Covid-19 Clinical Trial
Official title:
Association Between IL-12RB and TNF-alpha Gene Polymorphism With Susceptibility and Progress of Covid-19 SARS-CoV-2: A Case Control Study
A novel coronavirus was identified in late 2019 in Wuhan, China On 11 February, The
International Committee on Taxonomy of Viruses (ICTV) announced that the official
classification of the new coronavirus (2019-nCoV) is called severe acute respiratory syndrome
coronavirus 2 (SARS-CoV-2). The World Health Organization (WHO) announced on the same day
that the official name of the disease caused by the virus is Corona Virus Disease-19
(COVID-19). WHO has declared the infection a Pandemic on March 11, 2020. Based on previous
studies on SARS in 2003 and SARS-MERS 2013 there was a genetic polymorphism associated with
the susceptibility and severity of the disease.
Interleukin-12 (IL-12) is a cytokine secreted by activated phagocytes and dendritic cells. It
plays a pivotal role in promoting Th1-type immune responses and cell-mediated immunity. IL-12
triggers many biological functions: it stimulates the proliferation of activated T- and
NK-cells, enhances T- and NK-cell-mediated cytolytic activity, and induces the production of
IFN-γ by both T-and NK-cells. The interferon-γ production induced by IL-12 forms a major link
between innate and adaptive immunity. A recent study revealed that interferon-mediated
immunopathological events are associated with atypical innate and adaptive immune responses
in SARS patients.
Also, TNF-α is a key mediator of the inflammatory response and is critical for host defense
against a wide variety of pathogenic microbes. However, the over-expression of this cytokine
may lead to badness in disease recovery. The dual role of TNF, acting as an agent of both
innate immunity and inflammatory pathology, poses a considerable challenge for gene
regulation.
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