[Centigonal]

Herpes viruses like HSV are notoriously difficult to target with medication bc they encode themselves into DNA inside the nuclei of long-lived human nerve cells. Between outbreaks, they basically exist only as rogue DNA floating inside mostly-healthy cells in the nerve ganglia. At some point, something triggers the nerve cell to transcribe the rogue DNA, producing new viruses and beginning a new outbreak.

[mrtesthah]

IM-250 (Adibelivir) is a helicase-primase inhibitor that targets latent HSV so well it may actually permanently reduce the pool of viable latent HSV genomes.

[shevy-java]

Nope - because it can not target the genome. So it is, by definition, not a permanent reduction. Any inhibitor is a protein; unless such a protein modifies the DNA, one only cures a symptom, not the cause, by definition. HAART with regards to the HI virus has a similar problem.

Note that even on commercial sites they point this out:

https://www.medchemexpress.com/im-250.html

"Adibelivir (IM-250) is an orally active helicase-primase inhibitor. Adibelivir is effective against HSV infection and reduces reactivation of latent HSV."

See the word "reduces". Nowhere does it insinuate "permanently"; besides, permanently is simply a misnomer here. Even "latent" is a misnomer; it simply is integrated DNA. The only way to get rid of it is to cut this DNA out. Which therapeutic does so with efficiency? Even CRISPR-Cas9 has off-target effects. There are no permanent cures, and insinuating otherwise by using "permanently", is simply and factually incorrect.

[mrtesthah]

Technically they are circular episomes — not integrated into chromosomal DNA like HIV.

And we do know that it’s possible to reduce the pool of reactivation-competent HSV genomes by the presence of IFNα during primary infection:

https://pmc.ncbi.nlm.nih.gov/articles/PMC12764766/

This causes PML-NB formation → more viral genomes with H3K9me3 + ATRX → resists eviction by the H3K9me3S10ph “methyl/phospho switch” → stops Phase I HSV transcription (and VP16 expression).

Who’s to say an HPI like IM-250 isn’t altering epigenetic markers in viral episomes in this way? Innovative Molecules’ own press release states that some sort of permanent or semi-permanent modification may take place:

https://www.pharmaceutical-technology.com/analyst-comment/es...

>Furthermore, testing in animal models showed that adibelivir affected the latent viral reservoir, suggesting that it has potential as a long-term curative therapy for HSV.