Abstract
Background:
The incursion of Chikungunya (CHIKV) and Zika (ZIKV) viruses into Latin America and the Caribbean (LAC) after 2013 created complex epidemics with high attack rates, severe complications, and persistent transmission. While individual aspects have been studied, a synthesized understanding of the interacting viral, ecological, and social drivers sustaining these arboviruses in the region remains lacking.
Objectives:
To critically synthesize evidence on the incursion and establishment of CHIKV and ZIKV in LAC through an integrative framework examining the interaction between viral adaptation and structural vulnerabilities.
Design:
Systematic review following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 guidelines.
Data sources and methods:
We systematically searched PubMed, EMBASE, Scopus, and LILACS, supplemented by gray literature from PAHO, WHO, and CDC, for studies published between January 2013 and December 2025. Eligible studies included observational studies, surveillance data analyses, outbreak reports, modeling studies, and genomic epidemiology focusing on CHIKV/ZIKV incursion, transmission dynamics, establishment, burden, or socio-ecological determinants in LAC populations. Two independent reviewers performed screening, data extraction, and quality assessment using Joanna Briggs Institute tools. A critical narrative synthesis was conducted using the novel Structural Vulnerability and Pathogen Plasticity framework.
Results:
Eighteen studies met inclusion criteria. Pathogen plasticity—evidenced by multiple independent introductions, genetic variability, and cryptic transmission (e.g., an unreported 2017 ZIKV outbreak in Cuba uncovered through travel-genomic surveillance)—exploited profound structural vulnerabilities. These included weak surveillance systems (detection rates as low as 1%–6% for ZIKV), inadequate water and sanitation infrastructure driving a knowledge-practice gap (75.2% knowledge vs 30.7% adequate practices), and socioeconomic inequities that concentrated disease burden. Severe impacts were disproportionately borne by marginalized groups, quantified by a 9.0-year disparity in average Years of Life Lost between Black (22.0 years) and White (13.0 years) Brazilians with Chikungunya. Despite the epidemic’s waning, 58% of analyzed locations remain at high risk for future ZIKV outbreaks due to discrepancies between environmental suitability and population immunity. A critical geographical evidence bias was identified: 13 studies (72%) were conducted in Latin America (primarily Brazil and Colombia), while only 5 (28%) focused on the Caribbean region, limiting generalizability to smaller island states.
Conclusion:
The establishment of CHIKV and ZIKV in LAC represents a biosocial process wherein adaptable pathogens exploit and reinforce structural inequities. Achieving durable resilience requires integrated surveillance platforms that monitor both pathogens and social vulnerabilities, coupled with fundamental investment in water, sanitation, waste management, and equitable healthcare infrastructure to interrupt the vicious cycle of arboviral emergence.
Trial registration:
PROSPERO CRD420251242134 (available at: https://www.crd.york.ac.uk/PROSPERO/view/CRD420251242134).
Plain language summary
This review examined how two mosquito-borne diseases (Chikungunya and Zika) spread and became established in Latin America and the Caribbean after 2013. We studied not only the viruses themselves but also how they interacted with social and environmental conditions. Our key finding is that the spread and impact of these diseases were heavily shaped by social inequality. The viruses spread fastest and caused the most severe harm in areas with weak infrastructure: neighborhoods with unreliable tap water, poor waste collection, and limited healthcare access. For example, people without reliable water are forced to store it in containers, which become breeding sites for mosquitoes. We also found that the burden of severe illness and death fell disproportionately on poorer communities and marginalized racial groups. In Brazil, Black individuals lost an average of nine more years of life to Chikungunya than White individuals. Although the major Zika outbreak has faded, our analysis shows that over half of the locations studied remain at high risk for future outbreaks, because immunity in the population is uneven and poorly understood. The central message is that controlling diseases like Chikungunya and Zika requires more than vaccines, insecticides, or public health advisories. Lasting protection depends on fixing the foundation: investing in reliable water systems, regular waste collection, equitable healthcare, and stronger community-focused disease monitoring. Only by addressing these root social and environmental causes can we break the cycle of outbreaks and build healthier, more resilient communities.
Keywords
Introduction
More than 700,000 deaths annually are attributed to vector-borne diseases globally, with Aedes-transmitted arboviruses such as dengue (DENV), Chikungunya (CHIKV), and Zika (ZIKV) constituting a major public health burden in tropical and subtropical regions. 1 The rapid incursion of CHIKV and ZIKV into Latin America and the Caribbean (LAC) from 2014 to 2017 created complex epidemics characterized by high attack rates, novel severe complications, and heterogeneous transmission dynamics that overwhelmed health systems and exposed deep-seated social inequities.2,3
While substantial research has documented clinical outcomes and epidemiological features, the literature often remains compartmentalized. Virological studies trace viral lineages (e.g., Villero-Wolf et al. 4 ), computational models map theoretical spread (e.g., Zhang et al. 5 ) and public health analyses highlight social risk factors (e.g., Carabali et al. 6 ). This fragmentation has resulted in a gap: a synthesized understanding of the synergistic processes enabling the establishment and persistence of these arboviruses in LAC is lacking. We posit that successful entrenchment emerges from the dynamic interaction between pathogen plasticity—the capacity of viruses to evolve and adapt—and structural vulnerability—the societal conditions that increase population exposure and susceptibility.7,8
This structural vulnerability and pathogen plasticity framework suggests arbovirus establishment is a biosocial outcome, not a mere biological inevitability. Pathogen plasticity exploits preexisting structural vulnerabilities (e.g., unplanned urbanization, poor water access), creating a feedback loop that sustains transmission and amplifies burden. Existing systematic reviews have either focused on specific clinical outcomes or provided broad summaries without such an integrative, critical lens. 8 Consequently, policymakers lack a coherent model to anticipate resurgence or design interventions targeting root biosocial drivers.
To address this gap, this systematic review aims to critically synthesize evidence on the incursion and establishment of CHIKV and ZIKV in LAC through the proposed integrative framework. We focused on CHIKV and ZIKV due to their synchronous, pandemic-scale emergence in the Americas post-2013, which presented a unique natural experiment in the biosocial dynamics of Aedes-borne virus establishment, distinct from the longer, more complex endemic history of dengue in the region. We seek to answer four key questions regarding: (1) the interaction of viral genetics, mobility, and ecology shaping invasion patterns; (2) the distribution of burden mediated by structural vulnerabilities; (3) evidence for viral mechanisms contributing to persistence; and (4) the knowledge-practice gap as a reflection of structural constraints. By integrating evidence across disciplines, this review aims to move beyond description and provide a novel framework for building durable, equitable resilience against arboviral threats.
Methods
Study design
This systematic review was conducted to investigate the incursion, spread, and establishment of CHIKV and ZIKV viruses in LAC. The review protocol was prospectively registered with the International Prospective Register of Systematic Reviews (https://www.crd.york.ac.uk/PROSPERO/view/CRD420251242134) and was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 guidelines. 9
Eligibility criteria
Studies were selected based on the eligibility criteria detailed in Table 1.
Study eligibility criteria.
LAC, Latin America and the Caribbean.
The review was restricted to studies published in English. While this introduces a potential language bias, it was necessitated by practical constraints in translation resources and the need for accurate interpretation of complex methodological details. To mitigate this, our search included regional databases (LILACS) and grey literature from major international organizations (PAHO, WHO) that publish authoritative English-language reports on the region. The implications of this limitation are explicitly discussed in the Limitations Section.
Information sources and search strategy
A comprehensive, systematic search was conducted across four electronic databases: PubMed, EMBASE, Scopus, and LILACS (Latin American and Caribbean Health Sciences Literature). To capture gray literature and unpublished data, supplementary searches were conducted in the online repositories of the Pan American Health Organization (PAHO), the World Health Organization (WHO), the Centers for Disease Control and Prevention (CDC), and relevant national health ministry bulletins from LAC countries.
The search strategy was developed with a medical librarian and used a combination of Medical Subject Headings (MeSH) and free-text keywords related to the viruses (CHIKV, ZIKV), the geographic region (LAC and all constituent countries), and core epidemiological concepts (outbreak, transmission, establishment, and epidemiology). The search date was from inception (September) to December 18, 2025. The PubMed search strategy is presented below as an example; it was adapted for syntax and controlled vocabulary in other databases.
Sample pubmed search strategy
The full search strategies for all databases are provided in Supplemental File 2.
Study selection process
All identified records were imported into Covidence, a systematic review software for deduplication and management. The selection process involved two independent reviewers (AH & MZR) in two stages:
Title/abstract screening: Records were screened against eligibility criteria. Conflicts were resolved by consensus or consultation with a third reviewer.
Full-text screening: Potentially eligible studies were retrieved and assessed in full. Reasons for exclusion at this stage were documented.
The process was documented using a PRISMA 2020 flow diagram, detailing the number of records identified, screened, assessed for eligibility, and included. The PRISMA checklist is provided in Supplemental File 1.
Data extraction process
Data from included studies were extracted by two independent reviewers using a standardized, piloted extraction form in Microsoft Excel. Any discrepancies were resolved through discussion. The standardized data extraction form is available from the corresponding author upon request. The extracted data included:
Study identifiers: Authors, year, title, journal.
Methodology: Study design, setting, timeframe, population, and sample size.
Virus and context: Virus type, outbreak phase (introduction, peak, endemic).
Key findings: Categorized according to the review framework:
○ Pathogen plasticity: Genomic data, lineage, mutations, cross-reactivity/interference. ○ Transmission Dynamics: Introduction routes, spatial spread patterns, reproduction number (R), modeling assumptions. ○ Burden: Attack rates, seroprevalence, hospitalization, mortality, Years of Life Lost (YLL), and congenital outcomes. ○ Structural vulnerability: Socioeconomic, racial/ethnic, and gender disparities; environmental and infrastructural determinants; knowledge-practice gaps.
Limitations: Key methodological limitations as noted by the study authors.
Quality assessment (risk of bias)
The methodological quality and risk of bias of included studies were assessed independently by two reviewers (AH and MZR) using standardized tools from the Joanna Briggs Institute (JBI), selected according to study design 10 :
JBI Checklist for Analytical Cross-Sectional Studies
JBI Checklist for Cohort Studies
JBI Checklist for Case Series
JBI Checklist for Prevalence Studies
A custom appraisal tool was adapted for modeling and genomic studies, to assess transparency, data sources, validation, and assumption justification.
Studies were rated as having “Low,” “Moderate,” or “High” risk of bias. This assessment was not used to exclude studies but to critically inform the interpretation and weighting of evidence during the narrative synthesis. The quality of evidence supporting major thematic conclusions was explicitly characterized. The full JBI checklist is provided in Supplemental File 3.
Data synthesis
A meta-analysis was deemed unfeasible due to extreme heterogeneity in study designs, outcomes measured (e.g., genomic sequences, years of life lost, survey percentages), and metrics reported, which precluded statistical pooling. The narrative synthesis approach allows for the integration of this diverse evidence within a coherent theoretical framework.
A critical narrative synthesis was conducted, structured around the Structural Vulnerability and Pathogen Plasticity framework. The synthesis process involved:
Data organization: Extracted data were organized into evidence tables (see Tables 2 and 3) and categorized by the framework’s domains.
Critical integration: Within each domain, findings were compared and contrasted. The methodological strengths and limitations (as assessed in the quality assessment) were integrated to evaluate the robustness and generalizability of each finding. For example, conclusions drawn from high-quality national cohort studies were given greater weight than those from small, biased cross-sectional surveys.
Thematic development and interaction analysis: Patterns and discrepancies were analyzed to develop thematic findings. Crucially, we then examined interactions between domains (e.g., How does a specific viral mutation [Plasticity] potentially amplify burden in a context of poor housing [Vulnerability]?). This step moved the synthesis from the descriptive summary to an explanatory analysis.
Generation of a conceptual model: The synthesized evidence was used to iteratively refine and illustrate the proposed framework, showing how the components interact to drive establishment and burden.
The synthesis aimed to answer the predefined review questions, with conclusions explicitly linked to the strength of the underlying evidence.
Characteristics of included studies (categorized by framework domain).
Synthesis of major findings and critical appraisal of evidence.
Results
Study selection and characteristics
The systematic search yielded 2847 records from databases and grey literature sources. After deduplication, 1923 titles and abstracts were screened for eligibility. Of these, 102 full-text articles were assessed, resulting in the inclusion of 18 studies that met all criteria. The selection process is detailed in the PRISMA 2020 flow diagram (Figure 1). A critical finding was a significant geographical evidence bias: of the 18 studies, 13 (72%) were conducted in Latin America (primarily Brazil and Colombia), while only 5 (28%) focused on the Caribbean region. This limits the generalizability of findings to the diverse epidemiological contexts of smaller island states.
PRISMA 2020 flow diagram of study selection.
The included studies employed diverse methodologies. Table 2 summarizes the key characteristics, while Table 3 details their major findings, categorized according to the Structural Vulnerability and Pathogen Plasticity framework. The subsequent narrative synthesis critically integrates these findings, explicitly weighing the strength of evidence from different study designs as assessed by the Joanna Briggs Institute (JBI) tools.
Synthesis of evidence through the critical framework
Pathogen plasticity and invasion dynamics: Pattern and uncertainty
The evidence on initial incursion and spread, primarily from modeling and genomic studies, reveals a consistent pattern but is fundamentally constrained by the poor quality of underlying surveillance data, a key structural vulnerability.
Points of introduction and spread mechanisms: Modeling studies consistently identify major international travel hubs and densely populated coastal cities as epicenters of initial introduction.5,11 The subsequent spatial spread was best explained by gravity models relying on human mobility data, 12 suggesting short- to medium-distance travel was a primary driver. However, this conclusion is critically limited: these models depend on clinically reported case data, which studies estimate have a detection rate of only 1%–6% for ZIKV. 5 This profound under-ascertainment means the inferred spatial parameters represent a vast underestimation of true transmission networks, particularly in under-resourced areas.
Genomic evidence of plasticity and cryptic transmission: Genomic studies provided direct evidence of pathogen plasticity. Multiple, independent introductions of both CHIKV (Asian genotype) and ZIKV were documented.4,14 The most compelling evidence of plasticity exploiting surveillance gaps came from Grubaugh et al., 13 who integrated travel data with genomics to uncover a large, unreported ZIKV outbreak in Cuba in 2017. This demonstrates that pathogen plasticity enables silent transmission where structural surveillance capacity is weak.
The clinical burden and its unequal distribution: High-quality evidence of inequity
Evidence on disease burden from large Brazilian cohort studies offers robust, population-level data but confirms that burden is not biological fate but socially patterned.
Severe morbidity and mortality: The burden of severe disease is substantial. A nationwide Brazilian cohort found children with CZS had a mortality rate 11.3 times higher than unaffected children. 16 For CHIKV, a parallel cohort quantified an in-hospital case-fatality rate of 4.9%, rising to 14.1% among men aged 85–89. 17 The strength of this evidence is high due to the cohorts’ scale. However, a key limitation is pervasive misclassification: only 40% of cases in the CHIKV/dengue cohort were lab-confirmed, 17 a structural flaw in health data systems that obscures true etiology.
Structural vulnerability manifested in health outcomes: The burden mapped directly onto social disadvantage. The same Brazilian cohort quantified a stark disparity in average years of life lost (aYLL): Black individuals with chikungunya lost 22.0 years on average, compared to 13.0 years for White individuals. 17 Spatial analyses confirmed that chikungunya cases were significantly more concentrated in low socioeconomic neighborhoods. 6 This pattern, robust across studies, indicates that structural factors channel exposure and amplify suffering.
The knowledge-practice gap as a structural phenomenon
Evidence from cross-sectional surveys highlights a critical disconnect rooted in infrastructure, not ignorance.
The gap between awareness and action: A study in southeastern Mexico found that while 75.2% of households had adequate knowledge, only 30.7% reported adequate preventive practices. 22 This gap was structurally mediated: inadequate public water supply forced the water storage that created breeding sites. This evidence illustrates how structural deficiencies transform public health guidance into impossible demands, shifting the locus of responsibility from the individual to the system.
Viral interactions and the uncertain immunity landscape
Evidence on viral cross-interaction presents a compelling hypothesis that remains difficult to validate due to surveillance limitations.
Cross-protection and its implications: Modeling suggested the massive ZIKV epidemic was followed by a significant, temporary suppression of dengue, positing immune-mediated cross-protection. 23 This is a key example of population-level pathogen interaction. However, the authors note competing hypotheses cannot be ruled out due to limitations in serological data specificity. This underscores a major evidence gap: our understanding of the true postepidemic immunity landscape—and thus future vulnerability—remains opaque, a direct consequence of inadequate diagnostic and serosurveillance infrastructure.
Integrated critical appraisal of the evidence base
The quality assessment reveals a tiered evidence landscape. The highest rigor is in large, national cohort studies (e.g., Paixao et al. 16 ; Cerqueira-Silva et al. 17 ) which provide powerful estimates of burden and disparity but lack granular data. Modeling and genomic studies (e.g., Charniga et al. 11 ; Grubaugh et al. 13 ) offer innovative insights but are wholly dependent on the poor-quality primary surveillance data fed into them. Cross-sectional studies (e.g., Causa et al. 22 ) provide crucial context but are limited by design.
A unifying, critical limitation across almost all studies is the reliance on passive, clinically based surveillance systems prone to underreporting and misdiagnosis. This fundamental data problem propagates uncertainty through all analyses. Therefore, the synthesized findings must be interpreted as the visible patterns of much larger, partially obscured epidemics, with the most severe burdens and cryptic transmissions likely occurring in the most structurally vulnerable blind spots of the surveillance system.
Discussion
Synthesized through the Structural Vulnerability and Pathogen Plasticity framework, this review explains how CHIKV and ZIKV became established in LAC not by virological destiny, but by exploiting preexisting social and infrastructural fault lines. The epidemiological patterns—from invasion speed to mortality concentration—emerge from the interplay between adaptable pathogens and a vulnerable human landscape.
The interdependence of spread and surveillance blind spots
Modeling studies indicate invasion followed pathways through urban hubs, driven by human mobility.11,12 However, these models rely on clinically reported cases, estimated to represent only 1%–6% of total ZIKV infections. 5 Thus, the detected spread is biased toward areas with better reporting. The integration of genomics with travel surveillance, which uncovered a silent outbreak in Cuba, 13 is paradigmatic: pathogen plasticity realizes its full potential where structural vulnerabilities in surveillance exist. The primary challenge is therefore repairing systemic surveillance blind spots.
From clinical burden to biomarker of social inequity
The review documents a severe disease burden.16,17 More critically, this burden is inequitably distributed. The disparity in years of life lost—22.0 years for Black Brazilians versus 13.0 for White Brazilians with chikungunya 17 —transforms arboviral disease into a biomarker of structural marginalization. This pattern is reinforced by the spatial concentration of cases in low-SES neighborhoods. 6 Substandard housing, precarious water storage, and constrained healthcare access create permissive environments for intense transmission and worse outcomes.
The knowledge-practice gap: A symptom of systemic failure
The disconnect between high knowledge (75.2%) and low preventive practice (30.7%), linked to inadequate water infrastructure, 22 is central to our framework. This gap is frequently misdiagnosed as a problem of compliance. Our synthesis redefines it as a logical consequence of structural vulnerability. When public health directives conflict with survival strategies, the rational choice is to secure water, not mosquitoes. Closing the gap requires investment in reliable water systems and dignified housing, making the healthy choice feasible.
The unresolved landscape of immunity and future vulnerability
A key finding is the tension between the epidemic’s wane and high resurgence risk. While modeling suggests high immunity halted ZIKV, 12 seroprevalence analyses indicate 58% of locations remain highly vulnerable. 25 This paradox stems from inadequate measurement tools (e.g., serological cross-reactivity) and heterogeneous immunity. Evidence of ZIKV conferring temporary cross-protection against dengue 23 adds ecological complexity. The uncertain immunity landscape means predicting outbreaks requires mapping social and immunological variations, not just viral clockwork.
The vicious cycle of pathogen plasticity and structural vulnerability
The establishment of CHIKV and ZIKV in LAC can be visualized as a vicious cycle (Figure 2). Pathogen plasticity exploits structural vulnerabilities to initiate transmission, which inflicts a disproportionate burden on marginalized groups, deepening health inequities. The resources needed to break the cycle are least available in these same communities, thereby reinforcing the structural vulnerabilities that facilitate future outbreaks.26,27 This framework clarifies that technical solutions will have limited impact if deployed into the same vulnerable context. Exiting the cycle requires fortifying the structural landscape against pathogen exploitation.
The vicious cycle of pathogen plasticity and structural vulnerability in arboviral establishment.
Recommendations for public health response
The synthesis of evidence through the Structural Vulnerability and Pathogen Plasticity framework necessitates a paradigm shift from reactive, pathogen-centric control to proactive, system-level resilience. Effective public health action must target the interconnected vulnerabilities that pathogens exploit. We propose the following integrated, multilevel recommendations:
Reimagine surveillance: From case detection to system diagnosis
Public health surveillance must evolve to diagnose the social and infrastructural preconditions of outbreaks, not just the pathogens themselves. We recommend the development of Integrated Biostructural Surveillance Platforms. These systems should pair established syndromic and laboratory-based arbovirus monitoring (e.g., sentinel serosurveillance, genomic sequencing) with continuous, geo-referenced tracking of structural vulnerability indices. Key indices should include neighborhood-level data on water supply reliability, housing density, waste collection frequency, poverty metrics, and healthcare access. This would enable predictive risk mapping based on the convergence of viral presence and socio-ecological susceptibility. Such a system, informed by the success of integrated travel-genomic surveillance in uncovering cryptic outbreaks, 13 would allow for proactive, resource-efficient interventions—such as targeted vector control and community mobilization—before transmission becomes clinically detectable.
2. Invest in foundational infrastructure to close the knowledge-practice gap
Vector control strategies must address the structural roots of transmission. We recommend a transition from behavior-focused messaging to structural vector control interventions that make the healthy choice the feasible choice. National and municipal authorities must prioritize investment in reliable, continuous piped water systems and regularized waste management to eliminate the necessity for unsafe water storage and discard of containers. This directly addresses the evidence that preventive practices are constrained by infrastructural failure, not knowledge.22,28,29 Concurrently, community engagement should shift from top-down instruction to co-design of feasible solutions (e.g., safe larvicides for stored water, community-led cleanup campaigns). Furthermore, to mitigate inequitable exposure, personal protective measures (e.g., insecticide-treated screens, repellents) should be subsidized and distributed through social protection programs to low-income households.
3. Implement stratified and adaptive health system protocols
Health systems must adapt to the heterogeneous risk landscape. We recommend the adoption of Stratified Clinical Management and Preparedness Protocols.
For clinical care: Develop and disseminate guidelines that recognize distinct at-risk populations, informed by evidence on differential outcomes. This includes gender-specific guidance for CHIKV management 19 and protocols that prioritize monitoring for patients at age extremes and with comorbidities, who face the highest risk of severe outcomes. 17
For preparedness: Establish adaptive frameworks for rapid response to ZIKV resurgence. Regulatory and research agencies should preapprove protocols for Rapid-Response Vaccine and Therapeutic Efficacy Trials, enabling immediate activation upon genomic confirmation of local transmission. 30 This overcomes the ethical and logistical paralysis of testing interventions during interepidemic periods, a challenge highlighted by Ferguson et al. 24
4. Prioritize research on immunity landscapes and intersectoral evaluation
To resolve the paradox of persistent vulnerability, strategic research investments are critical.
Immunity mapping: Support the development, validation, and widespread deployment of highly specific serological assays to distinguish between flavivirus infections (e.g., ZIKV vs DENV). Fund longitudinal serosurveillance cohorts in diverse ecological and social settings to generate accurate maps of population susceptibility and understand the durability and interactions of arbovirus immunity.
Intervention evaluation: Champion and fund research that evaluates the health impact of intersectoral actions, such as urban upgrading projects or water system expansions. Building the evidence base for how investments in social determinants directly reduce arbovirus burden is essential for justifying and guiding long-term policy.
While these recommendations demand significant political will and multisectoral investment, they are targeted at the foundational drivers of risk identified in this review. Shifting from outbreak firefighting to fortifying the structural landscape is the essential pathway to durable and equitable health security against Aedes-borne arboviruses.
Limitations of the review
This review has several important limitations that must be considered when interpreting its findings and conclusions. The most significant methodological constraints pertain to language and geographic bias, the analytical approach, and the inherent limitations of the primary evidence base.
First, the decision to include only English-language publications introduces a potential language and publication bias. Given that Spanish, Portuguese, and French are the primary languages of scientific and public health reporting in LAC, this restriction likely omits pertinent data from local health bulletins, regional journals, and governmental reports. This may skew the synthesized perspective toward countries with stronger English-language publication records or towards research disseminated through international channels. Although our search strategy included regional databases (LILACS) and gray literature from major international organizations (e.g., PAHO, WHO) to mitigate this, the exclusion remains a notable constraint on the comprehensiveness of the evidence.
Second, the review identified a pronounced geographic imbalance in the available literature. Thirteen of the 18 included studies (72%) were from Latin American countries, predominantly Brazil and Colombia, while only five (28%) focused on the Caribbean region. This imbalance limits the generalizability of our conclusions across the heterogeneous socio-ecological contexts of LAC. It is particularly concerning as it may under-represent the unique structural vulnerabilities of small island developing states, such as those related to geographic isolation, limited health system capacity, and distinct infrastructure challenges. Consequently, the applicability of our framework to these settings requires further validation.
Third, while a narrative synthesis was the most appropriate method given the extreme heterogeneity in study designs, populations, and outcome measures (e.g., genomic sequences, years of life lost, survey data), this approach inherently involves a degree of subjective interpretation in theme development and evidence weighting. We mitigated this through independent review, piloting of extraction forms, and the explicit integration of a critical quality appraisal (using JBI tools) into the synthesis. However, this remains a limitation compared to a quantitative meta-analysis, which was precluded by the nature of the data.
Furthermore, while the framework highlights ecological interactions, the review is short on a detailed analysis of independent environmental and climatic drivers of transmission, such as rainfall patterns, temperature variability, and land-use change. Although factors like water storage (an infrastructural issue) are discussed, broader climatic variables were not systematically synthesized as primary determinants, representing a gap in the scope of the reviewed evidence.
Finally, the review’s findings are ultimately constrained by the collective limitations of the primary studies themselves. A unifying critical flaw across the evidence base is the widespread reliance on passive, clinically based surveillance systems, which are prone to profound underreporting (estimated at 1%–6% for ZIKV), clinical misclassification between arboviruses, and a general lack of serological precision. These fundamental data problems propagate uncertainty through all subsequent analyses, from genomic modeling to burden estimates. Therefore, our synthesis necessarily reflects the visible patterns of larger, partially obscured epidemics, with the most severe burdens and cryptic transmissions likely occurring in the surveillance system’s blind spots—often the most structurally vulnerable communities.
Conclusion
This review synthesizes evidence to illuminate a dual challenge for Latin America and the Caribbean: managing the unresolved vulnerability to Zika virus resurgence while mitigating the severe and inequitable endemic burden of Chikungunya. The central insight is that the epidemiology of these arboviruses cannot be deciphered through a purely biological lens. The rapid subsidence of ZIKV remains enigmatic, with high-risk vulnerability persisting in many areas, underscoring that future outbreaks cannot be confidently predicted with current surveillance. Conversely, the burden of CHIKV is predictable in its injustice, consistently mapping onto the fault lines of race and socioeconomic status. The identified knowledge-practice gap is a symptom of structural failure, not communication failure.
The overarching significance of this work is its demonstration that arboviral establishment and burden are driven less by novel pathogen characteristics and more by the persistent structural and social inequities they exploit. The current period of low incidence is not an endpoint but a crucial interlude. Transforming transient immunity into enduring public health resilience requires a fundamental pivot from short-term vector control to long-term structural investment, integrating surveillance of social determinants with viral monitoring. Only by fortifying the structural landscape can the region disrupt the vicious cycle of pathogen plasticity and build equitable defense against Aedes-borne arboviruses.
Supplemental Material
sj-pdf-1-tai-10.1177_20499361261438240 – Supplemental material for Beyond the epidemic curve: a critical systematic review of the structural, ecological, and viral determinants sustaining Chikungunya and Zika viruses in Latin America and the Caribbean
Supplemental material, sj-pdf-1-tai-10.1177_20499361261438240 for Beyond the epidemic curve: a critical systematic review of the structural, ecological, and viral determinants sustaining Chikungunya and Zika viruses in Latin America and the Caribbean by Danladi C. Husaini, Aneesah A. Herbert, Marjorie Z. Rivera, Jahaira Nunez, Arlen Coc, Joel H. Chiroma and Orish E. Orisakwe in Therapeutic Advances in Infectious Disease
Supplemental Material
sj-pdf-2-tai-10.1177_20499361261438240 – Supplemental material for Beyond the epidemic curve: a critical systematic review of the structural, ecological, and viral determinants sustaining Chikungunya and Zika viruses in Latin America and the Caribbean
Supplemental material, sj-pdf-2-tai-10.1177_20499361261438240 for Beyond the epidemic curve: a critical systematic review of the structural, ecological, and viral determinants sustaining Chikungunya and Zika viruses in Latin America and the Caribbean by Danladi C. Husaini, Aneesah A. Herbert, Marjorie Z. Rivera, Jahaira Nunez, Arlen Coc, Joel H. Chiroma and Orish E. Orisakwe in Therapeutic Advances in Infectious Disease
Supplemental Material
sj-pdf-3-tai-10.1177_20499361261438240 – Supplemental material for Beyond the epidemic curve: a critical systematic review of the structural, ecological, and viral determinants sustaining Chikungunya and Zika viruses in Latin America and the Caribbean
Supplemental material, sj-pdf-3-tai-10.1177_20499361261438240 for Beyond the epidemic curve: a critical systematic review of the structural, ecological, and viral determinants sustaining Chikungunya and Zika viruses in Latin America and the Caribbean by Danladi C. Husaini, Aneesah A. Herbert, Marjorie Z. Rivera, Jahaira Nunez, Arlen Coc, Joel H. Chiroma and Orish E. Orisakwe in Therapeutic Advances in Infectious Disease
Footnotes
References
Supplementary Material
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