I think ECDC gave the right answer, read more here. 

High risk patients, namely 65+ and with chronic conditions (e.g., cardiovascular diseases, HTA, respiratory disease, diabetes, cancer) must be better protected from getting COVID-19

Preventive precautions are essential but social distancing and face masks (see ECDC guidance) play an crucial role.

A study comparing the stability of the SARS-CoV2 showed half-life of virus as follows .

Aerosol 1.2 hours at 65% RH

Stainless Steel 5.6 hours at 40% RH

Plastic 6.8 hours at 40% RH

Cardboard over 3.5 hours 40% RH

Copper less than 1 hour 40% RH

No studies have tested viral stability on our hands.

There appears to be some cross reactivity of anti-SARS antibody to SARS-CoV2. See this paper for more information. 

Antibodies that bind to viral spike antigen and engage FcR of macrophages might cause immune enhancement. However, a potent neutralizing antibody against the receptor binding domain of the spike protein may be effective in preventing viral entry altogether and are less likely to engage in immune enhancement.

While SARS-CoV2 virus may be evolving, perhaps in a manner that could modulate its virulence in humans. There are at least two other main reasons why some people more susceptible than others and as such why we see such marked differences in disease (COVID-19) outcome. The first, and perhaps the most important, is that when a given national health system is robust and PCR-based testing can be done in a widespread manner, mortality falls to about 1-1.5%. This number is at least one order of magnitude higher when compared to the, non-related seasonal influenza. The other main factor is most likely related to “the metabolic status of the host” and there is an emerging notion that COVID-19 may well be a combination of an infectious/metabolic pathology. Its relative severity emerges as a two it (punch) system, with eventually devastating effects to the host depending on its metabolic status before infection (vigor). This was probably not appreciated to its full extent by some political leaders that lingered into taking action and are now suffering the consequences.

Yes, as for any other infectious disease. However, it may not explain per se why some people more susceptible then others.

This is very likely target indeed, as proposed by Akiko Iwasaki.

That is a one million dollar question. The reverse of that medal is why are older people more susceptible. The answer is, we do not know.

The immunogenic properties of BCG, a very safe tuberculosis vaccine, are such that they would boost the innate immune response and this might confer some protection against SARS-CoV-2.  Clinical trials are ongoing to test this in at least four different countries.  A SARS-CoV-2-specific vaccine would certainly be better but this will likely take at least another 9 months to develop.

Repurposing approved drugs is the fastest way forward as the safety data are available.

WHO does not recommend chloroquine for treating COVID-19 and the limited data from early clinical trials are ambiguous due to the trial design.  More robust trials are in progress.  In any case, the window for therapeutic intervention with antiviral drugs is small and they would have to be administered very soon after infection.  If effective, and given prophylactically, they could be very valuable to protect health care workers.  Drugs to downregulate inflammation and reduce immunopathology would be most useful for managing severe cases.

It would unethical to intentionally infect young people with a virus for which there is known treatment or cure.  However, nature is doing this for us in the pandemic so investigating immune responses in infected and convalescent individuals could lead to the identification of neutralizing antibodies, for later therapeutic use, and help understand how we can protect people in the future.  Antibodies appear 3 days or later after COVID symptoms. Numerous attempts to develop vaccines are underway using SARS-CoV-2 DNA, RNA, proteins, and different viral and bacterial vectors.