<![CDATA[Indonesia is one of the countries in the Southeast Asian region that contributes the largest malaria cases after India. In 2022, there has been the highest increase in cases in the last 3 years. Various molecular findings and malaria genomization projects are now increasingly being researched in a number of research centers around the world. However, only a few systematic reviews are available regarding malaria in Indonesia. This article aims to explore the latest update of malaria pathogenesis, so that it is expected to be a reference in establishing proper diagnosis and deciding on therapy, as well as contributing to the development of tropical infection science in Indonesia. As one of parasite causing Malaria, P. falciparum has ability to carry out an unlimited antigen variation by altering gene expression on the surface of infected red blood cells. When infected, the morphology of red blood cells changes significantly compared to uninfected ones. One indicator of the severity of malaria is a significant reduction in the flexibility of red blood cells. Plasmodium products trigger host release of a number of cytokines that aggravate clinical manifestations. For this reason, treatment with anti-cytokines is thought to be able to overcome the clinical manifestations of severe malaria. Malaria toxin is an immunogen produced by parasites. This toxin will induce the host so that it releases molecules bound to the serum. The Pf155 antigen, also called ring-stage erythrocyte surface antigen (RESA), can also trigger TNF-. Thrombospondin, CD36, ICAM-1, and VCAM-1 which are receptors located on infected erythrocytes. The degree of parasitemia may change over time in malaria infection. Repeated infections followed by the appearance of other antigens are a way for plasmodium to trick the immune system.]]>
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