Yes, that’s definitely true. I only bring it up because the way you worded your initial comment seemed to imply that NHP use has been on the decline whereas the opposite appears to be true, at least in the US and China. I suspect the low overall use of NHPs compared to other animal models is more so due to the astronomical economic cost of housing NHPs, not so much because of ethical qualms.

I think your statement that “almost nobody works with primates anymore” isn’t really correct. Most of what ive been reading in the past hour suggests NHP use has remained relatively constant or even increased slightly over the past few decades.

This is purely anecdotal, but as a vaccine researcher I haven’t really noticed any significant decline in the use of NHPs in my field over the past decade. Everyone knows that NHP research isn’t ideal from an ethical standpoint but when it comes to testing a vaccine before trying it in humans, there’s really no better alternative.

Edit: source from USDA showing slight increase in NHP use over time in the US

I think it’s all a matter of opinion, where to draw the line on what is and isn’t considered life. But yes, I can see how one could consider them somewhere between alive and not. They meet many of the criteria we’ve somewhat arbitrarily defined for living things but miss others, such as having the ability to produce their own energy for survival and replication.

If you consider viruses “alive” then it’ll probably be a virus.

Circoviruses have a genome size of 0.89kbases (890 bases)

If you don’t count viruses, the bacteria mycoplasma genitalium has a genome size of ~580kbases (580,000)

For comparison, humans have a genome size of ~6.4Gbases (6,400,000,000) or 3.2Gbases if you want the haploid number (per another users comment)

Herpes isn’t a retrovirus. Nor is HPV, per OP’s specific example.

HIV and HTLV are the only circulating retroviruses known to integrate into the human genome. The only example of a non-retrovirus integrating into host DNA that I’m aware of (not to say there aren’t others) is HPV, which can unintentionally become integrated into host DNA due to DNA damage and subsequent repairs that incorporate the viral DNA. This isn’t so much a cause of poor clearance though, at least for HPV, as the integrated DNA isn’t capable of producing viable new HPV virions.

The strategy is going to be somewhat virus-specific.

As one user noted, retroviruses go dormant by integrating into your own genome, at which point it becomes nearly impossible to rid them completely. External stimuli causes your own cells to express the integrated viral genome, leading to production of new virus. HIV is going to be the most common example in humans.

Other viruses, like herpes, infect so-called immunoprivileged cells that are considered too vital to be damaged in an immune response. In the case of herpes, nerve cells become infected where the virus can lay dormant more easily, as nerves are immunoprivileged cells. Some viruses, like Zika and Ebola can infect the testes which are also privileged sites.

Another general strategy is for the virus to simply hang out in the nucleus of a cell and stop replicating. The nucleus is a nice place for a virus to hang out because (to my knowledge) there aren’t really any proteins involved in recognition of pathogens there. Such proteins are typically in the cytoplasm, within endosomes, or on the cell surface. Furthermore, if a virus stops replicating then there’s not much material for our immune system to recognize. That I know of offhand, herpes, HPV, and cytomegalovirus (and probably MANY others) all employ this strategy.

Most viruses that go latent also express proteins or RNAs that inhibit our body’s ability to recognize pathogens. These come in many different forms but as an example HPV expresses E6 and E7 proteins which cause the infected cell to express fewer genes involved in viral clearance. Another example is how ebolavirus VP35 protein blocks the RIG-I receptor (which recognizes viral RNA)

Last mechanism that comes to mind is that some viruses simply infect areas that aren’t easily accessible by our immune system. HPV infects the epithelia of the uterus in a particular region that has very high cell-turnover rate. Because epithelial cells are constantly being shed in this region, immune cells can’t really patrol it very efficiently.

Anyways I’m just going off memory with this response so sorry it’s all over the place. Hopefully there’s something useful.