First off no one should be stopping their ARB or ACEI drugs without the direction of their physicians. In particular there is a risk of decompensation of heart failure when these drugs are used in their treatment.
We know that the ace2 receptor is encoded on the X chromosome so women have more ace2 receptors than men but men are more susceptible to severe disease then woman. Although men indulge in more dangerous behaviours such as smoking and high alcohol intake it is looking now as though there is a true biological difference. One would therefore think that the ace2 upregulation by these drugs maybe more helpful than deleterious, and the paper you quoted discusses this.
Although patients with hypertension are over-represented I have yet to see data to say that the use of ARB or ACEI is higher in the infected population of hypertensives.
The theoretical risk of these drugs is that upregulating the number of receptors increase the attack points for the virus. On the other hand it is hard to imagine that if one receives an infective dose of virus it is unable to fully saturate the available ACE2 receptors available to it. Especially when it is thought that the inoculum is probably only a few hundred or few thousand virions.
Another observation is that medical staff are more affected then others which suggest that the initial viral load is important. This suggests that the virus takes out more ace 2 receptors with a higher infective dose, rather than viral replication subsequently takes out more ace2 receptors in the initial assault. So having more receptors may be beneficial.
In practice I have read that people are just stopping drugs based on their clinical conditions rather than theoretical considerations especially when the theory is not fully developed.