Abstract
Viruses hijack host factors for their high speed protein synthesis, but information about these factors is largely unknown. In searching for genes that are involved in viral replication, we carried out a forward genetic screen for Drosophila mutants that are more resistant or sensitive to Drosophila C virus (DCV) infection-caused death, and found a virus-resistant line in which the expression of pelo gene was deficient. Our mechanistic studies excluded the viral resistance of pelo deficient flies resulting from the known Drosophila anti-viral pathways, and revealed that pelo deficiency limits the high level synthesis of the DCV capsid proteins but has no or very little effect on the expression of some other viral proteins, bulk cellular proteins, and transfected exogenous genes. The restriction of replication of other types of viruses in pelo deficient flies was also observed, suggesting pelo is required for high level production of capsids of all kinds of viruses. We show that both pelo deficiency and high level DCV protein synthesis increase aberrant 80S ribosomes, and propose that the preferential requirement of pelo for high level synthesis of viral capsids is at least partly due to the role of pelo in dissociation of stalled 80S ribosomes and clearance of aberrant viral RNA and proteins. Our data demonstrated that pelo is a host factor that is required for high efficiency translation of viral capsids and targeting pelo could be a strategy for general inhibition of viral infection.
Highlights
Viruses are the most abundant intracellular pathogens on the earth
We found pelo is required for high efficiency synthesis of proteins of a number of viruses, suggesting that inhibition of pelo may mediate a general antiviral activity
We proposed that the function of pelo in quality control of protein synthesis is required for high efficiency viral protein synthesis
Summary
Viruses are the most abundant intracellular pathogens on the earth. They can infect all living organisms and hijack their host factors for replication [1]. In order to withstand virus infections, their hosts have evolved multiple antiviral defense mechanisms [2,3,4]. Scientists have been studying host-virus interactions in order to develop new and more effective strategies for the prevention and treatment of viral infection. Drosophila melanogaster has been shown to be a powerful model system in studying host-pathogen interactions [5]. Several antiviral innate immunity pathways and their corresponding molecular mechanisms have been deciphered in Drosophila. Inducible gene expressions in response to viral infection contribute to antiviral immunity, including the JAKSTAT pathway and the DExD/H-box helicase Dicer-2-mediated antiviral gene induction [15,16].
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