Preprint Open Access
A novel coronavirus, SARS-CoV-2 was identified in Wuhan, China. The disease caused by the virus can range in severity from asymptomatic to acute respiratory distress syndrome (ARDS) and death.
Primary dengue infection results in IgE mediated sensitization against dengue virus (DENV) proteins. These IgE bind to receptors on mast cells. Upon subsequent exposure to the antigen recognized by the IgE, mast cell degranulation occurs releasing mediators such as histamine. Therefore secondary dengue infection results in urticaria, increased vascular permeability, hypotension, dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). A case of “slow rolling anaphylaxis”.
Since vaccines contain animal proteins derived from animals infected with any number of viral diseases, one could develop IgE mediated sensitization to numerous viral proteins including coronavirus proteins. Therefore, receipt of such vaccines acts like a dengue “primary infection”. It results in IgE mediated sensitization directed against coronavirus proteins. Once sensitized, a SARS-CoV-2 infection therefore now becomes the equivalent of a secondary dengue infection and similarly can have a severe course for the same reason - IgE mediated mast cell degranulation and the immune cascade that follows.
There are many common observations between COVID-19 and dengue. Elevated levels of ferritin, interleukin-6 (IL-6), vascular endothelial growth factor (VEGF), D-dimer, coagulopathy, urticaria and ARDS are reported in both diseases.
There are many indicators that mast cell degranulation and histamine release may have a major role in COVID-19 and dengue severity. Mast cell stabilizers, antihistamines, Vitamin C, HCQ, azithromycin, ivermectin may address different aspects of this cascade and thus reduce disease severity. Disease mechanisms and immunopathology must be understood. Focusing on anti-viral action of drugs alone could be counter productive. For example, CQ had no effect on viraemia but decreased cases of DHF.