Acute severe respiratory syndrome coronavirus-2 (SARS-CoV-2)
infection causes coronavirus disease-2019 (COVID-19) which is associated with
inflammation,
thrombosis edema,
hemorrhage, intra-alveolar
fibrin deposition, and vascular and pulmonary damage. In
COVID-19, the coronavirus activates macrophages by inducing the generation of pro-inflammatory
cytokines [
interleukin (IL)-1,
IL-6,
IL-18 and TNF] that can damage endothelial cells, activate platelets and neutrophils to produce
thromboxane A2 (TxA2), and mediate
thrombus generation. In severe cases, all these phenomena can lead to patient death. The binding of SARS-CoV-2 to the
Toll Like Receptor (TLR) results in the release of pro-IL-1β that is cleaved by caspase-1, followed by the production of active mature IL-1β which is the most important
cytokine in causing
fever and
inflammation. Its activation in
COVID-19 can cause a "
cytokine storm" with serious biological and clinical consequences. Blockade of
IL-1 with inhibitory and anti-inflammatory
cytokines represents a new therapeutic strategy also for
COVID-19. Recently, very rare
allergic reactions to
vaccines have been reported, with phenomena of pulmonary
thrombosis. These side effects have raised substantial concern in the population. Highly allergic subjects should therefore be vaccinated under strict medical supervision.
COVID-19 has accelerated vaccine therapy but also the use of drugs and
monoclonal antibodies (mABs) which have been used in
COVID-19 therapy. They are primarily adopted to treat high-risk mild-to-moderate non-hospitalized patients, and it has been noted that the administration of two mABs gave better results. mABs, other than polyclonal plasma
antibodies from infected subjects with SARS-CoV-2, are produced in the laboratory and are intended to fight SARS-CoV-2. They bind specifically to the
antigenic determinant of the spike
protein, inhibiting the pathogenicity of the virus. The most suitable individuals for mAB
therapy are people at particular risk, such as the elderly and those with serious
chronic diseases including diabetics,
hypertension and
obesity, including subjects suffering from
cardiovascular diseases. These
antibodies have a well-predetermined target, they bind mainly to the
protein S (formed by the S1A, B, C and D subtypes), located on the viral surface, and to the S2
protein that acts as a fuser between the virus and the cell membrane. Since mABs are derived from a single splenic immune cell, they are identical and form a cell clone which can neutralize SARS-CoV-2 by binding to the
epitope of the virus. However, this
COVID-19 therapy may cause several side effects such as mild
pain,
bleeding, bruising of the skin, soreness, swelling, thrombotic-type episodes, arterial
hypertension, changes in heart activity, slowed bone marrow activity, impaired renal function,
diarrhea,
fatigue,
nausea,
vomiting,
allergic reaction,
fever, and possible subsequent
infection may occur at the site of injection. In conclusion, the studies promoting mAB
therapy in
COVID-19 are very promising but the results are not yet definitive and more investigations are needed to certify both their good neutralizing effects of SARS-CoV-2, and to eliminate, or at least mitigate, the harmful side effects.