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Evaluating the zoonotic spectrum of sandfly-borne phleboviruses, Africa 评估非洲白蛉传播的白蛉病毒的人畜共患谱。
IF 5.1 2区 医学 Q1 VIROLOGY Pub Date : 2025-10-13 DOI: 10.1016/j.coviro.2025.101494
Edwin O Ogola , Missiani Ochwoto , Tatenda Chiuya , Marshall E Bloom , David P Tchouassi
Sandfly-borne phleboviruses (SBPs) are an important cause of febrile diseases and neuroinvasive infections in humans, especially in endemic regions. They have been described in Central Asia, Africa, the Middle East, and the Mediterranean regions. Current investigations suggest that SBPs originated from Africa, albeit with little zoonotic threat information. Particularly pertinent is the recent identification of genetically diverse SBPs associated with human infection circulating in North and East Africa. Spread of these viruses to new regions may pose a significant risk to the local populations with little or no pre-existing immunity. Additionally, the lack of SBP detection methods at the point of care may lead to an incorrect diagnosis of malaria and influenza, inappropriate treatment, and an underestimated disease burden. Despite the availability of a wide range of analytic approaches that include cell culture, electron microscopy, and serological screening, diagnosis remains a challenge. Application of new molecular techniques such as next-generation sequencing (NGS) would enable description of new SBPs; however, correlation with additional field clinical data is needed to evaluate the zoonotic significance of any new SBPs. In this review, we provide a summary of the disease ecology of SBPs in Africa to concatenate the existing knowledge on transmission dynamics. The review also highlights the limited surveillance of SBPs in Africa, thus confirming the need for enhanced virus characterization incorporating advanced approaches such as capture-based target enrichment NGS, allowing for the detection of existing and novel SBPs, in addition to epidemiologic data on their clinical relevance.
白蛉传播的白蛉病毒(sbp)是人类发热性疾病和神经侵入性感染的重要原因,特别是在流行地区。它们在中亚、非洲、中东和地中海地区都有记载。目前的调查表明,sbp起源于非洲,尽管人畜共患威胁信息很少。尤其相关的是,最近在北非和东非发现了与人类感染相关的遗传多样性sbp。这些病毒传播到新的地区,可能会对先前很少或没有免疫力的当地人群构成重大风险。此外,在医疗点缺乏收缩压检测方法可能导致对疟疾和流感的错误诊断、不适当的治疗和低估疾病负担。尽管有广泛的分析方法,包括细胞培养、电子显微镜和血清学筛查,但诊断仍然是一个挑战。新一代测序(NGS)等新分子技术的应用将有助于描述新的sbp;然而,需要与其他现场临床数据的相关性来评估任何新的sbp的人畜共患意义。在这篇综述中,我们总结了非洲小蠊的疾病生态学,以连接现有的传播动力学知识。该审查还强调了非洲对sbp的有限监测,从而确认需要加强病毒特征鉴定,包括基于捕获的靶标富集NGS等先进方法,除了有关其临床相关性的流行病学数据外,还允许检测现有和新型sbp。
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引用次数: 0
Host-targeted antivirals as broad-spectrum inhibitors of respiratory viruses 宿主靶向抗病毒药物作为呼吸道病毒的广谱抑制剂。
IF 5.1 2区 医学 Q1 VIROLOGY Pub Date : 2025-10-01 DOI: 10.1016/j.coviro.2025.101492
Rudolf K Beran, Arya Vijjapurapu, Varsha Nair, Venice Du Pont
Respiratory viruses, including influenza virus, respiratory syncytial virus, human rhinovirus, and severe acute respiratory syndrome coronavirus 2, are among the leading causes of acute respiratory infections worldwide. Strategies for antiviral drug development include direct-acting antivirals (DAAs), which inhibit viral proteins, or host-targeting antivirals (HTAs), which target host factors required for the viral life cycle. DAAs are often virus-specific, leaving gaps for emerging viruses such as novel coronaviruses and influenza viruses, or less common respiratory viruses such as human metapneumovirus. Moreover, DAAs are prone to viral resistance due to the low fidelity of viral polymerases, whereas HTAs act on conserved host proteins that are less susceptible to viral escape due to greater genetic stability. A variety of HTAs are currently being investigated that target viral entry, replication, assembly, or egress. The key challenges for the development of effective broad-spectrum HTAs are related to safety and translation of in vitro potency to in vivo efficacy. This review examines host factors crucial for respiratory virus lifecycles — including sialic acid receptors, lipids, phosphoinositide kinases, mitogen-activated protein kinases, cellular helicases, and nucleotide biosynthesis pathways — and the small-molecule inhibitors and biologics that are being explored to target them.
呼吸道病毒,包括流感病毒、呼吸道合胞病毒、人鼻病毒和严重急性呼吸道综合征冠状病毒,是全世界急性呼吸道感染的主要原因之一。抗病毒药物开发的策略包括直接作用抗病毒药物(DAAs),其抑制病毒蛋白,或宿主靶向抗病毒药物(hta),其靶向病毒生命周期所需的宿主因子。daa通常是病毒特异性的,这为新出现的病毒(如新型冠状病毒和流感病毒)或不太常见的呼吸道病毒(如人偏肺病毒)留下了空白。此外,由于病毒聚合酶的保真度较低,DAAs容易产生病毒抗性,而hta作用于保守的宿主蛋白,由于遗传稳定性更高,这些蛋白对病毒逃逸不太敏感。目前正在研究针对病毒进入、复制、组装或出口的各种hta。开发有效的广谱hta的关键挑战与安全性和体外效力到体内功效的转化有关。本文综述了对呼吸道病毒生命周期至关重要的宿主因子,包括唾液酸受体、脂质、磷酸肌苷激酶、丝裂原活化蛋白激酶、细胞解旋酶和核苷酸生物合成途径,以及正在探索的针对这些因子的小分子抑制剂和生物制剂。
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引用次数: 0
Multiple roles of the matrix protein Z in arenavirus infection — a structural perspective 基质蛋白Z在沙粒病毒感染中的多重作用——一个结构视角
IF 5.1 2区 医学 Q1 VIROLOGY Pub Date : 2025-09-24 DOI: 10.1016/j.coviro.2025.101493
Annika Rammelt , Saskia Johanns , Lennart Sänger , Gabriele Diana , Maria Rosenthal
Arenaviridae (class of Bunyaviricetes) are a group of negative-sense single-stranded RNA viruses. They can cause severe human disease after zoonotic spillover from mostly rodent reservoirs, with no approved vaccines or antiviral treatments available. Limited understanding of the processes within an infected cell is hampering the development of medical countermeasures. Although arenaviruses contain only a few proteins, they all serve multiple purposes during the viral life cycle. Here, we focus on the matrix protein Z, a small protein with multiple important roles during infection. We summarize the current state of literature linking structure and function and highlight open questions.
沙粒病毒科(Bunyaviricetes纲)是一组负义单链RNA病毒。在大多数啮齿动物宿主的人畜共患病溢出后,它们可引起严重的人类疾病,而目前尚无批准的疫苗或抗病毒治疗方法。对受感染细胞内部过程的有限了解阻碍了医疗对策的发展。虽然沙粒病毒只含有少量蛋白质,但它们在病毒生命周期中都有多种用途。在这里,我们关注的是基质蛋白Z,这是一种在感染过程中具有多种重要作用的小蛋白。我们总结了文献连接结构和功能的现状,并突出了有待解决的问题。
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引用次数: 0
Virological and immunological determinants of hepatitis E virus infection outcomes 戊型肝炎病毒感染结果的病毒学和免疫学决定因素。
IF 5.1 2区 医学 Q1 VIROLOGY Pub Date : 2025-09-19 DOI: 10.1016/j.coviro.2025.101491
Xinjia Wang , Lu Bian , Eun Hee Ha , Lei Wang , Kyle O’Shaughnessy , Yifei Zheng , Zhuoying Feng , Wei Bo Chen , Xianfang Wu
Hepatitis E virus (HEV) is a leading cause of acute viral hepatitis worldwide, especially in regions with limited sanitation infrastructure. Unlike hepatitis B virus (HBV) and hepatitis C virus (HCV) — which frequently progress to chronic infections associated with cirrhosis and hepatocellular carcinoma — HEV typically leads to acute and self-resolving infection in immunocompetent individuals. This review explores the mechanistic underpinnings that distinguish HEV’s clinical trajectory from HBV and HCV, focusing on viral genome organization, replication strategies, immune evasion tactics, and host immune responses. Understanding these factors provides critical insights into the determinants of viral clearance versus persistence and may guide future vaccine and antiviral development.
戊型肝炎病毒(HEV)是全世界急性病毒性肝炎的主要病因,特别是在卫生基础设施有限的地区。与乙型肝炎病毒(HBV)和丙型肝炎病毒(HCV)不同,乙型肝炎病毒(HBV)和丙型肝炎病毒(HCV)经常发展为与肝硬化和肝细胞癌相关的慢性感染,HEV通常在免疫能力强的个体中导致急性和自解性感染。这篇综述探讨了区分HEV与HBV和HCV临床轨迹的机制基础,重点是病毒基因组组织、复制策略、免疫逃避策略和宿主免疫反应。了解这些因素有助于了解病毒清除与持续存在的决定因素,并可能指导未来疫苗和抗病毒药物的开发。
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引用次数: 0
Sequence variability of the K1 gene in Kaposi’s sarcoma-associated herpesvirus and its role in pathogenesis 卡波西氏肉瘤相关疱疹病毒K1基因序列变异及其在发病机制中的作用
IF 5.1 2区 医学 Q1 VIROLOGY Pub Date : 2025-09-17 DOI: 10.1016/j.coviro.2025.101489
Soyoung Choi , Jun Tae Song , Seung-Hyun Lee , Un Yung Choi
Infectious pathogens account for approximately 13% of all human cancers globally, with oncogenic viruses constituting the majority. Among them, Kaposi’s sarcoma-associated herpesvirus (KSHV), a gammaherpesvirus, remains a persistent public health concern. Although KSHV is endemic in sub-Saharan Africa, where it drives high rates of pediatric and endemic Kaposi’s sarcoma (KS), AIDS-related KS remains a significant burden among immunocompromised individuals, especially in areas with limited access to long-term antiretroviral therapy. Additionally, KSHV is etiologically linked to primary effusion lymphoma and multicentric Castleman disease, both increasingly observed in transplant recipients and individuals undergoing long-term immunosuppressive therapy. Despite decades of research, no approved vaccine or curative treatment is currently available. Among the KSHV-encoded proteins, the K1 oncoprotein, encoded by the first open reading frame of the viral genome, exhibits exceptional sequence diversity and plays a critical role in viral pathogenesis. K1 activates key host signaling pathways involved in angiogenesis, cellular transformation, and survival. Importantly, genetic variation within K1, particularly in its variable regions, forms the basis for classifying KSHV into distinct genotypes that show different geographic distributions and may have divergent pathogenic potentials. In this review, we provide an updated overview of functions of K1, highlight genotype-specific oncogenic mechanisms, and examine how K1 sequence diversity may shape viral evolution, host interactions, and clinical outcomes.
感染性病原体约占全球所有人类癌症的13%,其中致癌病毒占大多数。其中,卡波西肉瘤相关疱疹病毒(KSHV),一种伽玛疱疹病毒,仍然是一个持续的公共卫生问题。尽管KSHV在撒哈拉以南非洲流行,在那里它导致儿童和地方性卡波西肉瘤(KS)的高发率,但艾滋病相关的KS仍然是免疫功能低下个体的重大负担,特别是在获得长期抗逆转录病毒治疗有限的地区。此外,KSHV在病因学上与原发性积液性淋巴瘤和多中心Castleman病有关,这两种疾病在移植受体和接受长期免疫抑制治疗的个体中越来越多地观察到。尽管经过数十年的研究,目前还没有获得批准的疫苗或治疗方法。在kshv编码的蛋白中,由病毒基因组第一个开放阅读框编码的K1癌蛋白具有特殊的序列多样性,在病毒的发病机制中起着关键作用。K1激活涉及血管生成、细胞转化和存活的关键宿主信号通路。重要的是,K1内的遗传变异,特别是其可变区域的遗传变异,构成了将KSHV分类为不同基因型的基础,这些基因型表现出不同的地理分布,可能具有不同的致病潜力。在这篇综述中,我们提供了K1功能的最新概述,重点介绍了基因型特异性致癌机制,并研究了K1序列多样性如何影响病毒进化、宿主相互作用和临床结果。
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引用次数: 0
The Dengue NS1 epitope landscape: a blueprint for next-generation vaccines and therapeutics 登革热NS1表位景观:下一代疫苗和疗法的蓝图。
IF 5.1 2区 医学 Q1 VIROLOGY Pub Date : 2025-09-16 DOI: 10.1016/j.coviro.2025.101488
Romchat Kraivong , Sararat Hattakam , Somchai Thiemmeca , Panisadee Avirutnan
The dengue virus (DENV) nonstructural protein 1 (NS1) is a critical ‘double-edged sword’ in dengue pathogenesis and immunity. While a key driver of vascular pathology, it is also a major target for protective immune responses that lack the risk of antibody-dependent enhancement. Anti-NS1 antibodies can neutralize NS1’s pathogenic functions or clear infected cells; however, pathogenic responses can be driven by cross-reactive antibodies, causing cellular dysfunction or by NS1–antibody immune complexes triggering inflammatory damage. Concurrently, T-cell responses target conserved epitopes to drive viral clearance, though their efficacy is shaped by host HLA diversity. This review deconstructs the NS1 epitope landscape to provide a blueprint for rational countermeasure design. We emphasize how targeting immunogenic ‘hotspots’ can elicit balanced immunity, while also critically assessing the major translational hurdles, particularly the limitations of preclinical models, that must be overcome.
登革病毒(DENV)非结构蛋白1 (NS1)在登革热发病机制和免疫中是一把关键的“双刃剑”。虽然是血管病理的关键驱动因素,但它也是缺乏抗体依赖性增强风险的保护性免疫反应的主要靶点。抗NS1抗体可中和NS1的致病功能或清除感染细胞;然而,致病反应可由交叉反应性抗体驱动,导致细胞功能障碍或由ns1抗体免疫复合物引发炎症损伤。同时,t细胞反应以保守的表位为目标来驱动病毒清除,尽管它们的功效受宿主HLA多样性的影响。本文通过对NS1表位景观的解构,为合理的对策设计提供蓝图。我们强调靶向免疫原性“热点”如何引起平衡的免疫,同时也批判性地评估必须克服的主要转化障碍,特别是临床前模型的局限性。
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引用次数: 0
Intercellular highways of viral spread: tunneling nanotubes and extracellular vesicles at the maternal–fetal interface 病毒传播的细胞间高速公路:母胎界面的隧道纳米管和细胞外囊泡。
IF 5.1 2区 医学 Q1 VIROLOGY Pub Date : 2025-09-16 DOI: 10.1016/j.coviro.2025.101490
Long B Tran , Rafael T Michita , Deepak Kumar , Indira U Mysorekar
The placenta serves as both a conduit and a barrier, facilitating nutrient exchange while shielding the fetus from pathogens. Despite these defenses, several viruses, including ZIKV, CMV, HSV, HIV, LCMV, and HBV, can breach the placental barrier, while others like SARS-CoV-2 and RSV infect placental cells without consistent vertical transmission. Emerging evidence highlights two underexplored intercellular communication mechanisms, tunneling nanotubes (TNTs) and extracellular vesicles (EVs), as critical pathways exploited by viruses to disseminate, modulate immunity, and disrupt placental homeostasis. This review discusses how virally hijacked TNTs and EVs facilitate transmission and immune evasion at the maternal–fetal interface, emphasizing the need to further understand these mechanisms in the context of pregnancy and fetal health.
胎盘既是管道又是屏障,促进营养交换,同时保护胎儿免受病原体的侵害。尽管有这些防御措施,一些病毒,包括ZIKV、CMV、HSV、HIV、LCMV和HBV,可以突破胎盘屏障,而其他病毒,如SARS-CoV-2和RSV,感染胎盘细胞,但没有一致的垂直传播。新出现的证据强调了两个未被充分探索的细胞间通讯机制,隧道纳米管(TNTs)和细胞外囊泡(ev),是病毒传播、调节免疫和破坏胎盘稳态的关键途径。这篇综述讨论了病毒劫持的tnt和ev如何在母胎界面促进传播和免疫逃避,强调需要进一步了解这些机制在妊娠和胎儿健康的背景下。
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引用次数: 0
Nexus of virus and brain: recent advances in flavivirus and enterovirus neuro-infection 病毒与大脑的联系:黄病毒和肠病毒神经感染的最新进展
IF 5.1 2区 医学 Q1 VIROLOGY Pub Date : 2025-09-11 DOI: 10.1016/j.coviro.2025.101487
Cheryl Yi-Pin Lee , Fok-Moon Lum
The global prevalence of neurotropic viruses is increasing annually, with no effective treatments available. Viral entry into the brain involves a complex interplay of host and viral factors, such as tight junction complexes, immune regulators, and viral protein polymorphisms. After establishing an infection in the brain, neurotropic viruses can trigger immune cell activation, robust inflammatory responses, and synaptic disruption, contributing to both acute and chronic neuropathology, including accelerated neuronal ageing and neurodegeneration. A wealth of studies has focused on the molecular mechanisms underlying the neurovirulence and neuropathogenesis of clinically relevant neurotropic RNA viruses, revealing critical insights into their interactions with host cells and immune response. However, despite such advances, a disparity in knowledge on how these viruses enter the brain remains. In this review, significant progress within the last 2 years, as well as research niche and challenges in unravelling the neuropenetrance of clinically relevant neurotropic flaviviruses and enteroviruses in causing neuro-associated pathology will be discussed.
嗜神经病毒的全球流行率每年都在增加,但没有有效的治疗方法。病毒进入大脑涉及宿主和病毒因素的复杂相互作用,如紧密连接复合物、免疫调节因子和病毒蛋白多态性。在大脑中建立感染后,嗜神经病毒可以触发免疫细胞激活,强烈的炎症反应和突触破坏,导致急性和慢性神经病理,包括加速神经元老化和神经变性。大量的研究集中在临床相关嗜神经RNA病毒的神经毒力和神经发病机制的分子机制上,揭示了它们与宿主细胞和免疫反应相互作用的重要见解。然而,尽管取得了这些进展,但对这些病毒如何进入大脑的了解仍然存在差异。在这篇综述中,我们将讨论近2年来在揭示临床相关的嗜神经黄病毒和肠病毒在引起神经相关病理中的神经外显性方面取得的重大进展,以及研究领域和面临的挑战。
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引用次数: 0
Intracranial calcifications in congenital viral infections: mechanisms and cellular roles 先天性病毒感染的颅内钙化:机制和细胞作用
IF 5.1 2区 医学 Q1 VIROLOGY Pub Date : 2025-09-06 DOI: 10.1016/j.coviro.2025.101479
Michael Fraczek , Haley Breckenridge , Ivonne Melano , Elisabeth Squillacioti , Karin Nielsen-Saines , Violette Recinos , Weiqiang Chen
Intracranial calcifications (ICCs) are a characteristic neuropathological feature of several congenital viral infections, including Zika virus (ZIKV), cytomegalovirus (CMV), and lymphocytic choriomeningitis virus (LCMV). These lesions are linked to severe neurodevelopmental outcomes, such as microcephaly, epilepsy, and cognitive deficits, yet the mechanisms underlying their formation and resolution remain unclear. ICCs are thought to arise from an imbalance in osteogenic and osteolytic signaling in the developing brain. Recent work implicates pericytes as key targets of ZIKV, capable of osteogenic reprogramming and direct mineral deposition. However, the pathways leading to calcification in CMV and LCMV infections are less well understood. Microglia, the brain’s resident immune cells, have emerged as potential regulators of calcification. While microglia can limit mineral deposition in noninfectious models of neurodegeneration and injury, their role in the context of congenital viral infection remains speculative. Whether they act to contain calcification, participate in its resolution, or contribute to pathogenesis via neuroinflammatory signaling is still unknown. This short review summarizes current knowledge of ICC pathogenesis during congenital ZIKV, CMV, and LCMV infections, with a focus on emerging potential cellular mediators, such as pericytes and microglia. We discuss known mechanisms, gaps in knowledge, and opportunities to build more representative animal models to elucidate how different viral infections orchestrate calcification in the fetal brain. Clarifying these pathways may inform future therapeutic approaches to mitigate virus-induced neurodevelopmental disorders.
颅内钙化(ICCs)是几种先天性病毒感染的特征性神经病理特征,包括寨卡病毒(ZIKV)、巨细胞病毒(CMV)和淋巴细胞性脉络丛脑膜炎病毒(LCMV)。这些病变与严重的神经发育结果有关,如小头畸形、癫痫和认知缺陷,但其形成和消退的机制尚不清楚。ICCs被认为是由发育中的大脑中成骨和溶骨信号的不平衡引起的。最近的研究表明,周细胞是ZIKV的关键靶点,具有成骨重编程和直接矿物沉积的能力。然而,CMV和LCMV感染导致钙化的途径尚不清楚。小胶质细胞,大脑的常驻免疫细胞,已经成为钙化的潜在调节者。虽然小胶质细胞可以限制非感染性神经变性和损伤模型中的矿物质沉积,但它们在先天性病毒感染中的作用仍是推测性的。它们是抑制钙化、参与钙化的解决,还是通过神经炎症信号参与钙化的发病机制尚不清楚。这篇简短的综述总结了目前对先天性ZIKV、巨细胞病毒和LCMV感染中ICC发病机制的了解,重点是新出现的潜在细胞介质,如周细胞和小胶质细胞。我们讨论了已知的机制,知识上的差距,以及建立更有代表性的动物模型来阐明不同病毒感染如何协调胎儿大脑钙化的机会。阐明这些途径可能为未来的治疗方法提供信息,以减轻病毒诱导的神经发育障碍。
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引用次数: 0
Human T-cell leukemia virus type I: modulation of viral gene expression and perturbation of host signaling pathways lead to persistent infection 人类t细胞白血病病毒I型:病毒基因表达的调节和宿主信号通路的扰动导致持续感染
IF 5.1 2区 医学 Q1 VIROLOGY Pub Date : 2025-09-06 DOI: 10.1016/j.coviro.2025.101480
Takafumi Shichijo, Jun-ichirou Yasunaga
Human T-cell leukemia virus type I (HTLV-1) was the first human pathogenic retrovirus to be discovered. HTLV-1 induces a T-cell malignancy, adult T-cell leukemia-lymphoma (ATL), and inflammatory diseases, such as HTLV-1-associated myelopathy (HAM), HTLV-1 uveitis (HU), and HTLV-1-associated pulmonary disease (HAPD). Importantly, HTLV-1 maintains persistent infection by regulating viral gene expression and disrupting host signaling pathways — activities that are closely linked to its pathogenicity. By modulating the expression of viral genes, including tax and HTLV-1 bZIP factor (HBZ), HTLV-1 enables itself to evade host immune attack and to promote the clonal expansion of infected cells. In addition, HTLV-1 perturbs host signaling pathways, such as the transforming growth factor (TGF)-β signaling pathway, the IL-10/JAK/STAT signaling pathway, the nuclear factor-kappa B signaling pathway, the Wnt signaling pathway, and the Rb/E2F signaling pathway. Among these pathways, the first two have recently been demonstrated to be significant in the development of ATL. HBZ enhances the activation of the TGF-β signaling pathway and the production of an immunosuppressive cytokine, IL-10, activities which not only help the virus evade the host immune system but also contribute to the proliferation of HTLV-1–infected cells themselves. In addition, HBZ converts HTLV-1–infected cells into Treg-like cells, which further enhances their survival. Overall, HTLV-1 promotes the long-term survival of infected cells in vivo by regulating viral gene expression and disrupting host signaling pathways, thereby accelerating the development of HTLV-1-associated disease.
人类t细胞白血病病毒I型(HTLV-1)是第一个被发现的人类致病性逆转录病毒。HTLV-1诱导t细胞恶性肿瘤、成人t细胞白血病淋巴瘤(ATL)和炎症性疾病,如HTLV-1相关脊髓病(HAM)、HTLV-1葡萄膜炎(HU)和HTLV-1相关肺部疾病(HAPD)。重要的是,HTLV-1通过调节病毒基因表达和破坏宿主信号通路来维持持续感染,这些活动与它的致病性密切相关。HTLV-1通过调节包括tax和HTLV-1 bZIP因子(HBZ)在内的病毒基因的表达,使自身能够逃避宿主免疫攻击并促进被感染细胞的克隆扩增。此外,HTLV-1还干扰宿主信号通路,如转化生长因子(TGF)-β信号通路、IL-10/JAK/STAT信号通路、核因子- κ B信号通路、Wnt信号通路、Rb/E2F信号通路等。在这些途径中,前两种途径最近被证明在ATL的发展中具有重要意义。HBZ增强TGF-β信号通路的激活和免疫抑制细胞因子IL-10的产生,这些活性不仅有助于病毒逃避宿主免疫系统,而且有助于htlv -1感染细胞本身的增殖。此外,HBZ可将htlv -1感染的细胞转化为treg样细胞,进一步提高其存活率。总之,HTLV-1通过调节病毒基因表达和破坏宿主信号通路,促进被感染细胞在体内的长期存活,从而加速HTLV-1相关疾病的发展。
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引用次数: 0
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