Similarities between the effect of SARS-CoV-2 and HCV on the cellular level, and the possible role of ion channels in COVID19 progression: a review of potential targets for diagnosis and treatment
https://www.tandfonline.com/doi/full/10.1080/19336950.2020.1837439
Therapies targeted at the p7 ion channel
p7, similar to SARS-CoV-2 E protein, is an HCV protein that plays a role in viral assembly and release of mature virions. In addition to this, the p7 protein is conserved across all genotypes of HCV, making it a potentially effective therapeutic target for HCV....A recent study, however, discovered that amantadine and its new analogue, rimantadine, are too small to fit the binding pocket of p7 and may not be as effective in vivo [50]. Developing a larger analogue of these inhibitors may thus help circumvent this potential setback and prove useful for SARS-CoV-2 treatment.
Amiloride is a guanidium compound that functions to block the Na+ channel in epithelial tissues to facilitate Na reabsorption in the kidney in a manner that depletes Na but not K within the body. Amiloride has been shown previously to inhibit release of viral particles in the Vpu protein of HIV-1 via inhibition of the ion channel activity that results from the virus budding [51]. Vpu has also been shown to be similar to p7 of HCV, which has prompted the investigation of amiloride activity in terms of its ability to inhibit p7.
A molecular dynamic modeling study has shown that a derivative of amiloride BITT225 has strong hydrophobic interaction with p7, which may translate to in vivo inhibition of p7 [52]. However, this remains to be tested in human studies. (my note: I assume human studies refers to Covid-19)
I've been away for a bit, so I don't know if this article has been posted yet from the 12th Oct. Goes into great detail about the similarities of Covid-019 and HCV. As we know BIT has had a strong focus on HCV and now Covid, and the interaction shows how BIT appear to be on the right track for a successful outcome for both (and more)
