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Faria, N. R.

Publications and source records attributed to Faria, N. R..

16 recordsLinked to original sources

Phylodynamic analysis reveals asymmetric and accelerating global spread of dengue virus

Dengue virus (DENV) continues to expand globally, with increasing incidence in both endemic and non-endemic countries. Leveraging a large global dataset of DENV genomes starting from the 1940s, we reconstructed global and regional patterns of DENV spread using phylogeographic and phylodynamic methods. Our analyses reveal that the current global diversity of urban DENV originated in Asia in the first half of the 20th century. During the more than 100 years since, we find that the highest density of between-country spread occurs within Asia and the region continues to be a global source, seeding transmission in Africa and the Americas. Global spread is, however, not balanced. Even though there is more travel to South America, we show that DENV lineages primarily enter North America (mostly from South Asia) through a link defined by seasonal synchrony across the Northern Hemisphere. Along with a substantial increase in global travel starting ~2010, the rate of spread to the Americas is increasing, establishing new lineages associated with large recent outbreaks. DENV lineages do not frequently spread back to Asia from the Americas or Africa, and we posit this is due to higher genetic diversity in Asia, leading to stiffer competition for invading lineages. Within the Americas, the network of DENV dispersal initiates in North America, primarily the Caribbean, and then is maintained by major hubs in South America. Overall, we find that travel volume, rather than climate factors, is mostly responsible for long-term patterns of DENV spread globally and within the Americas. Our results highlight key nodes in the global dynamics of DENV lineages, and suggest spread will continue to accelerate in a more connected world.

genomics↗

Genomic Epidemiology of Canine Distemper Virus (CDV) in Neotropical Primates in Brazil Reveals Multiple Spillover Events and Convergent Evolution at Hemagglutinin Residue 519

Canine distemper virus (CDV; Morbillivirus canis) is a multi-host paramyxovirus primarily maintained in the order Carnivora. However, recent outbreaks in Neotropical primates suggest recurrent cross-species spillover into non-human primates. Between May and July 2022, seven marmosets (Callithrix penicillata) were found dead in urban and peri-urban areas of Montes Claros, Minas Gerais, Brazil. Viral metagenomic sequencing recovered two near complete CDV genomes directly from liver samples. Maximum likelihood and Bayesian phylogenetic analyses placed these genomes within the South American CDV lineage and supported at least three independent zoonotic introductions into Callithrix populations. Domestic dogs (Canis lupus familiaris) were inferred as the most likely source and the crab-eating fox (Cerdocyon thous) as a probable bridge host. Ancestral-state reconstruction identified a substitution at position 519 of the hemagglutinin (H) protein (R519I in the two primate clades and R519G in a singleton primate sequence). In silico modelling of the marmoset signaling lymphocytic activation molecule (SLAM) complex was consistent with a modest reorganisation of the receptor-binding head in the 519-substituted variants (ipTM = 0.82), generating a testable hypothesis that this residue may contribute to adaptation at the primate SLAM receptor interface and is associated with altered predicted docking orientation for the receptor. Together, these findings suggest that residue 519 is a candidate marker of CDV adaptation to Neotropical primates and emphasise the importance of integrating genomic surveillance with domestic dog vaccination efforts under a One Health framework to reduce the threat of CDV spillover to vulnerable wildlife populations.

genomics↗

Better data, better trees: GenBank-GISAID deduplication and source-specific artifact masking in viral genomics

GenBank and GISAID are the primary repositories for viral genomic data, but integrating records across them remains a challenge. The same sequence could be made available in both databases without any cross-reference linking the two entries. Consequently, there is no systematic way to identify this redundancy, which compromises the compilation of representative, non-redundant large-scale datasets. In parallel, the growth of viral genomic data has increased the risk of systematic technical artifacts introduced during sequencing or assembly. These artifacts can inflate substitution rate estimates and degrade temporal signal, biasing evolutionary rate estimates. To address both challenges, here we present a formal, reproducible workflow integrating two newly developed complementary tools: G2G matcher for cross-repository harmonization and Lab-Specific Bias FILTer (LSBFILT) for masking of laboratory-specific artifacts. Using the Eastern/Central/South African (ECSA) chikungunya virus lineage as a proof-of-concept, we demonstrate that our integrated workflow restores temporal signal and provides a robust, curated dataset for downstream phylodynamic analyses. Critically, restricting masking of homoplastic sites to specific sequences reduces the substitution rate estimate from an inflated 8.517 x 10-4 to 5.078 x 10-4 substitutions/site/year and increases the coefficient of determination (R2) of the root-to-tip regression analysis from 0.353 to 0.677. By enabling systematic cross-repository harmonization and source-specific artifact masking, we provide the molecular epidemiological community with scalable tools to reconcile fragmented genomic data and reduce technical biases, fostering more accurate and reproducible phylogenetic analysis. G2G matcher is available at https://github.com/andrezaleite/G2G-Matcher, and LSBFILT at https://github.com/khourious/LSBFILT.

bioinformatics↗

Lessons from a multilaboratorial task force for diagnosis of a fatal toxoplasmosis outbreak in captive primates in Brazil

As exemplified by the Coronavirus Disease 2019 (COVID-19) pandemic, infectious diseases may emerge and spread rapidly, often causing serious economic losses and public health concerns. In fact, disease outbreaks have become increasingly common, especially those of zoonotic origin. The Brazilian Ministry of Health is responsible for national epizootic surveillance. However, the systems focus primarily on diseases affecting humans has led to the neglect of other zoonotic diseases. In this report, we present an integrated investigation of an outbreak that occurred during the first year of the COVID-19 pandemic among captive neotropical primates housed at a primatology center in Brazil. After presenting a range of non-specific clinical signs, including fever, prostration, inappetence, and abdominal pain, ten primates from five different species died within approximately four days. Despite the state of health emergency due to the pandemic, a network of volunteer researchers was established to investigate the outbreak. A wide range of high-resolution techniques was used for different pathogens, including SARS-CoV-2 (RTq-PCR, ELISA and IHC), Toxoplasma gondii (IHC and IFA) and Escherichia coli (IFA), as well as a portable Metagenomic Sequencing utilizing Nanopore Technology. Within a span of four days after necropsies, we successfully identified T. gondii as the causative agent of this outbreak. This case highlights some of the obstacles faced with the current Brazilian surveillance system, which is still limited. A cross-platform interdisciplinary investigation could be a possible model for future epizootic investigations in non-human animals. Author summaryThe Brazilian epizootic surveillance system, under the regulation of the Ministry of Health, has been established to address a national list of compulsory notifiable diseases. However, focusing mainly on the risks to humans causes other zoonoses to be neglected. Here we present an outbreak that occurred during the first year of the COVID-19 pandemic that affected eleven neotropical primates (NP) belonging to six different species. Within four days of exhibiting a range of non-specific clinical signs, including fever, prostration, inappetence, and abdominal pain, ten NPs died. Despite testing negative for pathogens included in the national surveillance policy, a collaborative group of researchers investigated the outbreak in detail. Using integrated diagnostic techniques, we identified Toxoplasma gondii as the causative agent four days after necropsy. Toxoplasmosis causes devastating acute death outbreaks in neotropical primates and is currently absent in the national guidelines. This unified effort proved the effectiveness of a multidisciplinary collaborative surveillance network in facilitating precise diagnoses.

microbiology↗

Madariaga and Venezuelan equine encephalitis virus seroprevalence in rodent enzootic hosts in Eastern and Western Panama

While rodents are primary reservoirs of Venezuelan equine encephalitis virus (VEEV), their role in Madariaga virus (MADV) transmission remains uncertain, particularly given their overlapping geographic distribution. This study explores the interplay of alphavirus prevalence, rodent diversity, and land use within Darien and Western Panama provinces. A total of three locations were selected for rodent sampling in Darien province: Los Pavitos, El Real de Santa Maria and Santa Librada. Two sites were selected in Western Panama province: El Cacao and Ciri Grande. We used plaque reduction neutralization tests to assess MADV and VEEV seroprevalences in 599 rodents of 16 species across five study sites. MADV seroprevalence was observed at higher rates in Los Pavitos (Darien province), 9.0%, 95% CI: 3.6-17.6, while VEEV seroprevalence was elevated in El Cacao (Western Panama province), 27.3%, 95% CI: 16.1-40.9, and El Real de Santa Maria (Darien province), 20.4%, 95% CI: 12.6-29.7. Species like Oryzomys coesi, 23.1%, 95% CI: 5.0-53.8, and Transandinomys bolivaris, 20.0%, 95% CI: 0.5-71.6 displayed higher MADV seroprevalences than other species, whereas Transandinomys bolivaris, 80.0%, 95% CI: 28.3-99.4, and Proechimys semispinosus, 27.3%, 95% CI: 17.0-39.6, exhibited higher VEEV seroprevalences. Our findings provide support to the notion that rodents are vertebrate reservoirs of MADV and reveal spatial variations in alphavirus seropositivity among rodent species, with different provinces exhibiting distinct rates for MADV and VEEV. Moreover, specific rodent species are linked to unique seroprevalence patterns for these viruses, suggesting that rodent diversity and environmental conditions might play a significant role in shaping alphavirus distribution.

microbiology↗

Early identification of dengue virus lineage replacement in Brazil using portable genomic surveillance

Over 400 million people are estimated to be at risk of acquiring dengue virus (DENV). Despite efforts to mitigate the impact of DENV epidemics, the virus remains a public health problem in the Americas: more than one million DENV cases were reported in the continent between January and July 2019 DENV was first detected in Brazil in 1982, and Brazil has reported 88% (1,127,244 cases) of all DENV cases in the Americas during 2019 to date. Sao Paulo state in the southeast of Brazil has reported nearly half of all DENV infections in the country. Here we characterised the genetic diversity of DENV strains circulating in Sao Paulo state in 2019, at the epicentre of the ongoing DENV epidemic. Using portable nanopore sequencing we generated 20 new DENV genome sequences from viremic patients with suspected dengue infection residing in two of the most-affected municipalities, Araraquara and Sao Jose do Rio Preto. We conducted a comprehensive phylogenetic analysis with 1,630 global DENV strains to better understand the evolutionary history of the DENV lineages that currently circulate in the region. The new outbreak strains were classified as DENV2 genotype III (American/Asian genotype). Notably, phylogenetic analysis indicated that the 2019 outbreak is the result of a novel DENV lineage that was recently introduced to Brazil from the Caribbean region. Our genetic analysis further indicates that the introduction and onwards spread of the outbreak lineage (named here DENV2-III BR-4) indicates a new DENV2 lineage replacement in Brazil. Dating phylogeographic analysis suggests that DENV2-III BR-4 was introduced to Brazil in or around early 2014, possibly from the Caribbean region. Our study describes the early detection of a newly introduced and rapidly-expanding DENV2 virus lineage in Brazil.\n\nAuthor SummaryDengue is the most important mosquito-borne viral disease of humans. The disease is caused by the dengue virus (DENV) that is classified within genus Flavivirus. DENV infections are caused by 4 serotypes (DENV 1-4) that are genetically related but antigenically distinct. Dengue infection results in a variety of symptoms that range from mild fever to dengue hemorrhagic fever and/or dengue shock syndrome (DHF/DSS). Clinical outcomes are associated with different types of infection, viral serotypes, genotypes, lineages, and host genetic factors. As a re-emerging infectious disease, DENV has become a serious threat to public health in the Americas, and particularly in Brazil, where it was introduced in the 1980s and became well established due to the country-wide re-infestation of the Aedes aegypti mosquito vector species. During the first six months of 2019, 1,282,183 DENV cases were reported in the Americas, with Brazil reporting a staggering 1,127,244 (88%) of all dengue cases in the continent. To date, no information exists on the genetic composition of the DENV lineage or lineages causing the current epidemic. Here we use portable sequencing to rapidly generate virus genome data from cases occurring in two different are severely-affected municipalities in Sao Paulo state, Brazil. We find that the 2019 dengue outbreak in Brazil is caused by a newly introduced DENV serotype 2 genotype III (Asian/American) that seems to be replacing previously-circulating DENV2 lineages. We discuss the potential implications of our results regarding the current outbreak in the context of previous outbreaks in the same region.

genomics↗

The evolutionary dynamics of Oropouche Virus (OROV) in South America

The Amazon basin is host to numerous arthropod-borne viral pathogens that cause febrile disease in humans. Among these, Oropouche orthobunyavirus (OROV) is a relatively understudied member of the Peribunyavirales that causes periodic outbreaks in human populations in Brazil and other South American countries. Although several studies have described the genetic diversity of the virus, the evolutionary processes that shape the viral genome remain poorly understood. Here we present a comprehensive study of the genomic dynamics of OROV that encompasses phylogenetic analysis, evolutionary rate estimates, inference of natural selective pressures, recombination and reassortment, and structural analysis of OROV variants. Our study includes all available published sequences, as well as a set of new OROV genomes sequences obtained from patients in Ecuador, representing the first set of viral genomes from this country. Our results show that differing evolutionary processes on the three segments that encompass the viral genome lead to variable evolutionary rates and TMRCAs that could be explained by cryptic reassortment. We also present the discovery of previously unobserved putative N-linked glycosylation sites, and codons which evolve under positive selection on the viral surface proteins, and discuss the potential role of these features in the evolution of the virus through a combined phylogenetic and structural approach.

evolutionary biology↗

Emergence of the Zika virus Asian lineage in Angola

Research In ContextO_ST_ABSEvidence before this studyC_ST_ABSWe searched PubMed without language restrictions using the keywords Zika and Africa for papers published to October 2018. We also checked available Situation Report publications from WHO for evidence of Zika virus (ZIKV) or congenital Zika disease in Africa. ZIKV African lineage has been detected within Africa since the mid 20th century, yet evidence for spread of the ZIKV Asian lineage within Africa is limited. Two countries in Africa (Cabo Verde and Angola) have reported ZIKV cases that are believed to be caused by a newly introduced Asian lineage virus. Sequence data are critical for confirming and understanding the spread of ZIKV Asian lineage within Africa, but these data are currently limited to a single 193bp fragment of the ZIKV NS1 gene from Angola. In addition, whilst epidemiological data on ZIKV and suspected microcephaly cases have been reported in detail from Cabo Verde, data from Angola are extremely limited.\n\nAdded value of this studyWe provide a detailed report of detected ZIKV acute cases and suspected microcephaly cases in Angola. We sequence ZIKV genomes from three acutely infected cases. These represent the first three Asian lineage genomes available from Africa, one of which was acquired from a baby with confirmed microcephaly. Analysis of these sequences suggests that ZIKV may have been introduced to Angola between July 2015 and June 2016, after which it likely circulated for at least one year. This provides the first genetic confirmation of autochthonous ZIKV Asian lineage transmission within Africa. We suggest that the virus was more likely introduced to Angola directly from Brazil, rather than from Cabo Verde. Our analyses from Angola, only the second African country to report presence of the Asian virus lineage, therefore improve our understanding of the extent and clinical impact of ZIKV Asian lineage in the continent.\n\nImplications of all the available evidenceThe circulation of ZIKV Asian lineage within parts of sub-Saharan Africa is concerning given the potential for continued viral spread across much of the continent. Available evidence suggests that ZIKV has circulated and caused cases of microcephaly in Cabo Verde and in Angola. Detecting additional ZIKV transmission using only clinical data on suspected microcephaly or clusters of mild illness may be challenging in countries where systems for reporting birth defects are limited and infectious disease burden is high. Further spread of the ZIKV Asian lineage would likely not be detected unless molecular surveillance systems for ZIKV are implemented to routinely monitor ZIKV transmission in Africa. Implementation of such a surveillance system is especially important in countries that are linked by high human mobility to areas that have experienced recent or ongoing outbreaks of ZIKV.\n\nAbstractO_ST_ABSBackgroundC_ST_ABSZika virus (ZIKV) infections and suspected microcephaly cases have been recently reported in Angola, but no data are available on the origins, epidemiology, and diversity of the virus.\n\nMethodsSerum samples from 54 suspected ZIKV cases, 76 suspected microcephaly cases, and 24 mothers of infants with suspected microcephaly were received by the Angolan Ministry of Health. Computed tomographic brain imaging and serological assays (PRNT) were conducted on one microcephalic infant. All sera were tested for ZIKV by RT-qPCR. 349 samples from HIV+ patients and 336 samples from patients suspected of chikungunya virus or dengue virus infection were also tested. Portable sequencing was used to generate Angolan ZIKV genome sequences, including from a ZIKV+ neonate with microcephaly born in Portugal to an Angolan resident. Genetic and mobility data were analysed to investigate the date of introduction and geographic origin of ZIKV in Angola.\n\nFindingsFour autochthonous cases were ZIKV positive via RT-qPCR, with all positive samples collected between December 2016 and June 2017. Viral genomes were generated for two of these cases, and from the neonate with microcephaly identified in Portugal. Genetic analyses and other data indicate that ZIKV was introduced to Angola from Brazil between July 2015 and June 2016. This introduction likely initiated local ZIKV circulation in Angola that continued until June 2017. The scanned microcephaly case showed brain abnormalities consistent with congenital Zika syndrome and serological evidence for maternal ZIKV infection.\n\nInterpretationOur analyses confirm the autochthonous transmission of the ZIKV Asian lineage in continental Africa. Conducting ZIKV surveillance throughout Africa is critical in the light of presented evidence for autochthonous ZIKV transmission in Angola, and associated microcephaly cases.\n\nFundingRoyal Society, Wellcome Trust, CNPq, CAPES, ERC, Oxford Martin School, Global Challenges Research Fund, Africa Oxford, and John Fell Fund.

epidemiology↗

MVSE: an R-package that estimates a climate-driven mosquito-borne viral suitability index.

BackgroundViruses such as dengue, Zika, yellow fever and chikungunya depend on mosquitoes for transmission. Their epidemics typically present periodic patterns, linked to the underlying mosquito population dynamics, which are known to be driven by natural climate fluctuations. Understanding how climate dictates the timing and potential of viral transmission is essential for preparedness of public health systems and design of control strategies.\n\nResultsWe developed the Mosquito-borne Viral Suitability Estimator (MVSE) software package for the R programming environment. The package estimates a suitability index based on a climate-driven mathematical expression for the basic reproductive number (R0) of a well established mathematical model for the transmission dynamics of mosquito-borne viruses. By accounting for local humidity and temperature, as well as viral, vector and human priors, suitability can be estimated for specific host and viral species, as well as different regions of the globe.\n\nConclusionsHere, we describe the background theory and biological interpretation of the new suitability index, as well as the implementation, basic functionality, research and educational potentials of the MVSE R-package. The package is freely available under the GPL 3.0 license.

epidemiology↗

Genomic and epidemiological monitoring of yellow fever virus transmission potential

The yellow fever virus (YFV) epidemic that began in Dec 2016 in Brazil is the largest in decades. The recent discovery of YFV in Brazilian Aedes sp. vectors highlights the urgent need to monitor the risk of re-establishment of domestic YFV transmission in the Americas. We use a suite of epidemiological, spatial and genomic approaches to characterize YFV transmission. We show that the age- and sex-distribution of human cases in Brazil is characteristic of sylvatic transmission. Analysis of YFV cases combined with genomes generated locally using a new protocol reveals an early phase of sylvatic YFV transmission restricted to Minas Gerais, followed in late 2016 by a rise in viral spillover to humans, and the southwards spatial expansion of the epidemic towards previously YFV-free areas. Our results establish a framework for monitoring YFV transmission in real-time, contributing to the global strategy of eliminating future yellow fever epidemics.

epidemiology↗

Zika virus outbreak in Cabo Verde Islands, West Africa: early epidemiological findings

IntroductionThe Zika virus (ZIKV) outbreak in the island nation of Cabo Verde was of unprecedented magnitude in Africa and the first to be associated with microcephaly in the continent.\n\nMethodsUsing a simple mathematical framework we present a first epidemiological assessment of attack and observation rates from 7,580 ZIKV notified cases and 18 microcephaly reports between July 2015 and May 2016.\n\nResultsIn line with observations from the Americas and elsewhere, the single-wave Cabo Verdean ZIKV epidemic was characterized by a basic reproductive number of 1.85 (95% CI, 1.5 -2.2), with overall the attack rate of 51.1% (range 42.1 - 61.1) and observation rate of 2.7% (range 2.29 - 3.33).\n\nConclusionCurrent herd-immunity may not be sufficient to prevent future small-to-medium epidemics in Cabo Verde. Together with a small observation rate, these results highlight the need for rapid and integrated epidemiological, molecular and genomic surveillance to tackle forthcoming outbreaks of ZIKV and other arboviruses.

epidemiology↗

Phylodynamic assessment of intervention strategies for the West African Ebola virus outbreak

This preprint has been reviewed and recommended by Peer Community In Evolutionary Biology (http://dx.doi.org/10.24072/pci.evolbiol.100046). The recent Ebola virus (EBOV) outbreak in West Africa witnessed considerable efforts to obtain viral genomic data as the epidemic was unfolding. If such data can be deployed in real-time, molecular epidemiological investigations could play a role in complementing contact tracing undertaken by public health agencies. Analysing the EBOV genomes accumulated to date can also deliver insights into epidemic dynamics. Such analyses have been shown that metapopulation dynamics were critical for EBOV dispersal between rural and urban areas during the epidemic, but the implications for specific intervention scenarios remain unclear. Here, we address this issue using a collection of phylodynamic approaches. We show that long-distance dispersal events (between administrative areas >250 km apart) were not crucial for epidemic expansion and that preventing viral lineage movement to any given administrative area would, in most cases, have had little impact. However, urban areas - specifically those encompassing the three capital cities and their suburbs - were critical in attracting and further disseminating the virus: preventing viral lineage movement to all three simultaneously would have contained epidemic size by two-thirds. Using continuous phylogeographic reconstructions we estimate a distance kernel for EBOV spread and reveal considerable heterogeneity in dispersal velocity through time. We also show that announcements of border closures were followed by a significant but transient effect on international virus dispersal. By quantifying the hypothetical impact of different intervention strategies as well as the impact of barriers on dispersal frequency, our study illustrates how phylodynamic analyses can help to address specific epidemiological and outbreak control questions.

epidemiology↗

Emergence and persistence of the Chikungunya virus East-Central-South-African genotype in Northeast Brazil

We investigate an outbreak of exanthematous illness in Maceio, Alagoas, using molecular surveillance. Of 273 samples, 76% tested RT-qPCR positive for Chikungunya virus. Phylogenetic analysis reveals that the outbreak was caused by the East-Central-South-African genotype, and that this lineage has likely persisted since mid-2014 in Northeast Brazil.\n\nArticle summary lineTransmission of the Chikungunya virus East-Central-South-African genotype has been ongoing in the Northeast region of Brazil since mid-2014.

epidemiology↗

Epidemic establishment and cryptic transmission of Zika virus in Brazil and the Americas

Zika virus (ZIKV) transmission in the Americas was first confirmed in May 2015 in Northeast Brazil1. Brazil has the highest number of reported ZIKV cases worldwide (>200,000 by 24 Dec 20162) as well as the greatest number of cases associated with microcephaly and other birth defects (2,366 confirmed cases by 31 Dec 20162). Following the initial detection of ZIKV in Brazil, 47 countries and territories in the Americas have reported local ZIKV transmission, with 22 of these reporting ZIKV-associated severe disease3. Yet the origin and epidemic history of ZIKV in Brazil and the Americas remain poorly understood, despite the value of such information for interpreting past trends in reported microcephaly. To address this we generated 53 complete or partial ZIKV genomes, mostly from Brazil, including data generated by the ZiBRA project - a mobile genomics lab that travelled across Northeast Brazil in 2016. One sequence represents the earliest confirmed ZIKV infection in Brazil. Joint analyses of viral genomes with ecological and epidemiological data estimate that the ZIKV epidemic first became established in NE Brazil by March 2014 and likely disseminated from there, both nationally and internationally, before the first detection of ZIKV in the Americas. Estimated dates of the international spread of ZIKV from Brazil coincide with periods of high vector suitability in recipient regions and indicate the duration of pre-detection cryptic transmission in those regions. NE Brazils role in the establishment of ZIKV in the Americas is further supported by geographic analysis of ZIKV transmission potential and by estimates of the virus basic reproduction number.\n\nOne Sentence SummaryVirus genomes reveal the establishment of Zika virus in Northeast Brazil and the Americas, and provide an appropriate timeframe for baseline (pre-Zika) microcephaly in different regions.

genomics↗

Epidemiological and ecological determinants of Zika virus transmission in an urban setting.

Zika has emerged as a global public health concern. Although its rapid geographic expansion can be attributed to the success of its Aedes mosquito vectors, local epidemiological drivers are still poorly understood. The city of Feira de Santana played a pivotal role in the early phases of the Chikungunya and Zika epidemics in Brazil. Here, using a climate-driven transmission model, we show that low Zika observation rates and a high vectorial capacity in this region were responsible for a high attack rate during the 2015 outbreak and the subsequent decline in cases in 2016, when the epidemic was peaking in the rest of the country. Our projections indicate that the balance between the loss of herd-immunity and the frequency of viral re-importation will dictate the transmission potential of Zika in this region in the near future. Sporadic outbreaks are expected but unlikely to be detected under current surveillance systems.

epidemiology↗