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 5 hours ago | parent [-]

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 2 minutes ago \| parent [-]
		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.