الفهرس 
IntroductionOnly 14 pages are availabe for public view
 |  | from | 200 |  |  |
| | | from | 200 | | |
Abstract
At the end of 2019, the severe acute respiratory syndrome
coronavirus 2 (SARS-CoV-2) originated in Wuhan, China. Since then, it
has been rapidly spreading worldwide and becoming a public health
concern worldwide. This disease leads to pneumonia infection named
coronavirus disease 2019 (COVID-19), posing an enormous threat to
global health. The virus can cause a wide range of clinical manifestations,
ranging from an asymptomatic condition to acute respiratory distress
syndrome (ARDS). COVID-19 can trigger a cytokine storm in pulmonary
tissues through hyperactivation of the immune system and the uncontrolled
release of cytokines. The phrase ―cytokine storm‖ is a descriptive term to
encompass a variety of events that may ultimately result in multi-organ
failure and death. Cytokine storms can cause a severe clinical complication
known as acute respiratory distress syndrome (ARDS).
Genetic factors might be associated with high levels of severe acute
respiratory syndrome coronavirus 2 (SARS-CoV-2) transmissions and
disease progression in the infected population. In COVID-19-associated
acute respiratory distress syndrome (CARDS), elevated plasma levels of
cytokines including IL-6 and TNF-α have been demonstrated and
associated with the severity of the clinical course.
The aim of this study was to evaluate the role of IL6 rs1800795
(174G/C gene) and TNF α rs1800629 (308 G/A gene) polymorphisms in
the progression of COVID-19, and to determine the relation between IL6
rs1800795 (174G/C gene) polymorphism and IL6 level in peripheral blood
of patients with covid-19.
One hundred Egyptian patients participated in this study; 30 Covid-
19 patients with mild disease (10 males& 20 females), 35 Covid-19 patients with moderate disease (19 males& 16 females), 35 Covid-19
patients with severe disease (19 males& 16 females).
All patients and controls were subjected to CT examination of the
chest (CT was graded according to CORADS staging) and the following
laboratory investigations: Complete blood count, CRP, D-dimmer, LDH,
ferritin, liver and kidney function tests, coagulation parameters and
molecular detection of COVID-19.
IL6 rs1800795 (174G/C gene) polymorphism was determined by
Mutagenically Separated PCR (MS-PCR) technique using the specific
primer mixtures according to the manufacturer protocol (Thermo Scientific,
EU/Lithuania). TNF α rs1800629 (308 G/A gene) polymorphism was
determined by RFLP-PCR using the specific primers and NcoI restriction
enzyme according to the manufacturer protocol (Thermo Scientific,
EU/Lithuania). IL6 serum level was done by Enzyme-Linked
Immunosorbent Assay.