ReviewMicroorganisms2026
Host Protein Palmitoylation: A Two-Edged Sword in the Pathogenesis of COVID-19.
Review in Microorganisms, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
0 citing papers in PubMed.
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Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protein palmitoylation is a two-edged sword in regulating Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection. On the one hand, SARS-CoV-2 hijacks the host's palmitoyl transferases (ZDHHC5/9/20) to modify its spike protein (S protein), enhancing its stability, membrane anchoring, and fusion, consequently facilitating SARS-CoV-2 entry, replication, and release. On the other hand, the host utilises this modification to activate antiviral defences: palmitoylation of the mitochondrial antiviral signalling protein (MAVS) leads to its accumulation in the mitochondria and initiates interferon signalling; palmitoylation of the stimulator of interferon genes (STING) is essential for its activation and transport; and palmitoylation of interferon-induced transmembrane protein 3 (IFITM3) increases its ability to inhibit SARS-CoV-2 membrane fusion. This defensive-offensive interplay within the same regulatory system offers fresh opportunities for targeted therapy, including the development of specific ZDHHC inhibitors, palmitoylated angiotensin-converting enzyme 2 (ACE2)-based decoy vesicles, and metabolic intervention approaches. In the future, it will be necessary to conduct in-depth analyses of the functions of key modification sites and develop precise regulatory strategies to address the ongoing threat posed by coronaviruses.
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