The Genetic Basis for Salivary Gland Barriers to Arboviral Transmission.
The Genetic Basis for Salivary Gland Barriers to Arboviral Transmission.
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DOI：
10.3390/insects12010073
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发表时间：
2021-01-15
期刊：
影响因子：
3
通讯作者：
Black WC 4th
中科院分区：
文献类型：
--
作者：
Sanchez-Vargas I;Olson KE;Black WC 4th
苔藓虫的唾液腺在进入唾液之前被虫媒病毒感染。蚊子唾液中的病毒可以在载体获得下一次血液时感染脊椎动物宿主。唾液腺感染和逃逸屏障（SGIB和SGEB，分别）已被确定为调节虫媒病毒的传播。SGIB表现为在具有播散性感染的蚊子的唾液腺中不存在病毒，而SGEB表现为即使唾液腺被感染，蚊子的唾液中也不存在病毒。埃及伊蚊和病毒之间的相互作用是动态的，与每个媒介种群和病毒变体的遗传背景有关。对SGIB和SGEB的遗传基础了解甚少。在这里，嵌套的，半同胞家庭的埃及伊蚊被用来估计遗传和环境的差异，其中女儿从一个单独的大坝不同，由于他们的表型的父亲。我们发现SGIB与登革病毒感染有很强的遗传基础，但与寨卡病毒或基孔肯雅病毒感染无关，其中所有唾液腺都被感染。SGEB对寨卡病毒或基孔肯雅病毒感染有中等遗传基础，但对登革热病毒感染没有遗传基础。节肢动物传播的病毒（虫媒病毒）感染蚊子的唾液腺，然后在病毒传播之前逃逸到唾液中。蚊媒病毒的传播可通过唾液腺感染屏障（SGIB）和唾液腺逃逸屏障（SGEB）进行调节。我们通过估计感染三种登革热2型（DENV 2）、两种基孔肯雅热（CHIKV）和两种寨卡病毒（ZIKV）基因型的埃及伊蚊半同胞家庭（Mapastepec，墨西哥）的定量遗传贡献，确定了SGIB和SGEB的影响。我们测定了感染后7天每个唾液腺和唾液的病毒滴度以及半同胞群体中的病毒流行率。CHIKV或ZIKV基因型不存在SGIB，而DENV 2基因型显示出低SGIB率。然而，由于半同胞家族中的加性遗传因素导致的病毒滴度和流行率在三种DENV 2基因型中的两种以及一种CHIKV和一种ZIKV基因型中显示出SGIB的显著狭义遗传力（h2）。在所有七种病毒株中检测到SGEB：60-88%的DENV 2和48-62%的CHIKV或ZIKV基因型感染。SGEB h2对于所有CHIKV或ZIKV基因型都是显著的，但对于任何DENV 2基因型都不显著。SGIBs和SGEBs表现出经典的基因间相互作用动力学，并受到蚊子和病毒中遗传因素的影响。
Mosquito salivary glands are infected with an arbovirus prior to entering saliva. The virus in the mosquito’s saliva can then infect a vertebrate host when the vector acquires its next bloodmeal. Salivary gland infection and escape barriers (SGIB and SGEB, respectively) have been identified that modulate arbovirus transmission. SGIB are manifest as the absence of virus in the salivary glands of mosquitoes having a disseminated infection, while SGEB are evident as an absence of virus in the saliva of mosquitoes even though salivary glands are infected. The interaction between Aedes aegypti and viruses is dynamic and related to the genetic background of each vector population and virus variant. There is little understanding of the genetic basis for SGIB and SGEB. Here, nested, half-sib families of Aedes aegypti were used to estimate genetic and environmental variances, in which daughters from an individual dam differ in their phenotype due to the sire. We found that SGIB has a strong genetic basis with dengue virus infections but not with Zika or chikungunya virus infections, in which all salivary glands became infected. SGEB has a moderate genetic basis for Zika or chikungunya infections but not with dengue virus infections. Arthropod-borne viruses (arboviruses) infect mosquito salivary glands and then escape to saliva prior to virus transmission. Arbovirus transmission from mosquitoes can be modulated by salivary gland infection barriers (SGIBs) and salivary gland escape barriers (SGEBs). We determined the influence of SGIBs and SGEBs by estimating the quantitative genetic contributions of Aedes aegypti half-sib families (Mapastepec, Mexico) infected with three dengue 2 (DENV2), two chikungunya (CHIKV), and two Zika (ZIKV) genotypes. We determined virus titer per salivary gland and saliva at seven days post-infection and virus prevalence in the half-sib population. CHIKV or ZIKV genotypes did not present SGIB, whereas DENV2 genotypes showed low rates of SGIB. However, virus titer and prevalence due to additive genetic factors in the half-sib family displayed a significant narrow-sense heritability (h2) for SGIB in two of the three DENV2 genotypes and one CHIKV and one ZIKV genotype. SGEBs were detected in all seven virus strains: 60–88% of DENV2 and 48–62% of CHIKV or ZIKV genotype infections. SGEB h2 was significant for all CHIKV or ZIKV genotypes but not for any of the DENV2 genotypes. SGIBs and SGEBs exhibited classical gene-by-gene interaction dynamics and are influenced by genetic factors in the mosquito and the virus.
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DOI：
10.4269/ajtmh.1966.15.989
发表时间：
1966-01-01
影响因子：
3.3
作者：
HURLBUT, HS
通讯作者：
HURLBUT, HS
影响因子：
2.6
作者：
Dickson, Laura B.;Campbell, Corey L.;Black, William C.
通讯作者：
Black, William C.
影响因子：
23.8
作者：
CHAMBERLAIN, R;SUDIA, WD
通讯作者：
SUDIA, WD
影响因子：
3.7
作者：
BOWERS, DF;ABELL, BA;BROWN, DT
通讯作者：
BROWN, DT
影响因子：
2.2
作者：
DEVINE, TERRY L.;VENARD, CARL E.;MYSER, WILLARD C.
通讯作者：
MYSER, WILLARD C.