COMPLEMENT LEVEL CHANGES AMONG IRAQI COVID-19 PATIENTS

Abstract

The complement system plays a significant role in the human innate immune system during the COVID-19 pandemic exhibits several protective effects against the virus in order to eliminate cellular debris, induced inflammation. On the other hand, it plays a significant role in the pathogenesis of COVID-19, primarily through its involvement in multi-organ dysfunction and increasing the likelihood of adverse clinical outcomes. In order to confirm that the complement system contributes to COVID-19 pathogenicity, it is essential to measure the concentration of complement system proteins in COVID-19 patient sera compared to healthy individuals. This study aims to evaluate and quantify the level of C1q, C3, C4, and Properdin between the patients diagnosed with COVID-19 and control groups, specifically focusing on the statistically significant variations in patients' outcomes compared to the non-significant changes. This study measured classical pathway activation markers (C1q, C3, C4, and Properdin) in 70 Iraqi patients with COVID-19 as well as 20 healthy controls. Levels were assessed by the ELISA technique in Medical City hospitals in Baghdad between December 2022 and May 2023. Patients infected with SARS-COV-2 reported decreased levels of (C1q, C3, and C4) in their blood when compared with controls, as shown in Figure 1. In addition, C1q, C3, and C4 levels showed a notable disparity between their levels in the sera of patients in comparison to the healthy control (p=0.0164), (p=0.0282), (p=0.0454) respectively, with no statistically significant difference seen in Properdin levels between the study groups (p=0.8837). Based on the available evidence, this work represents the initial investigation of C1q, C3, C4, and Properdin in COVID-19 patients in Iraq. In conclusion, according to the complement level in serum, there was a highly significant disparity between patients with COVID-19 and the control group, except for Properdin level. It might be due to the classical pathway's hyperactivation and complement protein consumption during infection.