Typical hypersensitive reactions of coronavirus and its vaccines
Hypersensitivity caused by COVID-19 and its vaccines |
there have been serious health conditions amongst the human population on
earth. Hypersensitivity is one of the mechanisms that SARS-CoV-2 is utilizing for
responding against corticosteroids (CS). In effect to unknown harmful
antigens, our body reacts by releasing inflammatory substances to inhibit any
potential damage to the host tissues by the antigen. However, in the case of
hypersensitivity reactions, tissue damage occurs in the host body due to either
a heightened or inappropriate immune response to an antigen. It practically
occurs during the time of cell-mediated as well as humoral responses. The
deaths, related to COVID-19, are majorly due to the creation of severe hypoxemic
conditions in individuals, causing a massive respiratory failure.
As per the research conducted in this field, the major pathogenesis for
the disease includes inflammatory storm. However,
hypersensitivity can also be considered to be another crucial mechanism that is
certainly involved in particular the severe cases of COVID-19. As stated by Tan and his team, hypersensitivity or allergic reactions can be
the outcome of a hyperactivated innate immune response that leads to increased levels of
inflammatory chemokines in serum. Cytokines like IL-1β, IL-6, and TNF-α are found to be
in elevated conditions during the inflammatory storm. Due to the increased
secretion of IL-6 and IL-1β, acute phase protein synthesis gets induced, which offers defense
against pathological damage. However, elevated secretion of such cytokines
causes damage to host cells, which ultimately leads to the exhaustion of
lymphocytes. Simultaneously, TNF-α has a cytotoxic effect, which is related to
chronic inflammation. All of these internal immune responses ultimately
lead to fatal respiratory conditions and organ failure in the body. In
addition to this, the researchers have also stated that COVID-19 can also be
related to hypersensitivity in the lungs, which is again related to the chances
of having chronic multisystem issues.
Hypersensitivity
type III is the one that is known to be related to the SARS-CoV-2 virus. Mahdi
mentioned that viral antigens (Ag) can cause infection to both T cells and
macrophages, leading them to secrete antibodies (Abs) like IgG and IgM. During the
acute phase of infection of this virus, these antibodies are created that, in
turn, lead to the entry and fusion of these viruses into the infected cells. Such
an induced Ag-Ab viral agglutination leads to complement activation for the
formation of the membrane attack complex (MAC). Henceforth, it can be
understood that the pathway for COVID-19 virus infection is related to the
complement activation path rather than antigen presentation and viral clearance
by phagocytosis. Furthermore, their research also mentioned that the Anti-S
protein:CoV immune complex formed by this virus also results in an abnormally
enhanced cytokine action in the body. Such cytokines include
IL-8 and MCP-1, which are lung macrophages. Due to the overproduction,
a cytokine
storm is raised in the lungs, and people then start experiencing lung
congestions and anaphylactic shocks.
When the world
is busy dealing with the COVID-19 virus and its infecting pathways, the
creation of a suitable vaccination became the most vital part to stop the
crisis. However, it has also been found that the causation of hypersensitivity is
not only related to the viral antigens but also its vaccines. Several cases of severe
anaphylactic have been reported by the usage of COVID-19 vaccines. From the
research of Hung and his
co-workers, it has been presented that the mast cell activation, caused by
the production of IgE might be the cause of immediate hypersensitivity.
COVID-19 vaccine excipients and compounds, like gelatin, could cause allergens
to elicit hypersensitivity reactions. The proposed mechanisms for
vaccine-induced immediate hypersensitivity reactions include IgE-mediated,
MRGPRX2-mediated, and complement-mediated. In addition to
this, another unknown mechanism for the causation of immediate
hypersensitivity reaction has been mentioned, which is found to be caused by
the release of effector mediators and mast cell degranulation.
Though
COVID-19 vaccines are highly effective in inhibiting the disease, research by Fernandez-Davila
and her team discovered that the Pfizer-BioNTech vaccine (BNT162b2)
was found to be causing hypersensitivity reactions. Polyethylene glycol (PEG) 2000 is
one of the excipients of the vaccine that can cause IgE-mediated anaphylaxis.
The phenomenon is rare and most of the hypersensitivity reactions are found to
be non-IgE
related. Such an occurrence can occur either by direct activation of
mast cells or by complement recognition of the allergic effector cells. Henceforth,
a certain part of the population has grown to have vaccine hesitancy due to
fear of allergic reactions. Through the research paper, it has also been
recommended that patients having a history of immediate hypersensitivity
reactions in the body need to have a consultation with an allergist before
vaccination. Furthermore, patients who have reacted to the COVID-19 vaccine
need to undergo skin testing either for the vaccine or its excipients.
Therefore, a thorough check-up of the patients’ history, be it an adult or
child, has to be done, specifically for individuals showing immediate (within 4
hours) allergic reactions to the SARS-CoV-2 vaccine.
The immediate
allergic reactions to the virus include cutaneous, cardiovascular,
gastrointestinal, and respiratory symptoms. As mentioned by Kelso,
examples of such symptoms are flushing, itching, coughing, hypotension, vomiting, nausea, diarrhea,
and abdominal pain. Other than these symptoms, there also can be mimics
of anaphylaxis, which include anxiety or vasovagal reactions. It has
also been mentioned that another mRNA vaccine, Moderna is associated with
hypersensitivity reactions. However, till now there has not been any
confirmation of the presence of a high risk level with the COVID-19 vaccines.