One universal antiviral to rule them all?

Viral evolution and resistance

• Multiple comments note viruses do evolve resistance, just like bacteria, via mutation and selection.
• However, resistance is constrained by physics/biology; some mechanisms can be “too lethal” for escape to be feasible.
• Strong, fast-acting antivirals or vaccines can actually reduce viral evolution by sharply limiting replication opportunities.
• Historical eradications (smallpox, rinderpest, near-eradication of polio) are cited as examples where escape did not occur in time.

Antibiotics vs antivirals

• Clarification that antibiotics target bacteria, not viruses, and bacterial resistance is helped by self-replication and horizontal gene transfer.
• Some antivirals target host-cell machinery essential for viral replication, which may offer fewer evolutionary escape routes.
• Debate over whether antibiotic overuse has made pathogens “worse” vs merely harder to treat; unclear in the thread.

Mechanism of the proposed antiviral

• Summaries emphasize this is an immune-boosting approach: mimic aspects of ISG15 deficiency to keep a small set of interferon-stimulated genes “on” briefly.
• Delivery is via mRNA in lipid nanoparticles, analogous in principle to mRNA vaccines.
• Ten antiviral genes were chosen that, in combination, strongly suppress viral replication in cells.

Safety, inflammation, and tradeoffs

• Major concern: chronic or broad inflammation is linked (in general) to serious disease; commenters worry about “playing with” a system that in full form causes interferonopathies, skin lesions, CNS effects, and higher bacterial susceptibility.
• Reassurance from others: intended use is short bursts (days) during acute infection or after exposure, not continuous activation.
• Several point out evolution’s failure to “auto-opt-in” to this state suggests non-trivial tradeoffs; long-term risks remain unknown.

Asymptomatic carriers and “Typhoid Mary” risk

• Question whether treated individuals could suppress symptoms yet still carry and transmit viruses, especially in healthcare settings.
• Some connect this to ISG15-deficient patients who show viral exposure without overt illness; others note confusion between inflammation-related disease and actual viral load.
• No clear consensus; flagged as an open risk that would need careful study.

Ecological and evolutionary role of viruses

• Thought experiment: eliminating all viruses could unleash bacterial overgrowth because bacteriophages regulate bacterial populations.
• Several note viruses’ deep roles in evolution (gene transfer, possible roles in placenta and memory), so a virus-free world might have unforeseen systemic consequences.
• Distinction is made between “all viruses” vs “human-tropic” viruses; the latter still leaves risk from new spillovers into an immunologically naïve population.

Comparison to other “universal antiviral” ideas

• DRACO is mentioned as an older broad-spectrum antiviral concept (apoptosis triggered by viral dsRNA) with stalled commercial development.
• Commenters see repeated cycles of “one drug to rule them all” hype; expectation is that reality will be many specialized tools rather than a single panacea.

Public trust and COVID-era context

• Some comments reflect persistent anxiety and misinformation around mRNA, lipid nanoparticles, and vaccine side effects.
• Others respond that serious adverse effects from COVID vaccines are extremely rare compared to common drugs, and that mRNA/LNP are now well-studied platforms.
• Several predict that any “universal” antiviral will face intense political and cultural pushback, not just scientific scrutiny.

Likely niche and deployment

• Many envision this as a targeted, time-limited intervention: e.g., for high-risk exposures (Ebola, rabies, future pandemics) or specialized workers, not mass continuous prophylaxis.
• Overall tone: cautious optimism about the concept, tempered by concern over immune overactivation, long-term safety, and real-world evolutionary responses.