Depression prevalence estimates in Spain (1995-2021): a systematic review.

Mosquitoes are responsible for a disproportionate burden of human infectious diseases due to the wide range of pathogens transmitted during blood-feeding. These include viruses such as yellow fever, Zika, dengue, and chikungunya, transmitted primarily by mosquitoes of the genus , as well as protozoan parasites such as spp., the causative agents of malaria that are transmitted by certain species of anopheline mosquitoes. Together, vector-borne diseases account for a substantial fraction of the global infectious disease burden, estimated at approximately 17% of all infectious diseases (), with mosquitoes representing some of the most important vectors. Although vector control strategies have substantially reduced transmission in multiple regions, the emergence of insecticide resistance in mosquito populations (, ) and drug resistance in parasites () have contributed to renewed transmission and control failure. In parallel, arboviral diseases have expanded geographically, driven in large part by vector range expansion, urbanization, and environmental change, which increase opportunities for transmission (–). These epidemiological realities have placed vector competence, the ability of a mosquito to acquire, maintain, and transmit a pathogen, at the center of infection biology. Yet vector competence is not a fixed property of the mosquito or the pathogen alone. It emerges from interactions among mosquito genotype, pathogen genotype, microbiota (–), environmental history, nutrition, reproductive state (, ), and tissue physiology (–). For immunology, this creates a central interpretive challenge: immune phenotypes measured in infected mosquitoes may reflect direct pathogen recognition, but they may also be shaped by the physiological consequences of blood feeding, including microbiota expansion, endocrine signaling, and tissue damage and repair processes. The dominant framework for insect immunity has largely been established in , where microbial recognition activates conserved signaling pathways such as Toll, Immune Deficiency (IMD), Janus kinase/signal transducer and activator of transcription (JAK/STAT), and c-Jun N-terminal kinase (JNK), which regulate antimicrobial peptide production, cellular immunity, epithelial renewal, and stress responses (–). This framework has provided essential conceptual and experimental language for insect immunology and has been productively translated across species. However, mosquitoes require additional interpretation because hematophagy places immune signaling within a distinct physiological context. Female mosquitoes alternate between sugar feeding and blood feeding, and the blood meal itself constitutes a large-scale transition involving nutritional overload, mechanical distension, oxidative stress, microbial expansion, endocrine activation, and reproductive reprogramming (–). Importantly, pathogen acquisition occurs within the same temporal window as this transition. As a result, conserved immune pathways in mosquitoes are not always deployed against infection in isolation, but within a blood-feeding context that can reshape the canonical insect-immunity models.