Eilat virus (EILV) causes superinfection exclusion against West NILE virus (WNV) in a strain specific manner in Culex tarsalis mosquitoes.
Eilat virus (EILV) causes superinfection exclusion against West NILE virus (WNV) in a strain specific manner in Culex tarsalis mosquitoes.
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埃拉特病毒 (EILV) 在跗库蚊中以毒株特异性方式引起对西尼罗河病毒 (WNV) 的重复感染排除。
DOI：
10.1101/2023.05.25.542294
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发表时间：
2023
期刊：
影响因子：
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通讯作者：
Rasgon,JasonL
中科院分区：
文献类型：
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作者：
Joseph,RenukaE;Bozic,Jovana;Werling,KristineL;Urakova,Nadya;Rasgon,JasonL
西尼罗河病毒(WNV)是美国蚊媒疾病的主要原因。目前还没有针对西尼罗河病毒的人类疫苗或疗法，媒介控制是控制西尼罗河病毒传播的主要策略。西尼罗河病毒载体迟钝库蚊也是昆虫特异性病毒(ISV)Eilat病毒(EILV)的合格宿主。像EILV这样的ISV可以在它们共享的蚊子宿主中与人类致病病毒相互作用并引起对人类致病病毒的重叠感染排斥(SIE)，从而改变对这些致病病毒的媒介能力。引起SIE的能力及其宿主限制使ISV成为针对蚊媒传播的致病病毒的潜在安全工具。在本研究中，我们在蚊虫C6/36 细胞和DC上测试了EILV是否引起SIE对西尼罗河病毒的攻击。鞑靼蚊子。西尼罗河病毒WN02-1956株和NY99株在C6/36 细胞中重叠感染48-72 h后，两株病毒的滴度都被EILV抑制。在我们的研究中测试的价值观。WN02-1956在两个M.O.的滴度。在C6/36 细胞中，这些值仍然受到抑制，而NY99细胞的值在接近最终时间点时出现了一些恢复。SIE的机制尚不清楚，但EILV被发现干扰了Ny99在C6/36 细胞上的附着，可能有助于抑制Ny99滴度。然而，在重叠感染条件下，EILV对WN02-1956的附着或两株WNV的内化都没有影响。Inc.在任一时间点，两株西尼罗河病毒的感染率均无显著差异。然而，在蚊子中，EILV在重叠感染后3 天提高了NY99感染滴度，但这种作用在重叠感染后7 天消失。而WN02-1956株在重叠感染后7 时，病毒滴度受到抑制。两个西尼罗河病毒株的传播和传播在任一时间点都没有受到EILV重叠感染的影响。总体而言，EILV在C6/36 细胞中引起对两种西尼罗河病毒株的SIE；然而，Inc.由于不同西尼罗河病毒株对共享资源的耗竭速度不同，EILV引起的沙门氏菌、SIE可能是毒株特有的。
West Nile virus (WNV) is the leading cause of mosquito-borne illness in the USA. There are currently no human vaccines or therapies available for WNV, and vector control is the primary strategy used to control WNV transmission. The WNV vectorCulex tarsalisis also a competent host for the insect-specific virus (ISV) Eilat virus (EILV). ISVs such as EILV can interact with and cause superinfection exclusion (SIE) against human pathogenic viruses in their shared mosquito host, altering vector competence for these pathogenic viruses. The ability to cause SIE and their host restriction make ISVs a potentially safe tool to target mosquito-borne pathogenic viruses. In the present study, we tested whether EILV causes SIE against WNV in mosquito C6/36 cells andC. tarsalismosquitoes. The titres of both WNV strains – WN02-1956 and NY99 – were suppressed by EILV in C6/36 cells as early as 48–72 h post-superinfection at both m.o.i. values tested in our study. The titres of WN02-1956 at both m.o.i. values remained suppressed in C6/36 cells, whereas those of NY99 showed some recovery towards the final timepoint. The mechanism of SIE remains unknown, but EILV was found to interfere with NY99 attachment in C6/36 cells, potentially contributing to the suppression of NY99 titres. However, EILV had no effect on the attachment of WN02-1956 or internalization of either WNV strain under superinfection conditions. InC. tarsalis, EILV did not affect the infection rate of either WNV strain at either timepoint. However, in mosquitoes,EILV enhanced NY99 infection titres at 3 days post-superinfection, but this effect disappeared at 7 days post-superinfection. In contrast, WN02-1956 infection titres were suppressed by EILV at 7 days post-superinfection. The dissemination and transmission of both WNV strains were not affected by superinfection with EILV at either timepoint. Overall, EILV caused SIE against both WNV strains in C6/36 cells; however, inC. tarsalis, SIE caused by EILV was strain specific potentially owing to differences in the rate of depletion of shared resources by the individual WNV strains.