Omicron variant has the mutation, D796Y. In HCoV-229E, the virus has a deletion, which suggests disease. This earlier science links to chloroquine and bafilomycin. Bafilomycin, like ivermectin, is a 16-membered macrolide, and HCoV-OC43 is the bovine-to-human species jump. It’s also a mistake to get amnesia about Fau Chi’s influenza and vaccine competition:
Blau DM, Holmes KV, Human Coronavirus HCoV-229E Enters Susceptible Cells Via the Endocytic Pathway, in The Nidoviruses: (Coronaviruses and Arteriviruses, Kluwer Academic, 2000)
’There are two serotypes of human coronaviruses, HCoV-229E and HCoV-OC43....In order to infect susceptible cells, the S glycoprotein of HCoV-229E binds to its receptor, human aminopeptidase N (hAPN) also known as CD13, a metalloprotease. After attachment, the viral envelope must fuse with a cellular membrane.
....We have studied the entry of HCoV-229E into polarized human colon cancer cells (Caco-2), and also show that the entry into MRC-5 human lung epithelial cells is inhibited by drugs that block the acidification of endosomes. These findings suggest that HCoV-229E undergoes endocytosis after binding to hAPN at the plasma membrane and the virion is then sorted into endosomes where fusion of viral envelope and endocytic membrane occcur.
If HCoV-229E enters by fusing with endocytic membranes, it is likely that these drugs will inhibit infection. Chloroquine, a weak base, and bafilomycin A1, a specific inhibitor of the vacuolar ATP-ase proton pump, both block acidification of endosomes. As seen in Table 2, treatment of MRC-5 cells with these drugs during virus adsorption inhibits viral infection, whereas treatment after viral replication has begun does not decrease the percent of cells expressing HCoV-229E antigen.
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It is thus possible that chloroquine and bafilomycin A1 affect not only the entry but also the release of the virus. Incubation in chloroquine or bafilomycin A1 before and during virus inoculation resulted in a decrease of viral titers when compared to untreated, inoculated cells. In contrast, when the drugs were added 8-12 hours post-inoculation, there was no significant decrease in viral yields compared to untreated, inoculated cells. These results show that lysosomotrophic drugs inhibit early at virus entry but at later times do not affect the release of virus....Influenza hemagglutinin (HA), its viral attachment protein, undergoes a conformational change at the low pH found in endosomes. This change allows fusion of the viral envelope with the endosomal membrane.’
