Researchers at Northwestern Medicine have discovered how poxviruses utilize host ribosomes for protein synthesis, a key process for their replication. Their study, published in Nature Microbiology, utilized advanced RNA sequencing and cryo-electron microscopy. They found that while the virus typically causes host shutoff to prioritize its own mRNA translation, some host mRNAs are still translated using a different initiation mechanism. The research identifies specific ribosomal proteins involved in this process, shedding light on the complex interplay between virus and host cells during infection and viral protein synthesis.
"What fascinates us is that all viruses are dependent on gaining access to host ribosomes, even poxviruses, which are highly unusual DNA viruses that are so self-sufficient in other processes."
"We found that at later times of infection, when the virus causes a phenomenon called host shutoff to favor viral mRNA translation, some host mRNAs continue to be translated, but they use a different, non-canonical mode of initiation to that of viral mRNAs."
"We found that poxvirus infection causes structural changes to how the 40S head domain moves during initiation."
"The findings provide new insight into how viruses can rewire cellular machinery, ensuring the production of key viral proteins while suppressing host defenses."
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