Department of Clinical Biochemistry, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Department of Microbiology and Virology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
J Med Microbiol. 2022 Apr;71(4). doi: 10.1099/jmm.0.001408.
Human T-cell lymphotropic virus type 1 (HTLV-1), a well-known member of the retroviridae family, potentially causes serious outcomes including adult T-cell leukaemia/lymphoma (ATLL) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM-TSP). Oxidative stress plays a key role in progression and clinical exacerbation of several chronic infections. We have previously shown a reduction in serum total antioxidant capacity (TAC) during HTLV-1 infection and this study was set out to investigate the reasons for TAC reduction. Oxidant/antioxidant imbalance during HTLV-1 infection may result from disruptions in oxidant levels or antioxidant defence system. This study aimed to analyse the key enzymes and oxidant molecules playing important roles in virus-induced oxidative stress. We measured serum activities of the major antioxidant enzymes; superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) as well as serum concentrations of the main oxidant markers: nitric oxide (NO) and malondialdehyde (MDA). Totally 40 HTLV-1 infected patients and 40 healthy controls were enrolled in this study. The patient group consisted of chronic carriers and patients with HAM-TSP (=20). The current study found that serum levels of MDA and NO were significantly higher in patient groups particularly in HAM-TSP patients (<0.05). In addition, a reductive trend was observed in the serum activities of CAT, SOD, and GPX in HTLV-1 infected patients compared with healthy controls (<0.05). Reduced activities of CAT, SOD, and GPX antioxidant enzymes along with the observed elevated concentrations of oxidant molecules may contribute to oxidative stress and worse outcomes during HTLV-1 infection.
人类 T 细胞嗜淋巴细胞病毒 1 型(HTLV-1),一种逆转录病毒科的知名成员,可能导致严重后果,包括成人 T 细胞白血病/淋巴瘤(ATLL)和 HTLV-1 相关脊髓病/热带痉挛性截瘫(HAM-TSP)。氧化应激在几种慢性感染的进展和临床恶化中起着关键作用。我们之前已经表明,在 HTLV-1 感染期间血清总抗氧化能力(TAC)降低,本研究旨在探讨 TAC 降低的原因。HTLV-1 感染期间的氧化剂/抗氧化剂失衡可能是由于氧化剂水平或抗氧化防御系统的破坏。本研究旨在分析在病毒诱导的氧化应激中起重要作用的关键酶和氧化剂分子。我们测量了主要抗氧化酶的血清活性;超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GPX)以及主要氧化剂标记物的血清浓度:一氧化氮(NO)和丙二醛(MDA)。总共纳入了 40 名 HTLV-1 感染患者和 40 名健康对照者进行这项研究。患者组包括慢性携带者和 HAM-TSP 患者(=20)。本研究发现,患者组,特别是 HAM-TSP 患者的血清 MDA 和 NO 水平显著升高(<0.05)。此外,与健康对照组相比,HTLV-1 感染患者的血清 CAT、SOD 和 GPX 活性呈下降趋势(<0.05)。CAT、SOD 和 GPX 抗氧化酶活性降低以及观察到的氧化剂分子浓度升高可能导致 HTLV-1 感染期间的氧化应激和更差的结果。