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During most eukaryotic translation processes, the small 40S ribosome subunit scans an mRNA from its 5' end until it encounters the first start AUG codon. The large 60S ribosomal subunit then joins the smaller one to initiate protein synthesis. The location of the translation initiation is largely determined by the nucleotides near the start codon as there may be multiple translation initiation sites present on the mRNA.  Marilyn Kozak discovered that the sequence RCCAUGG (where R...
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TMEM41B is a pan-flavivirus host factor.

H-Heinrich Hoffmann1, William M Schneider1, Kathryn Rozen-Gagnon1

  • 1Laboratory of Virology and Infectious Disease, The Rockefeller University, New York, NY, USA.

Biorxiv : the Preprint Server for Biology
|October 14, 2020
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This summary is machine-generated.

Transmembrane protein 41B (TMEM41B) is essential for flavivirus replication by aiding viral RNA complexes. Specific genetic variations in TMEM41B reduce flavivirus infection rates in East Asian populations.

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Area of Science:

  • Virology
  • Cell Biology
  • Genetics

Background:

  • Flaviviruses are a significant public health concern, causing regular outbreaks transmitted by mosquitoes and ticks.
  • Identifying host factors essential for flavivirus infection is crucial for developing antiviral strategies.

Approach:

  • Conducted genome-wide CRISPR-Cas9 loss-of-function screens to identify host genes required for flavivirus replication.
  • Focused on characterizing the roles of TMEM41B and VMP1 in the viral replication cycle.
  • Performed mechanistic studies to elucidate the function of TMEM41B in virus infection.

Key Points:

  • TMEM41B is required for the replication of all tested Flaviviridae family members and also for SARS-CoV-2 (Coronaviridae).
  • Single nucleotide polymorphisms (SNPs) in TMEM41B, common in East Asian populations, reduce flavivirus infection.
  • TMEM41B appears to be recruited to viral RNA replication complexes, facilitating membrane curvature for genome replication.

Conclusions:

  • TMEM41B and VMP1 are necessary for both autophagy and flavivirus infection, though autophagy itself is not required for flavivirus replication.
  • TMEM41B interacts with viral proteins and likely remodels membranes to support viral RNA replication complex formation.
  • TMEM41B deficiency exacerbates the innate immune response to high-multiplicity flavivirus infection.