Adult T-cell leukemia/lymphoma (ATLL)是由人类T淋巴病毒-1(HTLV-1)感染引起的CD4+T淋巴细胞的侵袭性恶性肿瘤。HTLV-1被带到世界卫生组织(WHO)和研究者那里，以解决其对全球公共卫生、致癌性和宿主免疫系统向自身免疫性的恶化的影响。在感染人群的少数人(3-5%)中，它可以引起炎性网络转向HTLV-1相关的髓病性脊髓病/热带痉挛性截瘫(HAM/TSP)，或者劫持感染的CD4+ T淋巴细胞转为T调节亚群，刺激抗炎信号网络，促进ATLL的发展。本综述对ATLL发病机制中的复杂信号网络进行了批判性讨论，以更好地解释致癌性，并介绍了ATLL发病机制中的主要候选人。至少有两种病毒因子，HTLV-1转录激活蛋白(TAX)和HTLV-1基本亮氨酸拉链因子(HBZ)，被认为参与了ATLL的表现形式，与宿主反应相互作用，并在有利于感染细胞生存和病毒传播的细胞信号调控方面失调。这些分子可以用作ATLL预后的潜在新生物标志物或治疗靶点。此外，本综述介绍的HTLV-1致癌性的挑战性方面，可能会为急性白血病发病机制的进一步研究开启新的途径。这些特征可以帮助在基因表达谱逐渐朝着合适的免疫反应转化时，发现有效的免疫疗法。

Adult T-cell leukemia/lymphoma (ATLL) is an aggressive malignancy of CD4+ T lymphocytes caused by human T lymphotropic virus type-1 (HTLV-1) infection. HTLV-1 was brought to the World Health Organization (WHO) and researchers to address its impact on global public health, oncogenicity, and deterioration of the host immune system toward autoimmunity. In a minority of the infected population (3-5%), it can induce inflammatory networks toward HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP), or hijacking the infected CD4+ T lymphocytes into T regulatory subpopulation, stimulating anti-inflammatory signaling networks, and prompting ATLL development. This review critically discusses the complex signaling networks in ATLL pathogenesis during virus-host interactions for better interpretation of oncogenicity and introduces the main candidates in the pathogenesis of ATLL. At least two viral factors, HTLV-1 trans-activator protein (TAX) and HTLV-1 basic leucine zipper factor (HBZ), are implicated in ATLL manifestation, interacting with host responses and deregulating cell signaling in favor of infected cell survival and virus dissemination. Such molecules can be used as potential novel biomarkers for ATLL prognosis or targets for therapy. Moreover, the challenging aspects of HTLV-1 oncogenesis introduced in this review could open new venues for further studies on acute leukemia pathogenesis. These features can aid in the discovery of effective immunotherapies when reversing the gene expression profile toward appropriate immune responses gradually becomes attainable.