HIV and ID Observations

I spend a lot of my time reading HIV clinical research papers. A lot. 

So here, for your viewing pleasure, is a poster I updated and modified from a brilliant xkcd web comic (using this tool), describing some common HIV clinical research themes.

Suitable for framing, it should prove helpful as you embark on your next research project.

A brief commentary on the contents of these papers:

1. Switching suppressed people with HIV (PWH) on antiretroviral therapy (ART) to almost anything maintains viral suppression. This is true for both biologic and behavioral reasons: there’s no viral replication at baseline, and only people with proven good medication adherence are eligible to participate. That means if it doesn’t work — like the raltegravir plus maraviroc switch — it’s pretty bad.
2. Older people with HIV have more comorbid medical problems — yes, aging sucks for everyone. Everyone! No exceptions to the rule, alas.
3. Here are a bunch of abnormal cytokines that nobody measures in clinical practice. They’re abnormal, yes. Clinical significance? Ummm … let me get back to you on that one. Or let me ask someone who loves cytokines, like the innovative and wonderful Dr. Irini Sereti.
4. Low-level viremia drives us crazy, so we studied it — but you still won’t know what to do.  I’m lucky to work with a guru of low-level viremia (among other things), Dr. Jonathan Li, a translational virologist and senior author on this fascinating study. He knows more about this annoying lab result — its causes and implications — than anyone on the planet. Good to have his number on speed dial, if “speed dial” is still a thing in a post-landline age.
5. Another unsuccessful broadly neutralizing antibody (bnAb) study, but this won’t keep us from trying again with something else. Let’s try an even broader one! One that’s more potent! Let’s “extendify” it, using techniques of “extendification”, so it can be given less often! Then it might work. But if not, we’ll try again!
6. Some phylogenetic trees and/or single-nucleotide polymorphisms (SNPs) that you won’t understand. Or at least, I won’t understand. Throw in a genomewide association study (GWAS) with a Manhattan plot, and let the confusion start.
7. Poor adherence to preexposure prophylaxis (PrEP) is associated with getting HIV (I know, shocker). These are important studies from a behavioral health perspective, such as this recent one. But let me put this a different way — what if you had a strategy that clearly worked, but it wasn’t used? Would it still work?
8. D’oh! Some people with HIV were diagnosed late because the clinicians caring for them for years never sent an HIV test. A remarkably common clinical error, even in 2023, sadly. Quoting this noted researcher in the title’s first syllable.
9. This HIV cure intervention using drugs you’ve never heard of looks really promising — in a mouse. Or if not panobinostat, vedolizumab, or ipilimumab, how about some CRISPR?
10. The incidence curves in this randomized trial of an HIV vaccine versus placebo overlap with depressing precision. Here’s the latest, alas. Oh well, it’s important to keep trying.
11. No, we still haven’t found a good use for maraviroc. But still trying! Trivia buffs will know the clever brand name of this rarely used antiretroviral agent — Selzentry. Get it?
12. Here’s a resistance mutation that only older HIV doctors have memorized. Guilty as charged. I’m still miffed that E138K is a resistance mutation for both nonnucleoside reverse-transcriptase inhibitors (NNRTIs) and integrase inhibitors. What’s up with that?

Ok, that’s a wrap. Am sure I left off some major themes, what else would you include?

Hey, dog lovers — is this you? (It’s definitely me.)

Greeting humans vs their dogs pic.twitter.com/NeGbEtd1n8

— Emma Pope (@emmerpope) September 21, 2022