The results from the molecular simulations seem to demonstrate that DHF can inhibit, non-competitively and in a reversible way, the binding of ACE2 with the Wild type SARS-CoV-2 virus RBD. However, since there is no evidence that DHF can establish covalent bonds with ACE2, it could be assumed that the DHF can spend a short time in ACE2 and later take another pose, in such case, it cannot perform an inhibition or even abandon it. Therefore, it can be said that DHF's inhibitory capacity could depend on the relation of it plasma concentration and the amount of ACE2 receptors present, that is dose-response effect. Figure shows that RBD mutations for the Beta and Delta variants have not increased the affinity of RBD for the ACE2 receptor, when compared to the Wild type SARS-CoV-2. In other words, the mutations present in the RBD of these variants do not seem to improve the binding energy of their RBD with the ACE2 receptor, so the increase in their contagious capacity may not be explained by this mechanism. On the other hand, the mutations present in the rest of the virion of the variants of this virus may contribute to this capacity. However, if we consider that the virus mutations in its RBD allow it to evade the protection offered by high levels of DHF or other folic acid's metabolites in human plasma. This might explain the higher infection rate observed with these new variants in the general population. If folate levels were an important factor in the relative resistance to infections by this virus in healthy people, this might be different in pregnant women, since their immune system is altered to avoid rejection of the fetus , and therefore, the prescribed supplements could no longer provide significant protection for the Delta and other variants, as it did for the Wild type SARS-CoV-2 .