We have successfully verified substances that narrow the entrance/exit of the coronavirus “nest.”
Drawing on two recent Nature papers about the virus’s DMV (double‑membrane vesicle)—a structure that is notoriously persistent yet remains under‑studied—we focused on the fact that there is only one service entrance accessible from outside (the “crown”). We ran our own AlphaFold2‑based simulations on a largely uncharacterized “second crown” and found that by mimicking substances the virus tends to export from its nest—in effect sending decoy cues—the diameter of the passage can be narrowed. This report summarizes those results.For the first time, we tackle the DMV—where SARS‑CoV‑2 is thought to hole up, keep copying itself, and drive stubborn inflammation—from a new angle: inducing shape change. Because the target and mode of action are completely different, the antiviral performance we evaluate here does not clash with existing antivirals. We simulated and assessed three compounds with minimal side‑effect profiles; one of them also supports neural regeneration and cognitive performance.
Using our latest GPU‑ready in‑house pipeline (DOI: 10.5281/zenodo.16760844) augmented with fluid‑dynamics analysis, we quantified how much the crown’s hydrodynamic resistance increases. To offset the limitation that this is not a lab experiment, we repeated the simulations with three random seeds and confirmed that the same result recurs each time.
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Physiological mechanisms evaluated
Geometric tunability of the outward DMV crown (nsp3–nsp4) formed by SARS‑CoV‑2.
Binding at the NAB–PLpro interface by three compounds and changes in DMV entrance/exit diameter mediated by allosteric responses.
Increase in hydrodynamic resistance affecting DMV “logistics” (nucleic acids, ions) and heightened stress on the environment that houses replicating RNA.
A new strategy for controlling chronic inflammation/persistent infection by intervening in long‑lived viral replication organelles.
For one compound: support for neuronal membrane phospholipid synthesis and synaptic plasticity (a brain‑nutrition/cognitive‑support aspect).
Who this is for
Readers interested in DMVs (“viral persistence nests”) in Long COVID.
Researchers/clinicians who want to understand the DMV pore and nsp3–nsp4 crown as a novel target.
Those interested in drug discovery or basic research using molecular dynamics (MD) and fluid‑dynamics analysis.
Clinical researchers seeking non‑competitive mechanisms that differ from existing antivirals.
General readers / wellness‑oriented audiences interested in bridging neural regeneration or cognitive improvement with antiviral strategy.
⚠ People who should exercise caution (consult a physician before introducing anything new)
Individuals with a history of purine‑metabolism or uric‑acid–related disorders (gout, hyperuricemia).
Those with underlying hepatic or renal disease affecting metabolism/excretion.
People under treatment for cancer or proliferative diseases (medical confirmation may be advisable).
Pregnant or breastfeeding individuals, children, and older adults—populations with high individual variability.
Anyone considering concurrent use with other supplements or medications (especially antivirals or immunosuppressants).
- Individuals who have previously experienced allergic symptoms or intolerance with supplements or vitamin complexes.
Disclaimer
This report is intended to provide insights into molecular mechanisms and physicochemical knowledge. It does not recommend or provide medical advice regarding specific health foods, supplements, or pharmaceuticals.
Before making any decisions about actual introduction or use, please consult with a qualified physician or healthcare professional.
Reading Antiviral Design Through Viral Geometry Morphomechanics
Language : English
Report number : 66
Category : Viral protein
Format : PDF
Pages : 43
Subject : World, Now
Period analyzed : ~September 2025



