[neom]

high mutation rate != high crossover rate, and immunological resistance != susceptibility to novel evolution. (it's actually the other way around)

Also to be super clear, I'm not saying rats are immune to bat viruses, I'm just saying in reality it's is too divergent for functional crossspecies transmission and both rats and bats already have their own established, evolved coronavirus ecosystems that solve the same problems (like furin cleavage above). It seems to me near impossible it could actually happen.

[mikeyouse]

It’s incredibly common for bats and rats to be coinfected with the same viruses… this is literally why we were looking at pangolins and raccoon dogs and mink for SC2 and at masked palm civets and ferrets for SC1. The term of art here is “intermediate host”.

The virus doesn’t need to make the animal sick to increase its human transmission risk, it just needs to infect its cells and be in the same host as other circulating viruses to get the crossover and recombination events.

From early host analysis,

> For a precursor virus to acquire the genomic features suitable for human ACE2 receptor binding, an animal host would likely have to have a high population density to allow natural selection to proceed efficiently (27). It is interesting to note that rodent betacoronaviruses have the polybasic cleavage site (38). Considering the above, surveillance and whole genomic analysis of CoVs from rodents are important to elucidate whether these species have any role in the transmission cycle of the virus and to detect the emergence of possible recombinants involving CoVs from these species and those from bats. However, there is not yet any evidence on the role of rodents or squirrels as intermediate hosts.

https://pmc.ncbi.nlm.nih.gov/articles/PMC7297130/

Or more direct examination of the FCS issue between rats and bats:

> Here, we examine the spike protein across coronaviruses identified in both bat and rodent species and address the role of furin as an activating protease. Utilizing two publicly available furin prediction algorithms (ProP and PiTou) and based on spike sequences reported in GenBank, we show that the S1/S2 furin cleavage site is typically not present in bat virus spike proteins but is common in rodent-associated sequences, and suggest this may have implications for zoonotic transfer. We provide a phylogenetic history of the Embecoviruses (betacoronavirus lineage 2a), including context for the use of furin as an activating protease for the viral spike protein. From a One Health perspective, continued rodent surveillance should be an important consideration in uncovering novel circulating coronaviruses.

https://www.sciencedirect.com/science/article/pii/S235277142...

[neom]

Too much conflation going on at this point, feels like we’re getting to the point of talking past each other. My understanding is: crossspecies jumps need cellular compatibility, not just proximity. Resistance makes a host a dead end, not a mixing vessel. “Intermediate host” means one the virus can actually replicate in, not just be near. And parallel evolution isn’t the same thing as recombination.

[mikeyouse]

I guess we are getting past each other. Not all viruses have the crosspieces compatibility, but many coronaviruses do. Rodents are extremely common intermediate hosts for bat viruses that later infect other animals. It’s a speculated source of a pig outbreak in China;

A possible scenario for such transmission may include bats infected with HKU2-like CoVs preying on insects near pig facilities, dropping contaminated feces that were later introduced into the pens somehow, by pig feed or some kind of animal (Fig. 4). According to our onsite observation in 2017, rodents were frequently visible in these pig farms. Notably, bat HKU2-like CoVs are clustered with rat CoVs in the genus Alphacoronavirus (Fig. 3). As we found that SeACoV infects different cell lines originating from rodents, and mice may be susceptible to SeACoV experimental infection (Yang et al., 2019b), we hypothesize that in such field conditions, rodents (especially wild rats) in the farms may eat pig feed contaminated by bat feces, becoming carriers of SeACoV (Fig. 4). Alternatively, if pigs became infected and shed SeACoV-positive feces, the virus could begin circulating in pig facilities. Contamination of pig feed, pig feces and water supplies by rodents could accumulate and develop into outbreaks of diarrhea in neonatal piglets (Fig. 4). Future studies on identifying HKU2-like CoV positive samples in rodents near pig farms are warranted to test this hypothesis.

Many rat coronaviruses are closer evolutionarily to specific bat coronaviruses than other closely related bat coronaviruses;

https://ars.els-cdn.com/content/image/1-s2.0-S01681702193067...