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

The result's identifiers

  • Result code in 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>

  • Alternative codes found

    RIV/60076658:12310/19:43899780

  • Result on the web

    <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>

Alternative languages

  • Result language

    angličtina

  • Original language name

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

  • Original language description

    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.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

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

Result continuities

  • Project

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2019

  • Confidentiality

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

Data specific for result type

  • Name of the periodical

    Insects

  • ISSN

    2075-4450

  • e-ISSN

  • Volume of the periodical

    10

  • Issue of the periodical within the volume

    10

  • Country of publishing house

    CH - SWITZERLAND

  • Number of pages

    15

  • Pages from-to

    339

  • UT code for WoS article

    000500573900033

  • EID of the result in the Scopus database

    2-s2.0-85073740534