Red blood cells (RBCs) are the most abundant cell type in human blood. Their primary function is to transport oxygen from the lungs to every tissue and organ, a task accomplished by the iron-containing protein hemoglobin. Research confirms that SARS-CoV-2 infection frequently impacts both the count and the function of these oxygen-carrying cells. Understanding this relationship helps clarify the severity and long-term effects of COVID-19.
Confirmed Changes in Red Blood Cell Levels
A frequent observation in patients with moderate to severe COVID-19 infection is a reduction in the red blood cell count, known as anemia. Observational studies revealed that a significant percentage of hospitalized patients develop anemia, with prevalence rates sometimes exceeding 60%. This condition is frequently categorized as Anemia of Chronic Disease (ACD) or Anemia of Inflammation.
This type of anemia differs from typical iron deficiency anemia, as it is driven by the body’s inflammatory response. Laboratory findings often show low levels of iron circulating in the blood, despite high levels of ferritin, the iron storage protein. The presence of anemia upon hospital admission has also been associated with a less favorable outcome in patients infected with SARS-CoV-2.
While a drop in red blood cell count is the most common change, some patients in the early stages might show a temporary increase in RBC concentration. This is often an effect of dehydration, where decreased blood plasma volume makes the relative number of blood cells appear higher. However, the sustained and clinically significant finding remains the development of anemia, which can persist for weeks or months after the acute infection has resolved.
How COVID-19 Affects RBC Production and Survival
The systemic inflammation triggered by SARS-CoV-2 is the primary driver behind the altered red blood cell profile. The immune system releases inflammatory signaling molecules that suppress the bone marrow. This suppression slows erythropoiesis, the production of new red blood cells, resulting in fewer cells generated to replace those that naturally age and die.
A major component of this inflammatory effect is the dysregulation of iron metabolism, a hallmark feature of Anemia of Chronic Disease. Systemic inflammation leads to increased production of hepcidin, a hormone that regulates iron availability. Elevated hepcidin acts to trap iron within immune cells and storage sites, preventing it from being released into the bloodstream.
This mechanism results in functional iron deficiency. The iron is unavailable for use in the bone marrow to synthesize new hemoglobin. The inability to access iron impairs the creation of healthy, oxygen-rich cells.
Beyond production issues, the inflammatory environment can also shorten the lifespan of existing red blood cells. The oxidative stress caused by the infection can damage the cell membranes and internal structures of circulating erythrocytes. This damage can lead to premature destruction (hemolysis), or trigger eryptosis, a form of programmed cell death for red blood cells. Suppressed production and accelerated destruction contribute to the overall reduction in the red blood cell count.
Health Consequences of Altered Red Blood Cell Counts
The reduction in the number of functional red blood cells directly impairs the body’s capacity to deliver oxygen. Low hemoglobin levels mean the blood cannot effectively carry enough oxygen to the body’s tissues. This diminished oxygen-carrying capacity contributes significantly to common symptoms like fatigue, muscle weakness, and persistent shortness of breath, which can linger long after the initial infection.
The quality of the red blood cells also influences the risk of blood clots. Studies show that red blood cells from infected patients often exhibit morphological changes, losing their normal flexible, biconcave shape. This loss of deformability means the cells struggle to squeeze through the body’s smallest blood vessels, the capillaries.
These altered, less flexible red blood cells can increase blood viscosity and promote cell-to-cell clumping. The damaged cells can also interact with the lining of blood vessels, activating clotting pathways. This can lead to the formation of microthrombi that obstruct blood flow in the microcirculation of various organs, further exacerbating tissue hypoxia. The combination of fewer cells and dysfunctional cells creates a dual problem that affects both oxygen delivery and the risk of thrombotic events.