About this Research Topic
In infected humans, parasites can, directly and indirectly, manipulate and subvert host immunity and cause diseases. For example, the interaction of Plasmodium falciparum ligands (at the host cell surface) with inhibitory receptors promotes parasite survival and suppresses host immune effector molecules to mediate immune evasion and suppress host immune effector molecules, in direct correlation with malaria severity. However, `protection' against a severe disease occurs early in life in areas where malaria is endemic. A protective immunity depends on antibody responses to proteins expressed by the parasite, which are extremely diverse. Nonetheless, mechanisms of protective immunity formation against malaria remain unclear. Conversely, vectors evolved mechanisms to survive when infected with parasites. Although insects are not endowed with an adaptive immune response, they possess an innate immunity system composed of both humoral and cell-mediated immune pathways which allow them to mount a generalized defense including inhibition of pathogen replication, enhancing pathogen lysis and phagocytosis, or binding of receptors to antigens produced by the invading pathogen. Immunity or natural resistance to parasites in some animals fully protects against infections either early in life or after a lifetime of exposure. For example, birds are naturally immune to the Chagas disease parasite Trypanosoma cruzi .
Knowledge of vector and parasite biology and vector-parasite interactions is beginning to stimulate new concepts and tools for control. However, the mechanisms and pathways through which the development of parasites within vectors may enhance vector-mediated immune control or regulate interactions are yet to be properly understood. In addition, although the mechanisms by which hosts respond to parasite exposure and acquire immunity remain unclear, naturally acquired immunity is related to host responses to parasite antigens. Low antibody levels targeting antigens are predictive of infection, which increases with exposure. This lays the basis for the identification of biomarkers of exposure and candidate antigens for new/improved sero-diagnostics or vaccine development. More so, genome-wide analysis of human pathogens for signatures of selection have been led to the discovery of new vaccine and drug candidates. Therefore, conceptual and technical advances in our understanding of both host- and vector-parasite interactions are essential to developing more effective tools for vector control, parasitic infections, as well as vaccine candidates for vector-borne parasitic diseases.
This Research Topic focuses on the latest research development on the immunobiology, diagnosis, and prevention of VBPDs. Considering the burden of VBPDs and the (re)emergence of some parasites which contribute largely to neglected parasitic infections, particular attention is paid to parasitic disease vectors with their parasites. These include but are not limited to anopheles-borne disease with Plasmodium; snail-borne diseases with Schistosoma, Clonorchis, Opisthorchis, Angiostrongylus, and Paragonimus ; sand fly-borne disease with Leishmania ; and tsetse fly- or triatomine bugs-borne diseases with Trypanosoma .
We welcome prospective authors to contribute Original Research articles and Review articles for this forthcoming Research Topic, covering the following topics:
(i) Immune regulation in the host-parasite or vector-parasite interactions;
(ii) Modulation of the vector immune system by midgut microbiota;
(iii) Molecular evolution of parasite antigens and mechanisms of immune evasion;
(iv) Serological assays for the detection of antibodies to vector-borne parasites;
(v) Vaccine candidates for vector-borne parasitic diseases.
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.