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.