Worth noting: this is 90% effective for HSV-1, but not tested on HSV-2. That’s on their radar for research. It’s nonetheless a breakthrough, and the Hutch has pulled off some interesting things in the past, so I’d imagine they’ll get there.
I’ve often thought that the people working on herpes treatments probably don’t get the credit they deserve
I read the article but I’m still confused how this works.
My understanding is the herpes virus DNA is integrated into our own. So once the gene editing molecules snip at the herpes virus damaging it, how does the chromosome get put back together?
Is it actually sniping at two places in the herpes genome in a way that the two ends match up and reform while cutting out a section in the middle?
My understanding is the herpes virus DNA is integrated into our own.
I’m not sure about the technique here (I’m sure part of the process puts it back together), but I just wanted to denote that this is how all retroviruses work - they infect a cell and incorporate themselves into the DNA, which is then replicated by normal cell processes.
Our DNA is littered with the corpses of many such remnants, and if we can figure out how to stop Herpes, it would be a path to also stopping HIV.
Meganucleases can work in quite a few ways. Typically speaking cleaving describes a process in which a section of genome is removed (cutting in two places), but not always. The article doesn’t go into too much detail of the specifics of the meganucleases used in this study, but the literature they cite might.
That’s a really good question, the article doesn’t go into specifics.
Then the body’s own repair systems recognize the damaged DNA as foreign and get rid of it.
This is somewhat ambiguous. It could mean that human DNA polymerases see the damaged DNA, scroll backwards and forwards to the START and STOP codons, and break the bonds to snip out the bits of viral DNA. Then endogenous DNA ligases patch the ends together. It could mean that it affects DNA in the viral particles themselves (but from the context in the article I don’t think this is the case). Or it could be the case that the process triggers apoptosis to eliminate the infected cells entirely; I don’t think this is the case because then you have necrotic tissue all over the place, and given that we’re talking about herpes viruses this means fragile skin in tender places… ouch. That’s kind of like using thermite to roast a marshmallow: Fun but overkill and potentially hazardous.
