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.
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.