion production, which preliminarily indicates that the ESCRT pathway is involved in IHNV release. [2]观察到较高的细胞内 DENV RNA、DENV E 蛋白和细胞内病毒粒子，而细胞外病毒粒子的产生相对低于对照。 [1] 在本研究中，抑制ESCRT成分的蛋白表达会降低细胞外病毒粒子的产生，这初步表明ESCRT通路参与了IHNV的释放。 [2]
Reduced Virion Production 减少病毒粒子的产生
Our results indicate that resveratrol treatment is capable of inhibiting VEEV replication, resulting in increased viability of Vero and U87MG cells as well as reduced virion production and viral RNA contents within host cells for at least 48 h with a single treatment. [1] Deletion and knockdown of PAN resulted in defects in viral replication and reduced virion production in the absence of PAN RNA. [2]我们的研究结果表明，白藜芦醇处理能够抑制 VEEV 复制，导致 Vero 和 U87MG 细胞的活力增加，并通过单次处理至少 48 小时降低宿主细胞内的病毒粒子产生和病毒 RNA 含量。 [1] PAN 的缺失和敲低导致病毒复制缺陷并在没有 PAN RNA 的情况下减少病毒粒子的产生。 [2]