Cheng Chih-Chieh, Sofiyatun Eny, Chen Wei-June, Wang Lian-Chen
Graduate Institute of Biomedical Sciences, Chang Gung University, Kwei-San, Tao-Yuan 33332, Taiwan.
Program in Tropical Medical Science, Gadjah Mada University, Yogyakartan 53482, Indonesia.
Antioxidants (Basel). 2021 Mar 5;10(3):395. doi: 10.3390/antiox10030395.
Dengue fever is a mosquito-borne viral disease of increasing global importance. The disease has caused heavy burdens due to frequent outbreaks in tropical and subtropical areas of the world. The dengue virus (DENV) is generally transmitted between human hosts via the bite of a mosquito vector, primarily and as a minor species. It is known that the virus needs to alternately infect mosquito and human cells. DENV-induced cell death is relevant to the pathogenesis in humans as infected cells undergo apoptosis. In contrast, mosquito cells mostly survive the infection; this allows infected mosquitoes to remain healthy enough to serve as an efficient vector in nature. Overexpression of antioxidant genes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione S-transferase (GST), glutaredoxin (Grx), thioredoxin (Trx), and protein disulfide isomerase (PDI) have been detected in DENV2-infected mosquito cells. Additional antioxidants, including GST, eukaryotic translation initiation factor 5A (eIF5a), and p53 isoform 2 (p53-2), and perhaps some others, are also involved in creating an intracellular environment suitable for cell replication and viral infection. Antiapoptotic effects involving inhibitor of apoptosis (IAP) upregulation and subsequent elevation of caspase-9 and caspase-3 activities also play crucial roles in the ability of mosquito cells to survive DENV infection. This article focused on the effects of intracellular responses in mosquito cells to infection primarily by DENVs. It may provide more information to better understand virus/cell interactions that can possibly elucidate the evolutionary pathway that led to the mosquito becoming a vector.
登革热是一种由蚊子传播的病毒性疾病，在全球范围内的重要性日益增加。由于在世界热带和亚热带地区频繁爆发，该疾病造成了沉重负担。登革病毒（DENV）通常通过蚊媒叮咬在人类宿主之间传播，主要是 ， 作为次要物种。已知该病毒需要交替感染蚊子和人类细胞。DENV诱导的细胞死亡与人类发病机制相关，因为受感染的细胞会发生凋亡。相比之下，蚊子细胞在感染后大多存活；这使得受感染的蚊子保持足够健康，能够在自然界中充当高效的传播媒介。在DENV2感染的蚊子细胞中检测到抗氧化基因如超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GPx）、谷胱甘肽S-转移酶（GST）、谷氧还蛋白（Grx）、硫氧还蛋白（Trx）和蛋白质二硫键异构酶（PDI）的过表达。其他抗氧化剂，包括GST、真核翻译起始因子5A（eIF5a）和p53亚型2（p53-2），以及可能的其他一些物质，也参与创造适合细胞复制和病毒感染的细胞内环境。涉及上调凋亡抑制因子（IAP）以及随后提高caspase-9和caspase-3活性的抗凋亡作用，在蚊子细胞抵抗DENV感染的能力中也起着关键作用。本文重点关注蚊子细胞内对主要由DENVs引起的感染的反应的影响。它可能提供更多信息，以更好地理解病毒/细胞相互作用，这可能有助于阐明导致蚊子成为传播媒介的进化途径。
