Red blood cell (RBC) intercellular interactions, i.e., self-aggregation and adherence to endothelial cells (EC), play important roles in microcirculation. These RBC flow properties are determined by cell membrane components, which are prone to damaging reactive oxygen species (ROS) produced in oxidative stress (OS) states. Alterations in RBC aggregability and adherence have been linked to the pathophysiology in numerous diseases associated with OS. We investigated RBC intercellular interactions in four OS states--thalassemia, treatment of RBC with phenyl-hydrazine or H2O2, and photodynamic virus inactivation of blood units. All these OS states increased RBC adherence to EC, but only part of them elevated their aggregability, while others abolished it. It is proposed that (1) different OS states might induce disparate effects on RBC intercellular interactions; (2) RBC aggregability and adherence to EC, although both intercellular interactions, are controlled by different cell surface factors.