Understanding Host–Pathogen–Vector Interactions with Chronic Asymptomatic Malaria Infections

Pathogenesis studies typically collect a single blood sample from malaria patients on arrival at hospital, giving us only snapshot of host–pathogen interactions. Human chronic asymptomatic infections, which represent the majority Plasmodium can provide multitimepoint samples to study continuous development host–pathogen–vector interaction. Such infections are very low parasitemia; hence, limited amount parasite biomass is available for experiments. However, today’s technologies powerful enough sequence genome and transcriptome parasite. Key biological questions could be answered with regular sampling carriers. This approach advance our understanding parasite–host–vector interactions molecular drivers – critical step eradication. The last standing will display effective adaptations selective forces. While substantial progress has been made in reducing mortality, eradication require elimination all parasites, including those infections. These chronic, low-density difficult detect, yet persist months. We argue that infection parasite’s best asset survival but it exploited if studied as new model Regular cohorts individuals means investigate within its natural host. State-of-the-art techniques now applied such may reveal key recurrent variation surface-exposed antigens by successive generations evade host immune system. presence circulating parasites an individual body temperature <38°C more than 48 h; also referred 'afebrile'. var allele generated mitotic ectopic recombination two genes. persistence multiplying over long period time without resolution. binding P. falciparum-infected erythrocytes other cells, endothelial cells. first Duffy-binding-like 5?-end almost Although total number unique DBL? sequences falciparum population virtually infinite, ~30 bp regions either end highly conserved. 'Universal primers' targeting these used amplify polymorphic region between, identification transcript quantitation. temporary halt intraerythrocytic cycle. this context, strategies avoiding detection and/or removal host’s system, particularly via antigenic variation. group displayed surface infected erythrocytes. They include encoded (~60 copies), rif (~180 stevor (~40 copies) gene families. family genes, mutually exclusive expression, coding erythrocyte membrane protein 1 (PfEMP1). PfEMP1 mediates cytoadherence or uninfected composed four seven DBL CIDR domains.