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抑制防御素 A 和 Cecropin A 对登革热病毒 1 感染埃及伊蚊的反应。

Inhibition of defensin A and cecropin A responses to dengue virus 1 infection in Aedes aegypti.

机构信息

Instituto de Investigaciones Biomédicas "Dr. Francisco Triana Alonso", Facultad de Ciencias de la Salud, Universidad de Carabobo, Maracay, Aragua, Venezuela.

出版信息

Biomedica. 2021 Mar 19;41(1):161-167. doi: 10.7705/biomedica.5491.

DOI:10.7705/biomedica.5491
PMID:33761199
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8055593/
Abstract

INTRODUCTION

It is essential to determine the interactions between viruses and mosquitoes to diminish dengue viral transmission. These interactions constitute a very complex system of highly regulated pathways known as the innate immune system of the mosquito, which produces antimicrobial peptides that act as effector molecules against bacterial and fungal infections. There is less information about such effects on virus infections.

OBJECTIVE

To determine the expression of two antimicrobial peptide genes, defensin A and cecropin A, in Aedes aegypti mosquitoes infected with DENV-1.

MATERIALS AND METHODS

We used the F1 generation of mosquitoes orally infected with DENV-1 and real-time PCR analysis to determine whether the defensin A and cecropin A genes played a role in controlling DENV-1 replication in Ae. aegypti. As a reference, we conducted similar experiments with the bacteria Escherichia coli.

RESULTS

Basal levels of defensin A and cecropin A mRNA were expressed in uninfected mosquitoes at different times post-blood feeding. The infected mosquitoes experienced reduced expression of these mRNA by at least eightfold when compared to uninfected control mosquitoes at all times post-infection. In contrast with the behavior of DENV-1, results showed that bacterial infection produced up-regulation of defensin and cecropin genes; however, the induction of transcripts occurred at later times (15 days).

CONCLUSION

DENV-1 virus inhibited the expression of defensin A and cecropin A genes in a wild Ae. aegypti population from Venezuela.

摘要

简介

了解病毒与蚊子之间的相互作用对于减少登革热病毒的传播至关重要。这些相互作用构成了一个非常复杂的系统，即蚊子的固有免疫系统，该系统产生了抗菌肽，作为针对细菌和真菌感染的效应分子。关于这些效应如何影响病毒感染的信息较少。

目的

确定感染 DENV-1 的埃及伊蚊中两种抗菌肽基因（防御素 A 和 Cecropin A）的表达。

材料和方法

我们使用经口感染 DENV-1 的 F1 代蚊子和实时 PCR 分析来确定防御素 A 和 Cecropin A 基因是否在控制埃及伊蚊中 DENV-1 复制方面发挥作用。作为参考，我们对细菌大肠杆菌进行了类似的实验。

结果

在未感染的蚊子中，防御素 A 和 Cecropin A mRNA 的基础水平在吸血后不同时间表达。与未感染的对照蚊子相比，感染后的蚊子在感染后所有时间点的这些 mRNA 表达均降低了至少 8 倍。与 DENV-1 的行为相反，结果表明细菌感染导致防御素和 Cecropin 基因的上调；然而，转录本的诱导发生在较晚的时间（15 天）。

结论

DENV-1 病毒抑制了委内瑞拉野生埃及伊蚊种群中防御素 A 和 Cecropin A 基因的表达。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e881/8055593/a0db6237985e/2590-7379-bio-41-01-5491-f3S.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e881/8055593/8df46b0f6750/2590-7379-bio-41-01-5491-f1S.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e881/8055593/c3133051a38f/2590-7379-bio-41-01-5491-f2S.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e881/8055593/3135d8d0cde1/2590-7379-bio-41-01-5491-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e881/8055593/13ae69b8566a/2590-7379-bio-41-01-5491-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e881/8055593/a0db6237985e/2590-7379-bio-41-01-5491-f3S.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e881/8055593/8df46b0f6750/2590-7379-bio-41-01-5491-f1S.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e881/8055593/c3133051a38f/2590-7379-bio-41-01-5491-f2S.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e881/8055593/3135d8d0cde1/2590-7379-bio-41-01-5491-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e881/8055593/13ae69b8566a/2590-7379-bio-41-01-5491-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e881/8055593/a0db6237985e/2590-7379-bio-41-01-5491-f3S.jpg

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