Here’s the most recent, directly relevant update I can confirm: GBP5 (interferon-inducible guanylate-binding protein 5 / interferon-inducible GTPase 5) has been reported to inhibit SARS‑CoV‑2 spike protein maturation by interfering with N‑linked glycosylation in the ER, leading to misfolding/retention and reduced virion assembly/release.[1][2]
The recent thread across these papers is that GBP5’s antiviral effect is mechanistic (ER glycosylation interference), not just “general interferon effects.”[2][1]
If you tell me whether you mean GBP5 specifically (human gene GBP5, official protein name) or you meant a different “interferon-inducible GTPase 5” ortholog/isoform, I can narrow to the exact entity and pull more targeted “latest news” for that specific protein.
Viral infection induces production of type I interferons and expression of interferon-stimulated genes (ISGs) that play key roles in inhibiting viral infection. Here, we show that the ISG guanylate-binding protein 5 (GBP5) inhibits N-linked ...
pmc.ncbi.nlm.nih.govViral infection induces production of type I interferons and expression of interferon-stimulated genes (ISGs) that play key roles in inhibiting viral infection. Here, we show that the ISG guanylate-binding protein 5 (GBP5) inhibits N-linked ...
pmc.ncbi.nlm.nih.govCell-autonomous immunity is essential for host organisms to defend themselves against invasive microbes. In vertebrates, both the adaptive and the innate branches of the immune system operate cell-autonomous defenses as key effector mechanisms that ...
pmc.ncbi.nlm.nih.gov