Mature red blood cells (RBCs) lack internal organelles and canonical defense mechanisms, making them both a fascinating host cell, in general, and an intriguing choice for the deadly malaria parasite Plasmodium falciparum (Pf), in particular. Pf, while growing inside its natural host, the human RBC, secretes multipurpose extracellular vesicles (EVs), yet their influence on this essential host cell remains unknown.
Cerebral malaria is an outcome of multifaceted and complicated condition. Cytoadherence is one critical factor in cerebral malaria pathology as high order cytoadherence complexes result in vascular congestion and cell apoptosis. Morphological abnormalities in uninfected RBCs can be a contributing factor to aggravate cytoadherence. Malaria pigment hemozoin is a potential bioactive molecule and the role of this pigment in cerebral malaria pathology is not completely understood. To understand this, primarily we investigated the impact of hemozoin pigment on uninfected RBCs.
Malaria, a protozoan disease led to numerous deaths and several new million cases raised due to the development of resistance as per the WHO malaria report 2019. This can be overcome by the development of an effective targeted plant-based delivery system through phytosomes that are effective in permeation and bioavailability to treat infected RBCs (parasitic cells).
The spleen is a complex secondary lymphoid organ that plays a crucial role in controlling blood-stage infection with Plasmodium parasites. It is tasked with sensing and removing parasitized RBCs, erythropoiesis, the activation and differentiation of adaptive immune cells, and the development of protective immunity, all in the face of an intense inflammatory environment.
Plasmodium (P.) falciparum infection mediated Epstein-Barr virus (EBV) reactivation is well established in malaria-endemic countries. We hypothesize that, during malaria onset, the reactivated EBV can infect human brain microvascular endothelial cells (HBECs). This may cause severe cerebral manifestations. We infected HBECs with EBV in vitro. The subsequent gene expression pattern of EBV, inflammatory and endothelial markers was analysed using qRT-PCR.