Identification of regulatory host genes involved in sigma virus replication using RNAi knockdown in Drosophila

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F60077344%3A_____%2F19%3A00519025" target="_blank" >RIV/60077344:_____/19:00519025 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/60076658:12310/19:43899780

Výsledek na webu

<a href="https://www.mdpi.com/2075-4450/10/10/339" target="_blank" >https://www.mdpi.com/2075-4450/10/10/339</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.3390/insects10100339" target="_blank" >10.3390/insects10100339</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Identification of regulatory host genes involved in sigma virus replication using RNAi knockdown in Drosophila

Popis výsledku v původním jazyce

The Drosophila melanogaster sigma virus, a member of the Rhabdoviridae family, specifically propagates itself in D. melanogaster. It contains six genes in the order of 3′-N–P–X–M–G–L-5′. The sigma virus is the only arthropod-specific virus of the Rhabdoviridae family. Sigma-virus-infected Drosophila may suffer from irreversible paralysis when exposed to a high CO2 concentration, but generally, no other symptoms are reported. A recent study reported that host gene expression in immune pathways was not changed in sigma-virus-infected Drosophila. However, that does not necessarily exclude their involvement in virus–host interactions. The present study aimed to identify host genes associated with sigma virus replication. Immune pathways JAK-STAT and IMD were selected for detailed study. It showed that the genome copy number of the sigma virus increased after knocking down the immune pathway genes domeless and PGRP-LC in Drosophila S2 cells. Also, the knockdown significantly up-regulated the expression of the L gene compared to the other viral genes. We propose that the immune pathways respond to sigma virus infection by altering L expression, hence suppressing viral replication. This effect was confirmed in vivo, when D. melanogaster individuals injected with dsdome and dsPGRP-LC showed not only an increase in sigma virus copy number, but also a reduced survival rate after CO2 treatment. Our study proved that host immunity affects viral replication, even in persistent infection. Knocking down the key components of the immune process deactivates immune controls, allowing the viral expression and replication. We propose that the immune system of D. melanogaster regulates the replication of sigma virus by affecting the L gene expression. Despite research showing minimal host–virus interaction in such cases, our study demonstrated that the viral replication in persistent infection continued to be influnced by host immune system.

Název v anglickém jazyce

Identification of regulatory host genes involved in sigma virus replication using RNAi knockdown in Drosophila

Popis výsledku anglicky

The Drosophila melanogaster sigma virus, a member of the Rhabdoviridae family, specifically propagates itself in D. melanogaster. It contains six genes in the order of 3′-N–P–X–M–G–L-5′. The sigma virus is the only arthropod-specific virus of the Rhabdoviridae family. Sigma-virus-infected Drosophila may suffer from irreversible paralysis when exposed to a high CO2 concentration, but generally, no other symptoms are reported. A recent study reported that host gene expression in immune pathways was not changed in sigma-virus-infected Drosophila. However, that does not necessarily exclude their involvement in virus–host interactions. The present study aimed to identify host genes associated with sigma virus replication. Immune pathways JAK-STAT and IMD were selected for detailed study. It showed that the genome copy number of the sigma virus increased after knocking down the immune pathway genes domeless and PGRP-LC in Drosophila S2 cells. Also, the knockdown significantly up-regulated the expression of the L gene compared to the other viral genes. We propose that the immune pathways respond to sigma virus infection by altering L expression, hence suppressing viral replication. This effect was confirmed in vivo, when D. melanogaster individuals injected with dsdome and dsPGRP-LC showed not only an increase in sigma virus copy number, but also a reduced survival rate after CO2 treatment. Our study proved that host immunity affects viral replication, even in persistent infection. Knocking down the key components of the immune process deactivates immune controls, allowing the viral expression and replication. We propose that the immune system of D. melanogaster regulates the replication of sigma virus by affecting the L gene expression. Despite research showing minimal host–virus interaction in such cases, our study demonstrated that the viral replication in persistent infection continued to be influnced by host immune system.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10603 - Genetics and heredity (medical genetics to be 3)

Projekt

—

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2019

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Insects

ISSN

2075-4450

e-ISSN

—

Svazek periodika

10

Číslo periodika v rámci svazku

10

Stát vydavatele periodika

CH - Švýcarská konfederace

Počet stran výsledku

15

Strana od-do

339

Kód UT WoS článku

000500573900033

EID výsledku v databázi Scopus

2-s2.0-85073740534