Interesting. I wonder if this would be applicable to other viruses that hide dormant like shingles or herpes.
Herpesvirus latency is really complicated, more so than HIV. It hides in more tissues and particularly in nerves, which have some degree (debated) of immune privilege. Every type has different latency. Most types have multiple, very different methods of staying latent and stay more latent than HIV. We understand some of those methods, partially understand many of them, and still don't know a lot about others. A latent infection will probably still remain if too few of these pathways are activated at once.
> We therefore modified the lipid composition of the LNP to enhance potency. First, the ionisable lipid DLin-MC3-DMA (MC3) was replaced with SM-102, an ionisable lipid previously shown to lead to greater cytosolic mRNA delivery through enhanced endosomal escape [30]. Second, the SM-102-LNPs were further modified using ß-sitosterol, a naturally-occurring cholesterol analogue associated with enhanced mRNA delivery [31], to create a formulation referred to as LNP X (Fig. 1b).
[30]: https://pubmed.ncbi.nlm.nih.gov/29653760/
[31]: https://pubmed.ncbi.nlm.nih.gov/32080183/
Neither of those papers they cited were focused on HIV/T cells specifically. Maybe this will have no applications, or applications in HIV only, or be generally useful for hard to transfect cells, or be bad for HIV for some unforseen reason but useful elsewhere, or be a dead end, you never know. But yeah maybe if folks run into similar challenges for approaches to dealing with those viruses, maybe there's something from this work that could help them, who knows?