Red blood cells from COVID-19 patients suffer from increased oxidative stress and may have increased lactate influx.

TO THE EDITOR: Coronavirus disease (COVID-19) is caused by SARS-CoV-2, a novel, highly infectious, single stranded RNA virus. An inappropriate immune response characterised by the excess production of pro-inflammatory cytokines (‘cytokine storm’) is common in severe cases of COVID-19 [1]. Such severe disease is frequently complicated by coagulopathy, often progressing to DIC and multi-organ failure [2]. The ‘cytokine storm’ accompanying severe COVID-19 as well as increased serum ferritin levels may be important sources of endogenous oxidative stress [3, 4] Such excess oxidative stress may lead to tissue damage in the lungs and elsewhere by generation of reactive oxygen species (ROS) [5]. The potential role of red blood cells (RBCs) in the pathophysiology of COVID-19, especially their possible contribution to hypoxia and to the thrombotic complications remains uncertain. Both anemia and increase in RBC distribution width have now been associated with increased mortality in hospitalized patients with SARS-CoV-2 infection [6, 7]. In addition, increased oxidation of structural proteins and impairment of membrane lipid homeostasis is reported in RBCs of COVID-19 positive patients, which may alter RBC deformability, potentially contributing to the thromboembolic complications seen in severe forms of COVID-19 infection [8]. To further investigate the possible role of RBC dysfunction in COVID-19, we measured ROS in RBCs of patients infected with COVID-19 at our hospital and the effect of the anti-oxidant N-acetyl cysteine (NAC). To look for evidence of increased adherence of RBCs to endothelial cells (ECs) and platelets in COVID-19 which might contribute to thrombosis, we measured RBC surface expression of adhesion molecules CD44, CD242 (ICAM-4) and CD47, as these red blood cell surface proteins have been implicated in interactions with blood vessels and/or platelets [9]. We also measured surface expression of CD147, as a surrogate marker of the lactate transporter monocarboxylate transporter 1 (MCT1) [10].