| Summary: | The <i>Drosophila melanogaster</i> sigma virus, a member of the <i>Rhabdoviridae</i> family, specifically propagates itself in <i>D. melanogaster</i>. It contains six genes in the order of 3′-<i>N</i>−<i>P</i>−<i>X</i>−<i>M</i>−<i>G</i>−<i>L</i>-5′. The sigma virus is the only arthropod-specific virus of the <i>Rhabdoviridae</i> family. Sigma-virus-infected <i>Drosophila</i> may suffer from irreversible paralysis when exposed to a high CO<sub>2</sub> 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 <i>Drosophila</i>, which does not necessarily suggest that they are not involved 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. The results showed that the genome copy number of the sigma virus increased after knocking down the immune pathway genes <i>domeless</i> and <i>PGRP-LC</i> in <i>Drosophila</i> S2 cells. The knocking down of <i>domeless</i> and <i>PGRP-LC</i> significantly up-regulated the expression of the <i>L</i> gene compared to the other viral genes. We propose that the immune pathways respond to sigma virus infection by altering <i>L</i> expression, hence suppressing viral replication. This effect was further tested in vivo, when <i>D. melanogaster</i> individuals injected with ds<i>dome</i> and ds<i>PGRP-LC</i> showed not only an increase in sigma virus copy number, but also a reduced survival rate when treated with CO<sub>2</sub>. Our study proved that host immunity influences viral replication, even in persistent infection. Knocking down the key components of the immune process deactivates immune controls, thus facilitating viral expression and replication. We propose that the immunity system of <i>D. melanogaster</i> regulates the replication of the sigma virus by affecting the <i>L</i> gene expression. Studies have shown minimal host−virus interaction in persistent infection. However, our study demonstrated that the immunity continued to affect viral replication even in persistent infection because knocking down the key components of the immune process disabled the relevant immune controls and facilitated viral expression and replication.
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