DBCB

This is one of those cases where it's really hard to tell what could have happened, but I think the risk outweighed the benefits of doing so. Clinicians have to make decisions every step of the way, and the details of the case are so contradictory and hard to wrap one's head around (literally, nobody had ever seen a clinical picture of symptoms like this guy developed) that I think they decided it was better to be conservative and treat infection as a foregone conclusion and cull the Truvada rather than risk the strain becoming fully resistant and imbricated in the community. It seems like it wasn't fully able to thrive and reproduce in a system flush with Truvada, but it was able to at least hold its ground long enough that periodic bouts of immune modulation/drug level fluctuation allowed it to continue progressing. I think of it like musical chairs.

Theoretically, this has always been possible- both drugs in Truvada, Emitricitibine and Tenofovir, are NRTIs, rather than Fusion/Entry Inhibitors. I could go into the specifics of the HIV lifecycle, but the short of it is that technically, it doesn't stop the HIV from getting in and attempting to infect CD4/CD8 cells- rather, once the HIV is in, it prevents it from successfully translating its genetic material from RNA to DNA, at which point it would attempt to insert the DNA into the cell's genome. So, in theory, some hardy HIV virions could stick out for a while in a set of CD4/CD8 cells, until there is turnover and the cells die and are replaced with new ones. For the majority of these cells, that happens within weeks- but there is a subpopulation of these cells that has a turnover of about 8-9 months or so (give or take). So, if these fairly hardy HIV virions stuck it out long enough, and there was a dip in the amount of Truvada in the blood, some of them could end up getting their RNA translated and integrated (since the PrEP formulation doesn't include and integrase inhibitor)- at which point it would begin to reproduce, and since there would be no other drugs effective at other stages of the HIV life cycle, a localized infection could be sustained until there was enough of a dip for it to enter the blood stream. Typically, without PrEP, this takes 1-3 days (hence the "crucial window" for PEP), but with PrEP under the right conditions it could hold out. Again, this has always been a theoretical possibility- the chances of this happening are incredibly slim, because so, so many factors have to line up for it to work out this way (one of which is, of course, the amount of virus someone is exposed to and how many different strains are present). It's absolutely fascinating that it has occurred, if they're correct about it- but I don't know that the majority of people will have to worry about it. This is the 1% they're talking about when they say up to 99%. Also, forgive any mistakes, while I do work in science, it's been some time since I've had anything to do with virology/HIV specifically.

You could upload to Google Drive, and then privately share the link to us via DM

I second this request- I've been looking for this video everywhere, and can't find it. Seems like it was uploaded by one Tumblr user and reblogged, and so when it was removed that first time it disappeared everywhere.

These are Old English- I also came onto these by accident once, and now everything else pales in comparison! http://iblastinside.com/guide-to-poppers/english-us/