The gist of the thesis so far:

here is what we think is known so far.

ACE2 adjusts the amount of angiotensin II [given]

and when angiotensin II docks to its receptor [AT2] this results in a signal to increase your blood pressure.

this receptor [AT2] is where losartan does its job, it inhibits binding of angiotensin II to the AT2.

what the virus seems to do is dock with and disrupt the ACE2 protien, so your ability to adjust howmuch angiotensin II is free and available is disrupted.

what does this do? there is a lot more angiotensin II encountering the AT2 receptor, this causes blood pressure to go up, this causes the lungs to generate fibres between cells, this causes lung tissue to become less than optimum at being pliable elastic and permeable to gases.

This is not a good time to have a blood pressure spike. this is probably not a good time to do anything that increases the angiotensin II signal to the AT2 receptor.

your losartan _may_ actually help you.

now keep in mind this is ongoing way out to the very edge, preliminary research so dont do something risky like screwing around with these meds when this isnt even finished science.