Thread by @ElianaGolber

Several studies in situ in Italy suggest that #hydroxychloroquine and #azithromycin have determinant effects over the ribosome RNA poly3' aaa sensitive polymerases, that are protein assembly units from RNA messenger into proteins.

It appears based on evidence (n=250), [not a randomised double-blind studies], that these two drugs have a synergistic effect in the hosts cells that make the virus partially unable to kidnap the ribosomes polymerase protein assembly of our cells.

Hydroxychloroquine is a zinc Inophore, which means it allows the external Zn to go inside the cell. Zn by itself is not easy to be carried inside the cells, however high amounts of Zn+2 inside the cell have the ability to reduce attachment of RNA 3'aaa dependent polymerases.

Zn+2 appears to delay the ability of the virus to grow rapidly

While #Azytromicine seems to have a synergistic effect when used with Zn+2 Ionophores by targeting other ribosomal mechanism that down regulates the fixation of SARS-CoV-2 poly aaa 3' RNAm into our cells' polymerases

If the viral load remains low, the antigen presenter cells APC are able to work more efficiently in identifying and envelop the viruses, the subsequent presentation of antigens that lead to the receptor of the THC1 stimulating CD4 cells into releasing Interleukin12.

IL12 then activates the T Killer cells CD8, these cells induce apoptosis in infected cells that have parts of the virus in their membrane.

TH1 in CD4 also induce the formation of B Cells these induce a rapid formation of antibodies that can bind easily to those antigens.

Stopping the ability to rapidly infect cells by affecting the attachment of the RNAm of the virus to the ribosomes can be key to enable TH1 CD4 cells and CD8 cells to work without being overwhelmed by large viral loads.