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SARS-CoV-2 evolution influences GBP and IFITM sensitivity.

Dejan Mesner1, Ann-Kathrin Reuschl1, Matthew V X Whelan1

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SARS-CoV-2 variants evolved to escape innate immune restriction factors like Guanylate-binding proteins (GBP) 2 and 5. Omicron, however, is sensitive to these factors, indicating a trade-off for antibody escape.

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GBPIFITMSARS-CoV-2restrictionspike

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Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • SARS-CoV-2 viral entry depends on spike protein processing by host proteases.
  • Furin-cleavage site (FCS) optimization in spike enhances viral infectivity and transmission.
  • Interferon-inducible restriction factors, including Guanylate-binding proteins (GBP) 2 and 5, limit viral replication.

Purpose of the Study:

  • To investigate how SARS-CoV-2 variants interact with host restriction factors.
  • To determine the mechanisms by which variants like Alpha, Delta, and Omicron evade or are targeted by GBP2/5 and IFITM proteins.
  • To map the specific spike protein domains responsible for variant sensitivity to restriction factors.

Main Methods:

  • Analysis of spike protein cleavage by furin in the presence of GBP2/5.
  • Infectivity assays using early SARS-CoV-2 isolates and variants of concern (VOCs) with varying restriction factor expression.
  • Site-directed mutagenesis and chimeric spike protein construction to map functional domains.
  • Assessment of viral entry pathways (TMPRSS2-dependent vs. independent).

Main Results:

  • GBP2/5 interfere with furin-mediated spike cleavage and inhibit early SARS-CoV-2 isolates.
  • VOCs Alpha and Delta escape GBP2/5 restriction, linked to the D614G spike substitution.
  • Omicron remains sensitive to GBP2/5 and exhibits sensitivity to IFITM1, IFITM2, and IFITM3.
  • Omicron's S1 domain mediates GBP2/5 sensitivity, while the S2' domain dictates IFITM2/3 sensitivity and TMPRSS2-independent entry.

Conclusions:

  • SARS-CoV-2 evolution, particularly the D614G substitution, facilitates escape from GBP restriction.
  • Omicron's adaptations for antibody escape and altered tropism have increased its susceptibility to innate immune restriction factors targeting viral entry.
  • Understanding these interactions is crucial for developing effective antiviral strategies.