The most recent peer-reviewed findings I found about interferon-inducible GTPase 5 (GBP5) are from 2024–2025 studies showing GBP5 acts as an interferon-stimulated antiviral factor by interfering with viral protein glycosylation/maturation, particularly for SARS‑CoV‑2 spike.[1][2]
A 2025 study describes a mechanism where GBP5 inhibits N-linked glycosylation of SARS‑CoV‑2 spike (S protein) via effects on the OST-mediated glycosylation pathway, leading to misfolding/ER retention and reduced virion assembly/release.[1] A 2024 study reports a consistent conclusion: GBP5 inhibits SARS‑CoV‑2 virion assembly and release by interfering with S protein maturation, again tied to disruption of spike glycosylation and trafficking/processing.[2]
“Interferon-inducible GTPase 5” is commonly referred to as GBP5 (an interferon-inducible guanylate-binding protein).[2][1]
If you want, tell me whether you mean GBP5 in humans (Homo sapiens) and whether you care more about SARS‑CoV‑2, cancer/immunology, or basic interferon biology—and I can narrow the “latest news” to that subtopic.
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