Emerging Pathogens Institute, University of Florida, Gainesville, FL 32611, USA.
Department of Molecular Genetics & Microbiology, College of Medicine, University of Florida, Gainesville, FL 32603, USA.
Commun Biol. 2021 Jan 15;4(1):69. doi: 10.1038/s42003-020-01614-9.
Inter-host transmission of pathogenic arboviruses such as dengue virus (DENV) and Zika virus (ZIKV) requires systemic infection of the mosquito vector. Successful systemic infection requires initial viral entry and proliferation in the midgut cells of the mosquito followed by dissemination to secondary tissues and eventual entry into salivary glands. Lack of arbovirus proliferation in midgut cells has been observed in several Aedes aegypti strains, but the midgut antiviral responses underlying this phenomenon are not yet fully understood. We report here that there is a rapid induction of apoptosis (RIA) in the Aedes aegypti midgut epithelium within 2 hours of infection with DENV-2 or ZIKV in both in vivo blood-feeding and ex vivo midgut infection models. Inhibition of RIA led to increased virus proliferation in the midgut, implicating RIA as an innate immune mechanism mediating midgut infection in this mosquito vector.
宿主间传播的致病性虫媒病毒，如登革热病毒（DENV）和寨卡病毒（ZIKV），需要蚊子媒介的全身感染。成功的全身感染需要病毒最初在蚊子的中肠细胞中进入和增殖，然后传播到次级组织，并最终进入唾液腺。在几种埃及伊蚊株中观察到中肠细胞中缺乏虫媒病毒增殖，但这一现象背后的中肠抗病毒反应尚不完全清楚。我们在这里报告，在体内吸血和离体中肠感染模型中，感染 DENV-2 或 ZIKV 后 2 小时内，埃及伊蚊中肠上皮细胞中迅速诱导细胞凋亡（RIA）。抑制 RIA 导致中肠中病毒增殖增加，表明 RIA 作为一种先天免疫机制，介导了这种蚊子媒介的中肠感染。
