About this Research Topic
Neglected tropical diseases (NTDs) are diseases of poverty that impose a high socio-economic burden on more than 1 billion people worldwide according to the latest WHO reports, mainly in tropical and subtropical areas. Despite substantial progress in reducing the overall burden, new strategies to improve the current road maps toward eradication are obviously demanded. Among the 20 different diseases in this category, leishmaniasis remains an unresolved threat to global health with an estimated annual rate of 700,000 to one million new cases leading to 20,000 to 30,000 deaths each year.
Leishmaniasis is a vector-borne disease caused by the protozoan parasite of Leishmania genus. The parasite (with a dynamic genome) has evolved to advantage the vector sand fly transmission to successfully establish the disease. Decades of labor-intensive hard work has partially deconvoluted the intricacies of the host-pathogen interaction which is strongly controlled by different components deposited into the human skin through sand fly proboscis. These include sand fly saliva, parasite secretory gel carrying exosomes, parasite associated dsRNA viruses (LRV1 and LRV2) inoculated by parasite or parasite exosomes and even gut microbiota of the sand fly. Sand fly saliva, is composed of different immunomodulatory components among which chemotactic factors for neutrophils are recently characterized. LRVs trigger TLR-3 for pro-inflammatory cytokine production, gut microbiota induces IL-1b production via inflammosome activation and parasite dependent factors induce TLR-2, TLR-4 and TLR-7. The network of PRRS activated on one hand and the impact of the host factors including microbiota on immune response regulation on the other hand determines the outcome of the infection. Depending on the parasite and sand fly species and their components, the outcome might change. The cumulative consequence of this inflammatory response is the massive neutrophilic recruitment to the bite site which provides a permissive environment for disease establishment. To modulate this effect, the protective factors already defined include skin resident memory T cells (TRM) and long-lived T effector cells (TEFF) cells besides central (TCM) and Effector memory T cells (TEM). In the absence of the recently distinguished TRM and TEFF cells, permissive phagocytic cells lead to parasite propagation and disease establishment early after sand fly bite.
To improve the road map toward the disease elimination we need to put the ideas of researchers focused on different aspects of this complex host-parasite interaction together with better define strategies against the parasite, either as an effective prophylactic vaccine or treatment. We hope that this collection reach this aim with new concepts coming from expert researchers on Leishmania parasite and vector sand fly around the world.
Leishmaniasis is a vector-borne disease caused by the protozoan parasite of Leishmania genus. The parasite (with a dynamic genome) has evolved to advantage the vector sand fly transmission to successfully establish the disease. Decades of labor-intensive hard work has partially deconvoluted the intricacies of the host-pathogen interaction which is strongly controlled by different components deposited into the human skin through sand fly proboscis. These include sand fly saliva, parasite secretory gel carrying exosomes, parasite associated dsRNA viruses (LRV1 and LRV2) inoculated by parasite or parasite exosomes and even gut microbiota of the sand fly. Sand fly saliva, is composed of different immunomodulatory components among which chemotactic factors for neutrophils are recently characterized. LRVs trigger TLR-3 for pro-inflammatory cytokine production, gut microbiota induces IL-1b production via inflammosome activation and parasite dependent factors induce TLR-2, TLR-4 and TLR-7. The network of PRRS activated on one hand and the impact of the host factors including microbiota on immune response regulation on the other hand determines the outcome of the infection. Depending on the parasite and sand fly species and their components, the outcome might change. The cumulative consequence of this inflammatory response is the massive neutrophilic recruitment to the bite site which provides a permissive environment for disease establishment. To modulate this effect, the protective factors already defined include skin resident memory T cells (TRM) and long-lived T effector cells (TEFF) cells besides central (TCM) and Effector memory T cells (TEM). In the absence of the recently distinguished TRM and TEFF cells, permissive phagocytic cells lead to parasite propagation and disease establishment early after sand fly bite.
To improve the road map toward the disease elimination we need to put the ideas of researchers focused on different aspects of this complex host-parasite interaction together with better define strategies against the parasite, either as an effective prophylactic vaccine or treatment. We hope that this collection reach this aim with new concepts coming from expert researchers on Leishmania parasite and vector sand fly around the world.
Keywords: Leishmania, Vaccines, Drug development, Parasites, Parasitic infection, Leishmaniasis
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