Via Macromolecules: Cooperative Orthogonal Macromolecular Assemblies with Broad Spectrum Antiviral Activity, High Selectivity, and Resistance Mitigation. The abstract, with my bolding, and then a comment:
Treatment of viral infections continues to be elusive owing to the variance in virus structure (RNA, DNA, and enveloped and nonenveloped viruses) together with their ability to rapidly mutate and garner resistance.
Here we report a general strategy to prevent viral infection using multifunctional macromolecules that were designed to have mannose moieties that compete with viruses for immune cells, and basic amine groups that block viral entry through electrostatic interactions and prevent viral replication by neutralizing the endosomal pH.
We showed that cells treated with the antiviral polymers inhibited TIM receptors from trafficking virus, likely from electrostatic and hydrogen-bonding interactions, with EC50 values ranging from 2.6 to 6.8 mg/L, depending on the type of TIM receptors.
Molecular docking computations revealed an unexpected, and general, specific hydrogen-bonding interactions with viral surface proteins, and virus and cell binding assay demonstrated a significant reduction in infection after incubating virus or cells with the antiviral polymers.
Moreover, the mannose-functionalized macromolecules effectively prevented the virus from infecting the immune cells. Representative viruses from each category including dengue, influenza, Chikungunya, Enterovirus 71, Ebola, Marburg, and herpes simplex were surveyed, and viral infection was effectively prevented at polymer concentrations as low as 0.2 mg/L with very high selectivity (>5000) over mammalian cells.
The generality of these cooperative orthogonal interactions (electrostatic and hydrogen-bonding) provides broad-spectrum antiviral activity. As the antiviral mechanism is based on nonspecific supramolecular interactions between the amino acid residues and mannose/cationic moieties of the macromolecule, the ability to form the virus–polymer and polymer−cell assemblies can occur regardless of viral mutation, preventing drug resistance development.
In case the abstract is less than clear to you, here's the story in Popular Science that led me to this report.
I confess my first reaction was: What about the countless viruses we know nothing about, some of which might even be useful—even essential to our wellbeing? And my second reaction was:
One ring to rule them all, One ring to find them, One ring to bring them all, and in the darkness bind them.
When evolution has wired you to look for simple, dramatic solutions, those are the solutions you look for. I wish we'd been wired to look for better definitions of what a real problem is, and then to look for real solutions.
That said, if this is indeed the one ring to rule them all, and it stops viral disease dead, I will rejoice. Especially if old age is found to be caused by a virus inadvertently wiped out in the purge. And even if, newly rejuvenated, I then have to deal with the billions around the world who are no longer conveniently dying of viral diseases.
