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]
What’s new (recent publications)
- Nov 2025 (research report): GBP5 is described as an ISG that acts on viral protein glycosylation—specifically OST-mediated N-linked glycosylation of the SARS‑CoV‑2 spike protein, causing ER misfolding/retention and lowering virion assembly/release.[1]
- May 2024 (related paper): Similar mechanism: GBP5 is shown to inhibit SARS‑CoV‑2 virion assembly and release by disrupting spike protein maturation, again tied to N‑linked glycosylation / trafficking to post-Golgi compartments.[2]
Quick takeaway
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.