西尼罗河病毒(WNV)是美国蚊子传播疾病的主要原因。目前没有可用于WNV的人类疫苗或疗法,矢量控制是用于控制WNV传输的主要策略。WNV载体库蚊也是昆虫特异性病毒(ISV)埃拉特病毒(EILV)的合格宿主。ISV,如EILV可以与人类病原病毒相互作用,并在其共有的蚊子宿主中引起重复感染排斥(SIE)。改变这些致病病毒的载体能力。引起SIE的能力及其宿主限制使ISV成为靶向蚊媒致病病毒的潜在安全工具。在本研究中,我们测试了EILV是否在蚊子C6/36细胞和C.tarsalis蚊子中引起针对WNV的SIE。两种WNV菌株的滴度-WN02-1956和NY99-早在超感染后48-72小时就被C6/36细胞中的EILV抑制。在我们的研究中测试的值。在C6/36细胞中,WN02-1956在两个m.o.i.值下的滴度仍然被抑制,而NY99的那些在最后时间点显示出一些恢复。SIE的机制仍然未知,但发现EILV干扰C6/36细胞中的NY99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的附着或任一WNV菌株的内化没有影响。在C.tarsalis,EILV在任一时间点都不影响任一WNV毒株的感染率。然而,在蚊子中,EILV在重叠感染后3天提高了NY99感染滴度,但这种效果在超感染后7天消失。相比之下,在超感染后7天,WN02-1956感染滴度被EILV抑制。在任一时间点,两种WNV菌株的传播和传播均不受EILV超感染的影响。总的来说,EILV在C6/36细胞中对两种WNV毒株均引起SIE;然而,在C.tarsalis,EILV引起的SIE可能是菌株特异性的,这可能是由于单个WNV菌株对共享资源的耗竭率不同。
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 vector Culex tarsalis is 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 and C. tarsalis mosquitoes. 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. In C. 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, in C. 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.