The environmental side of the argument is well established. Rising temperatures accelerate mosquito development, survival, biting frequency, and the rate at which viruses replicate inside the insect, while altered rainfall and humidity determine where breeding sites persist. The invasive mosquito Aedes albopictus has expanded across much of temperate Europe, and climate projections indicate substantial growth in the area environmentally suitable for Aedes-borne transmission. Autochthonous outbreaks of dengue and chikungunya have already occurred repeatedly in France and Italy, concentrated in summer and early autumn when vector abundance peaks. Recent modeling suggests climatic suitability for chikungunya transmission in Europe may be broader than previously assumed, raising the probability of future outbreaks. Aedes aegypti, the more efficient vector, remains geographically restricted in Europe, but the continued spread of albopictus is steadily increasing the capacity of some regions to sustain local transmission.

Latin America and the Caribbean present a different picture. Much of the region already experiences widespread arboviral transmission, so climate change is expected less to create new transmission zones than to alter the timing, intensity, and geographic distribution of existing ones, with region-specific increases and decreases in suitability. Seasonal dynamics are strongly modulated by temperature and precipitation, while longer-term fluctuations have been linked to the El Niño-Southern Oscillation. The authors stress that substantial heterogeneity exists within both regions, and that environmental drivers interact with urbanization, land-use change, water management, and human mobility, meaning outbreaks tend to ignite when imported infections coincide with favorable ecological conditions and dense vector populations.

The heart of the Perspective, however, is immunogenetic. Host genetic variation contributes to differences in susceptibility to arboviral infection and severe disease, and the authors emphasize that these differences are polygenic rather than attributable to a few dominant susceptibility genes. Studies of dengue, chikungunya, and Zika have implicated variants involved in viral recognition, interferon signaling, cytokine regulation, Fc-receptor signaling, complement activation, and antigen presentation. Individual effect sizes are often modest, but their combined influence may shape susceptibility and severity across individuals and populations, although the extent of their contribution to population-level disease patterns remains unproven and requires further study.

Regions differ in these immune-related genetic architectures. Many populations in Latin America and the Caribbean are highly admixed, reflecting varying contributions from Indigenous American, African, and European ancestries, and analyses of ancestry-enriched variants suggest that historical infectious pressures have shaped the distribution of alleles involved in cytokine signaling, antigen presentation, and T-cell responses. European populations have experienced distinct demographic and pathogen-driven selective pressures of their own. Experimental work adds biological weight to these observations: one recent study found that genetic ancestry shaped dengue virus infection in human skin explants, with ancestry-associated variation in inflammatory responses and viral replication, indicating that early host-virus interactions may differ between populations even before their population-level consequences are clear.

Human leukocyte antigen variation adds another layer. HLA molecules determine which viral peptides are presented to T cells, making them central to adaptive immunity, and HLA diversity is strongly geographically structured. Associations have been reported between particular HLA alleles and dengue susceptibility and disease severity, but these associations vary across populations, with some showing substantial regional heterogeneity. As transmission expands into Europe, the authors argue, differences in immunogenetic background may contribute to variation in individual susceptibility and severity, though they caution that translating individual-level genetic associations into regional predictions of outbreak size or disease burden is not yet possible with existing data.

Immune history may matter even more than genetics. Pre-existing immunity to arboviruses can protect or harm. In dengue, non-neutralizing or sub-neutralizing antibodies can enhance viral uptake into Fc receptor-bearing cells, a mechanism associated with increased risk of severe disease during secondary heterologous infections, whereas broadly neutralizing antibodies directed against conserved epitopes are protective. Cross-reactive immunity is especially relevant for dengue and Zika because of their antigenic similarity: dengue antibodies can enhance Zika infection in laboratory settings, and cross-reactive responses between the two viruses may either protect or exacerbate disease. Prior exposure can also bias subsequent responses toward previously encountered epitopes, a phenomenon known as original antigenic sin. Beyond antibodies, CD4-positive and CD8-positive T cells contribute to viral clearance and memory, cross-reactive memory T cells have been implicated in both protection and immunopathology, and trained immunity, the epigenetic reprogramming of innate immune cells, may modulate susceptibility in ways that remain poorly understood.

Against this backdrop, the two regions diverge sharply. Many European populations remain largely immunologically naïve to dengue, chikungunya, and Zika because sustained transmission has historically been limited. Viral introductions may therefore encounter populations with little pre-existing immunity, increasing susceptibility, particularly when early transmission goes undetected, as historical dengue expansion in the Americas illustrated. Naïve populations facing chikungunya may also experience substantial burdens of chronic complications, which can persist years after acute infection, as prospective cohort work in Curaçao has documented. Conversely, decades of exposure across Latin America and the Caribbean have generated complex immune landscapes in which sequential infections, coinfections, and immune imprinting mean prior immunity may either protect against infection or contribute to severity depending on exposure history. The authors stress that immunological experience does not necessarily imply lower disease burden; it creates a more intricate susceptibility landscape that must be measured, not assumed.

These differences carry direct consequences for vaccination and preparedness. Dengue vaccines illustrate the challenge, since efficacy and safety depend strongly on pre-existing immunity, and strategies developed and evaluated in endemic, seropositive settings may not transfer directly to largely seronegative European populations. If sustained transmission becomes established in Europe, vaccination policies may need to incorporate serological status, local epidemiology, and population immune history. For chikungunya, vaccine development is advancing rapidly, though questions of long-term safety, effectiveness, and accessibility persist; for Zika, the absence of a licensed vaccine remains a critical gap given the congenital consequences of infection during pregnancy. The authors also call for more representative trial populations, noting that findings from one demographic and epidemiological setting may not generalize to populations with different ancestry compositions or exposure histories.

Preparedness priorities should therefore differ between regions while remaining complementary. In Europe, the emphasis should fall on early detection, outbreak investigation, and rapid response, supported by integrated surveillance systems that combine epidemiological, entomological, and climatic data. In Latin America and the Caribbean, reducing endemic burden requires stronger healthcare infrastructure, expanded access to diagnostics and vaccines, and sustained vector control programs, since historical experience shows how quickly burden can rise when control weakens. Genomic surveillance is expanding in the Americas through Pan American Health Organization initiatives but remains uneven, while long-term ecological and epidemiological studies in Europe are still limited. The authors acknowledge that comparable immunogenetic datasets across both regions are scarce and that uncertainty in climate projections limits the precision of risk estimates. Even so, their central message stands: future arboviral burden will be shaped by the interaction of climate-driven exposure with host genetics, immune memory, and public health capacity, and risk models that ignore host susceptibility will misjudge the epidemics to come, including those posed by emerging threats such as Oropouche virus.

Subject of Research: Genetic and immunological determinants of susceptibility to mosquito-borne viruses under climate change in Europe and Latin America-Caribbean

Article Title: Genetic and immunological determinants of mosquito-borne virus susceptibility and climate change: Europe and Latin America-Caribbean perspectives

Article References: Heinneman, J., & Duits, A. J. (2026). Genetic and immunological determinants of mosquito-borne virus susceptibility and climate change: Europe and Latin America-Caribbean perspectives. Frontiers in Virology, 6, Article 1965985. https://doi.org/10.3389/fviro.2026.1965985

Image Credits: AI Generated

DOI: 10.3389/fviro.2026.1965985

Keywords: dengue, chikungunya, Zika virus, climate change, Aedes mosquitoes, immunogenetics, HLA diversity, immune imprinting, antibody-dependent enhancement, vaccination, public health preparedness, Latin America and the Caribbean

The study, published as a scoping review in the International Journal for Equity in Health, examined 286 documents published between 2008 and 2026. Following the PRISMA-ScR reporting guidelines, the researchers applied the Joanna Briggs Institute’s population, concept, and context framework to answer four questions: how the term “driver” is used globally and regionally, how it relates to the established concept of social determinants of health, what methodological strategies researchers deploy to study it, and where the glaring gaps in knowledge lie. The protocol was registered on the Open Science Framework, and the work was carried out as part of an effort to build a Health Equity Status Report for the Americas.

The headline finding is a conceptual one. The authors describe an evolution in the literature toward what they call Social Drivers of Equity in Health, a reframing that treats drivers not as passive background conditions but as operational engines of power. In other words, a driver is not simply a factor that correlates with poor health; it is a force that sets the social determinants of health in motion. This distinction matters because the social determinants framework, influential since the World Health Organization’s landmark commission on the subject, tends to describe the conditions in which people are born, grow, work, and age. Drivers, by contrast, imply agency and causation, the mechanisms that produce and reproduce those conditions in the first place.

The numbers reveal just how muddled the terminology remains. The review found that 36.4 percent of the analyzed literature uses “driver” and “determinant” interchangeably, treating them as synonyms despite their different analytical implications. Meanwhile, 38.5 percent of studies identify drivers as independent forces that put social determinants into motion, a more mechanistic reading. The remaining studies occupy various intermediate positions. This inconsistency, the authors argue, challenges theoretical coherence and makes it difficult to operationalize health equity in policy terms. If researchers cannot agree on what a driver is, they cannot agree on what should be driven, or by whom, or toward what end.

Methodologically, the field shows both strengths and limitations. About a third of the reviewed documents, 33.3 percent, were primary quantitative studies, and 46 of them employed multivariate modeling designed to isolate structural effects from individual-level confounders. That is a technically demanding undertaking. Structural forces such as racism, class, and gender hierarchy are not measured directly; they must be inferred through proxies, interactions, and hierarchical models that account for people nested within neighborhoods, institutions, and nations. The fact that only a minority of studies attempt this rigor suggests that much of the literature remains descriptive, cataloging inequities rather than explaining the machinery that produces them.

When the authors turned to the regional picture, the results were striking. Within the Americas, structural racism appeared as the predominant engine of health inequity, cited in 80.0 percent of the relevant regional literature, followed closely by socioeconomic status at 79.3 percent. These findings align with a growing body of evidence showing that racialized populations across the hemisphere face systematically worse outcomes, from maternal mortality to chronic disease burden, even after accounting for income and education. The review’s framing treats these not as isolated risk factors but as relational dimensions of inequality that structure social positions, analyzed across the PROGRESS-Plus axes, a taxonomy covering place of residence, race and ethnicity, occupation, gender, religion, education, social capital, socioeconomic status, age, disability, and sexual orientation.

Perhaps the most forward-looking element of the analysis is its identification of emerging axes of inequality that traditional frameworks have been slow to capture. The PROGRESS-Plus analysis surfaced digital and commercial dimensions as novel mediators of geographic inequity. The digital dimension reflects the reality that access to broadband, telehealth, and health information increasingly determines who can participate in modern health systems, a divide laid bare during the COVID-19 pandemic. The commercial dimension points to the growing influence of industries, from ultra-processed food to tobacco and alcohol, whose products and marketing practices shape health far beyond the clinic. Both axes cut across geography, deepening divides between urban and rural populations and between wealthy and impoverished regions.

Beneath these findings lies what the authors call a significant research inequity. A staggering 79.3 percent of the regional evidence base is concentrated in the United States, leaving Latin America and the Caribbean substantially underrepresented. This is not a trivial bibliometric curiosity. The structural drivers of health inequity in a high-income federal democracy with a fragmented insurance system may differ profoundly from those in middle-income countries with universal health systems, large Indigenous populations, histories of colonial extraction, and high levels of informal employment. Policies built on a US-centric evidence base risk misdiagnosing the levers of change elsewhere in the hemisphere, perpetuating a form of epistemic dependency that mirrors the material inequities the field seeks to dismantle.

To resolve the tension between the term “driver” and established social determinants models, the authors propose a pragmatic compromise: a hierarchy of drivers organized along the familiar upstream, midstream, and downstream gradient. Upstream drivers would encompass the structural forces, legal frameworks, and institutional arrangements that shape the distribution of power and resources, with legal reforms and social protection systems identified as precise levers of intervention. Midstream drivers would cover the conditions of daily life in communities, schools, and workplaces, while downstream drivers would address individual-level factors. This layered architecture allows policymakers to locate where in the causal chain an intervention is aimed, and to recognize that downstream programs, however well designed, cannot compensate indefinitely for upstream forces that continuously regenerate inequity.

The review’s conclusions come with a caution. The term “driver,” for all its rhetorical energy, should be used carefully and only in articulation with robust theoretical frameworks, lest it become another vague buzzword in a field already crowded with them. Used well, the authors suggest, it can serve as an operational catalyst for structural intervention, translating the descriptive language of determinants into the action language of policy. The study itself models a degree of transparency worth noting: the authors disclose that they used an AI tool during data synthesis to refine driver categorizations and cluster theoretical frameworks, with all outputs critically reviewed and verified by the team. Funded by the Pan American Health Organization and the Robert Wood Johnson Foundation, the review arrives at a moment when governments across the hemisphere are grappling with post-pandemic reversals in life expectancy and widening gaps between the richest and poorest. Its central message is deceptively simple: to make health equity more than an aspiration, the hemisphere must first agree on what is actually doing the driving, and then reach for the levers, especially legal and social protections, that can change direction.

Subject of Research: Social drivers of health equity in the Americas

Article Title: Drivers of health equity in the Americas: a scoping review

Article References: Chapman, E., Araujo, M., Maylen, R.-B., Pardo, J. P., & Mujica, O. J. (2026). Drivers of health equity in the Americas: a scoping review. International Journal for Equity in Health. https://doi.org/10.1186/s12939-026-03031-6

Image Credits: AI Generated

DOI: 10.1186/s12939-026-03031-6

Keywords: health equity, social determinants of health, scoping review, structural racism, socioeconomic status, PROGRESS-Plus, Pan American Health Organization, Latin America and the Caribbean, health policy, digital divide, commercial determinants, public health