The WHO, CDC & Health Canada have all known since 2005 that the most effective & clinically proven treatment for inhibiting (to prevent or hold back from doing something) SARS-CoV-2 replication & infection is nitric oxide.
SARS-CoV-2 infects cells by attaching to a receptor on the lining of the airways called angiotensin-converting enzyme 2 (ACE2). This is the same mechanism by which SARS-CoV-1 infects cells. Nitric Oxide (NO) specifically alters a surface protein known as the spike protein, such that it cannot attach to the ACE2 receptor. This results in blocking viral entry into the cell as well as the subsequent replication of the virus. Since SARS-CoV-2 shares the same mechanism of cell entry, we can relatively confidently assume that NO would have a similar effect regarding this novel virus.
A 2005 study published in the National Library of Medicine demonstrated that Nitric Oxide “significantly inhibited the replication cycle of SARS-CoV in a concentration-dependent manner. We also show here that NO inhibits viral protein and RNA synthesis. Furthermore, we demonstrate that NO generated by inducible nitric oxide synthase, an enzyme that produces NO, inhibits the SARS-CoV replication cycle.
To increase nitric oxide in the minimally ill or even uninfected is to augment the body’s ability to create it. There are many pharmacologic ways to do this; however, potentially the most effective, cheapest, and lowest risk is to supplement with the precursor amino-acid L-arginine.
The WHO, CDC, Health Canada and other public health practitioners and officials already know that the nutritional supplement L-arginine is converted in the body into a chemical called nitric oxide.
we found that NO inhibits (prevents) the replication of SARS-CoV by two distinct mechanisms. Firstly, NO or its derivatives cause a reduction in the palmitoylation of nascently expressed spike (S) protein which affects the fusion between the S protein and its cognate receptor, angiotensin converting enzyme 2. Secondly, NO or its derivatives cause a reduction in viral RNA production in the early steps of viral replication, and this could possibly be due to an effect on one or both of the cysteine proteases encoded in Orf1a of SARS-CoV.”