7. Conclusions
Although the anti-microbial activity of Aβ and the possible role of viral infection in Aβ plaque formation have been reported, the effects of Aβ on the progression of COVID-19 remain unknown. The aforementioned background points to the fact that Aβ can bind to the SARS-CoV-2 virus, as has been shown for other viruses as well, however, this union predisposes to an increase in the host cell infection, which is different from what happens with other viruses, like HSV-1. Therefore, it is concluded that this is possibly the cause of the neurological disasters that have been seen in post-COVID patients.
Some works explain the effect how SARS-CoV-2 modulates the synthesis of Aβ. Others studies show that Aβ can bind to SARS-CoV-2 and to ACE2. From the literature, it can be observed that no work to date says that Aβ prevents infection by SARS-CoV-2. A study demonstrated an increase in viral infectivity after binding to ACE2 receptors; however, up to now, there are no other studies in this regard. To know in depth the mechanisms by which this event occurs is essential to be able to propose future antivirals. Previously the Aβ had been proposed as an antiviral, however, under this latest work this theory is broken. In some cases, it is a requirement that the Aβ be in contact with the cells and the virus at the time of infection, indicating that the peptide is necessary for the early stages of infection, as occurs in enveloped virus [60].
However, it is difficult to attribute the consequences to a single event, some facts will be directly derived from a direct way and others by collateral damage.
The studies presented here as a whole show strong information to conclude that SARS-CoV-2 is a virus that, once it enters the brain, promotes the synthesis of Aβ. This protein binds to SARS-CoV-2, a mechanism reproduced with other viruses, however, this binding facilitates its entry into the host cell and promotes viral replication, thus increasing the synthesis of more amyloid beta peptide and more viral progeny, promoting inflammation, and exacerbation of neuronal damage. On the other hand, in patients with Alzheimer’s, when the virus enters this environment rich in Aβ, it is already in an environment in which it can initially bind to the pre-existing Aβ and then promote viral replication and inflammation, exacerbating symptoms of Alzheimer’s (Figure 1). These mechanisms could explain the rapid outcome of patients with neurodegenerative diseases and those infected with SARS-CoV-2, and the possible association between COVID-19 and the tendency to suffer neurodegenerative diseases in the future.