thetranscendedman (@atranscendedman.bsky.social)

Researchers found SARS-CoV-2 hijacks the host protein HuR to boost early viral protein production. Blocking HuR cut viral RNA, lowered viral growth, and made remdesivir work better, pointing to a possible new antiviral target. journals.asm.org/doi/10.1128/...

loading . . .

HuR enhances SARS-CoV-2 non-structural protein translation through the genomic 5′-UTR, by promoting polypyrimidine tract-binding protein binding | Journal of Virology Viruses interact with various host proteins throughout their life cycle. A key protein is HuR, an RNA-binding protein regulating RNA stability and translation. HuR binds to viral RNAs at the 5′-UTR or 3′-UTR, influencing translation and replication. We identified conserved HuR binding sites in the SARS-CoV-2 5′-UTR across beta coronaviruses. This binding enhances translation initiation from the genomic 5′-UTR, increasing non-structural protein production essential for replication. Additionally, we discovered that another host protein, PTB, is recruited by HuR to the viral 5′-UTR, aiding ribosome loading. This regulation shows that the virus exploits HuR for its benefit. Targeting HuR may help control the SARS-CoV-2 life cycle. HuR knockout increased sensitivity to remdesivir, an antiviral drug. Using an antisense oligonucleotide to block HuR binding effectively reduced viral RNA levels. Our findings highlight HuR’s critical role in viral protein production regulation and its potential as a therapeutic target against SARS-CoV-2. https://journals.asm.org/doi/10.1128/jvi.00276-26