Thanks for the input. The shared cytoplasm condition is perfectly reasonable requirement, certainly, but it's also not a terribly high bar to clear. HIV does i

Thanks for the input. The shared cytoplasm condition is perfectly reasonable requirement, certainly, but it's also not a terribly high bar to clear. HIV does indeed prominently infect CD4+ T lymphocytes, but that is by no means the only cell type it infects. At the very least, both species have been described to infect macrophages (and both may display tendencies to promote cell fusion, in which case I would expect many normal categorizations of what a cell type is, are off). As for the polymerases being roughly equivalent, I have a hard time believing that. As I've understood it, coronavirus RNA polymerase does perform proofreading, and over the course of the pandemic there has been plenty of media statements of relief and optimism about SARS-CoV-2 evolution not being such a big problem because the genome seems to be relatively stable as RNA viruses go. Many of the people making those statements may have had more hopes than facts to back that up, by all means, but simply grabbing a few highly ranked search result on mutation rates (I don't have time to do a more proper review now, sorry) does seem to suggest SARS-CoV-2 was estimated to have a low mutation rate (https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC7387429/ https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC7387429/) at least early after the introduction to human. Admittedly, it's also reported that mutations which should be suspected to reduce the proofreading effectiveness appeared early (https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC8134885/ https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC8134885/). But on the other hand, HIV is change virtuoso, and one of the first things you hit with a search engine on that topic currently (https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.1002251 https://journals.plos.org/plosbiology/article?id=10.1371/jou...) has the following very interesting piece in the abstract: "extremely high mutation rate of (4.1 ± 1.7) × 10^{−3} per base per cell, the highest reported for any biological entity. Sequencing of plasma-derived sequences yielded a mutation frequency 44 times lower, indicating that a large fraction of viral genomes are lethally mutated and fail to reach plasma. We show that the HIV-1 reverse transcriptase contributes only 2% of mutations, whereas 98% result from editing by host cytidine deaminases of the A3 family." Evidently those cytidine deaminases act on viral DNA sequences as a host defense mechanism, so that source of mutations at least, would be distinguishing for an RNA dependent DNA polymerase such as HIV reverse transcriptase (which, by the way, apparently really doesn't do any proofreading), as compared to a coronavirus RNA dependent RNA polymerase. Now I'd be curious to see if B.1.1.529 mutations appear preferentially at positions which would have cytidine after reverse transcription. I guess that would be the guanosines in RNA original?