Biology subjects

Armstrong, M.

Publications and source records attributed to Armstrong, M..

At least 19 recordsLinked to original sources

bioRxiv2026

The Flame Retardant Triphenyl Phosphate Induces Varying Responses in Genetically Diverse Mouse Induced Pluripotent Stem Cells

Genetic variation impacts biological response to chemical and environmental exposures, contributing to differences in resistance or susceptibility. Forward genetic screens of genetically diverse cell populations can be used to identify the precise genetic variants that drive response variation. Cell lines from laboratory mouse genetic reference populations like the Diversity Outbred (DO) population are well powered for genetic mapping. Diverse stem cell panels are especially beneficial for studying early developmental effects of chemical exposures like triphenyl phosphate (TPHP), an organophosphate flame retardant linked to adverse developmental effects, including altered cell cycle in stem cells. Self-renewal and pluripotency are defining properties of stem cells during development; therefore, it is important to understand how chemicals like TPHP may alter these critical characteristics. To better understand the influence of genetic variation on TPHP exposure response, we utilized a genetically diverse panel of DO induced pluripotent stem cells (DO iPSCs). Our analyses characterize interline variation in gene expression through differential gene expression analysis and expression quantitative trait locus (eQTL) mapping. We identified genomic loci that contribute to variation in gene expression following TPHP exposure, including a regulatory hotspot on chromosome 15. Gene set enrichment highlighted several pathways affected by TPHP including lipid metabolism, steroid hormone signaling, and cell cycle. Our study shows that genetic variation modulates the effects of TPHP on gene expression and cell cycle in stem cells. Additionally, our work demonstrates that genetically diverse cell panels like the DO iPSC resource offer a tractable and scalable approach for identifying the genetic determinants of chemical toxicity.

genomics↗

bioRxiv2026

Molecular and genetic heterogeneity in iPSCs derived from an outbred laboratory mouse population

Genetically diverse panels of human pluripotent stem cells enable genetic dissection of cellular phenotypes, but comparable induced pluripotent stem cell (iPSC) resources in model organisms remain limited. We generated a panel of iPSCs from the Diversity Outbred (DO) mouse population and established 288 genetically unique lines that retain the allele frequency distribution, heterozygosity, and low population structure of the source population. The lines exhibit consistent growth, pluripotent gene expression profiles, and capacity to form embryoid bodies. Transcriptomic profiling of the lines revealed significant variation in gene expression driven in part by genetic background. We used expression quantitative trait locus (eQTL) mapping to identify over 10,000 regulatory loci that influence gene expression variation, including multiple distal eQTL hotspots that are key gene regulatory hubs and are shared with DO embryonic stem cells (ESCs). The largest hotspot, mediated by Lifr, showed a shift in founder allele effects relative to ESCs, consistent with differences in cellular state and culture conditions. These results establish the DO iPSC panel as a genetically diverse, publicly accessible platform derived from a laboratory mouse genetic reference population, enabling integration of in vitro cellular phenotypes with in vivo traits within a closed, outbred population.

genetics↗

bioRxiv2025

Regional adaptation to mosquito vectors shapes Plasmodium falciparum populations

Transmission of Plasmodium falciparum through mosquitoes represents the most severe population bottleneck in the parasites life cycle, yet the genetic basis of parasite-vector compatibility remains poorly understood. Here, we show that mosquito species-specific transmissibility depends on allelic variation in multiple P. falciparum genes expressed during midgut invasion, beyond the well-studied Pfs47. Using an allelic replacement strategy, we targeted highly geographically differentiated SNPs in P. falciparum that match regional variation in vector community composition. Transmissibility was compared across four mosquito species representing distinct geographic ranges (An. gambiae, An. stephensi, An. minimus, and An. albimanus). Two of five tested polymorphisms showed increased oocyst and sporozoite burdens in sympatric parasite-vector combinations compared to allopatric ones. Both substitutions occurred in ookinete micronemal proteins, CTRP and WARP, within von Willebrand factor A domains, suggesting that regional allelic variation modulates Plasmodium-vector compatibility by altering midgut adhesion interactions. These findings reveal that vector compatibility is a polygenic trait shaped by molecular interactions across several loci. Understanding this complexity refines models of parasite adaptation and can inform the design of transmission-blocking interventions effective across diverse vector-parasite combinations.

microbiology↗

bioRxiv2025

Multiple stressors in the Anthropocene: Urban evolutionary history modifies sensitivity to the toxic effects of crude oil exposure in killifish

Persistence of wild species in human-altered environments is difficult, in part because challenges to fitness are complex when multiple environmental changes occur simultaneously, which is common in the Anthropocene. This complexity is difficult to conceptualize because the nature of environmental change is often highly context specific. A mechanism-guided approach may help to shape intuition and predictions about complexity; fitness challenges posed by co-occurring stressors with similar mechanisms of action may be less severe than for those with different mechanisms of action. We approach these considerations within the context of ecotoxicology because this field is built upon a rich mechanistic foundation. We hypothesized that evolved resistance to one class of common toxicants would afford resilience to the fitness impacts of another class of common toxicants that shares mechanisms of toxicity. Fundulus killifish populations in urban estuaries have repeatedly evolved resistance to persistent organic pollutants including PCBs. Since PCBs and some of the toxicants that constitute crude oil (e.g., high molecular weight PAHs) exert toxicity through perturbation of AHR signaling, we predicted that PCB resistant populations would also be resilient to crude oil toxicity. Common garden comparative oil exposure experiments, including killifish populations with different exposure histories, showed that most killifish populations were sensitive to fitness impacts (reproduction and development) caused by oil exposure, but that fish from the PCB-resistant population were insensitive. Population differences in toxic outcomes were not compatible with random-neutral expectations. Transcriptomics revealed that the molecular mechanisms that contributed to population variation in PAH resilience were shared with those that contribute to evolved variation in PCB resilience. We conclude that the fitness challenge posed by environmental pollutants is effectively reduced when those chemicals share mechanisms that affect fitness. Mechanistic considerations may help to scale predictions regarding the fitness challenges posed by stressors that may co-occur in human-altered environments.

evolutionary biology↗

bioRxiv2024

Upregulation of a nonsense mediated decay (NMD) insensitive CFTR mRNA isoform has therapeutic potential for the treatment of 3 Prime CFTR PTC variants

BackgroundNonsense or Premature Termination Codon (PTC) mutations of the CFTR gene are pathogenic and found in [~]10% of North American people with cystic fibrosis. PTC mutations induce Nonsense-Mediated mRNA Decay (NMD), leading to a substantial ([~]80-90%) reduction in full-length mRNA. This reduction is a key contributor to PTC mutation-related pathology. Various approaches to evade NMD and preserve the impacted mRNA transcript have been explored but have not progressed to clinical development, leaving NMD a significant hurdle for PTC readthrough therapy. MethodsAntisense oligonucleotides (ASOs) were tiled across intron 22 splice donor (SD) and acceptor (SA) sites of the CFTR gene. Immortalized airway cells were treated with SD and SA ASOs, and those yielding the greatest increase in a CFTR NMD-insensitive mRNA isoform (e22 trunc mRNA) were tested in combinations. Top SD/SA ASO pairs were assessed for their impact on e22 trunc mRNA via ddPCR, e22 trunc protein via western blot, and CFTR-mediated chloride (Cl-) transport via transepithelial electrophysiological measurements in immortalized and primary human bronchial epithelial (hBE) cell cultures. ResultsWe demonstrate that e22 trunc mRNA generates a truncated CFTR protein whose Cl- transport function can be enhanced with elexacaftor/tezacaftor/ivacaftor (ETI) treatment. ASO and ETI treatment in combination restore [~]20% and 25% of wild-type CFTR Cl- transport function in immortalized epithelial and primary hBE cells homozygous for CFTR W1282X, respectively. ConclusionsThis study lays the groundwork for advancing ASO-mediated upregulation of e22 trunc mRNA and protein as a therapeutic approach for cystic fibrosis caused by 3-terminal CFTR PTC mutations.

genomics↗

bioRxiv2024

Transcriptional profiling during infection of potato NLRs and Phytophthora infestans effectors using cDNA enrichment sequencing

An accurate assessment of host and pathogen gene expression during infection is critical for understanding the molecular aspects of host-pathogen interactions. Often, pathogen-derived transcripts are difficult to ascertain at early infection stages owing to the unfavourable transcript representation compared to the host genes. In this study, we compare two sequencing techniques, RNAseq and enrichment sequencing (RenSeq and PenSeq) of cDNA, to investigate gene expression patterns in the doubled monoploid potato (DM) infected with the late blight pathogen Phytophthora infestans. Our results reveal distinct advantages of cDNA RenSeq and PenSeq over traditional RNAseq in terms of target gene representation and transcriptional quantification at early infection stages. Throughout the infection time course, cDNA enrichment sequencing enables transcriptomic analyses for more targeted host and pathogen genes. For highly expressed genes that were sampled in parallel by both cDNA enrichment and RNAseq, a high level of concordance in expression profiles is observed, indicative of at least semi-quantitative gene expression representation following enrichment.

molecular biology↗

bioRxiv2023

Identification and mapping of Rpi-blb4 in diploid wild potato species Solanum bulbocastanum

More than 170 years after causing the potato famine in Ireland, late blight is still considered one of the most devastating crop diseases. Commercial potato breeding efforts depend on natural sources of resistance to protect crops from the rapidly evolving late blight pathogen, Phytophthora infestans. We have identified and mapped a novel broad-spectrum disease resistance gene effective against P. infestans from the wild, diploid potato species Solanum bulbocastanum. Diagnostic resistance gene enrichment sequencing (dRenSeq) was used to confirm the uniqueness of the identified resistance. RenSeq and GenSeq-based mapping of the resistance, referred to as Rpi-blb4, alongside recombinant screening, positioned the locus responsible for the resistance to potato Chromosome 5. The interval spans approximately 2.3 MB and corresponds to the DM reference genome positions of 11.25 and 13.56 Mb.

genetics↗

bioRxiv2023

Short- and long-term high-fat diet exposure differentially alters phasic and tonic GABAergic signalling onto lateral orbitofrontal pyramidal neurons

The chronic consumption of caloric dense high-fat foods is a major contributor to increased body weight, obesity, and other chronic health conditions. The orbitofrontal cortex (OFC) is critical in guiding decisions about food intake and is altered with diet-induced obesity. Obese rodents have altered morphological and synaptic electrophysiological properties in the lateral orbitofrontal cortex (lOFC). Yet the time course by which exposure to a high-fat diet (HFD) induces these changes is poorly understood. Here male mice are exposed to either short- (7 day) or long-term (90 day) HFD. Long-term HFD exposure increases body weight, and glucose signaling compared to short-term HFD or a standard chow control diet (SCD). Both short and long-term HFD exposure increased the excitability of lOFC pyramidal neurons. However, phasic and tonic GABAergic signalling was differentially altered depending on HFD exposure length, such that tonic GABAergic signaling was decreased with early exposure to the HFD and phasic signaling was changed with long-term diet exposure. Furthermore, alterations in the short-term diet exposure were transient, as removal of the diet restored electrophysiological characteristics similar to mice fed SCD whereas long-term HFD electrophysiological changes were persistent and remained after HFD removal. Finally, we demonstrate that changes in reward devaluation occur early with diet exposure. Together, these results suggest that the duration of HFD exposure differentially alters lOFC function and provides mechanistic insights into the susceptibility of the OFC to impairments in outcome devaluation. Significant statementThis study provides mechanistic insight on the impact of short- and long-term high fat diet (HFD) exposure on GABAergic function in the lateral orbitofrontal cortex (lOFC), a region known to guide decision making. We find short-term HFD exposure induces transient changes in firing and tonic GABA action on lOFC pyramidal neurons, whereas long-term HFD induces obesity and has lasting changes on firing, tonic GABA and inhibitory synaptic transmission onto lOFC neurons. Given that GABAergic signaling in the lOFC can influence decision making around food, these results have important implications in present society as palatable energy dense foods are abundantly available.

neuroscience↗

bioRxiv2022

Novel populations of Tr1 cells contribute to the resolution of acute influenza A virus infection.

Type I regulatory (Tr1) cells contribute to immune suppression in the context of chronic infection, autoimmunity, and transplant tolerance. However, their physiological relevance in the resolution of acute respiratory infection is not understood. Here, we identify Tr1 cells accumulating in the lung parenchyma during resolution of the response to sublethal influenza A virus infection in mice. Tr1 cells were dependent on IL-27R and in their absence recovery from IAV-induced weight loss is impaired. Notably, these Tr1 cells did not necessarily co-express the typical Tr1 markers LAG-3 and CD49b, with four distinct populations of Tr1 cells apparent in the lungs. Each population was suppressive and were differentially dependent on IL-10 to mediate suppression. Transcriptional analysis revealed a core Tr1 gene signature in each population and distinct expression profiles indicative of different states of activation and differentiation. Finally, sort-transfer experiments indicated non-linear plasticity between these subsets of Tr1 cells. Together, these data support Tr1 cells contributing to the resolution of acute inflammation and define novel Tr1 cell phenotypes in acute infection.

immunology↗

bioRxiv2022

BatCount: A software program to count moving animals

One of the biggest challenges with species conservation is collecting accurate and efficient information on population sizes, especially from species that are difficult to count. Bats worldwide are declining due to disease, habitat destruction, and climate change, and many species lack reliable population information to guide management decisions. Current approaches for estimating population sizes of bats in densely occupied colonies are time-intensive, may negatively impact the population due to disturbance, and/or have low accuracy. Research-based video tracking options are rarely used by conservation or management agencies for animal counting due to the perceived training required to operate. In this paper, we present BatCount, a free software program created in direct consultation with end-users designed to automatically count aggregations of bats at cave roosts with a streamlined and user-friendly interface. We report on the software package and provide performance metrics for different recording habitat conditions. Our analysis demonstrates that BatCount is an efficient and reliable option for counting bats in flight and has important implications for range- and species-wide population monitoring. Furthermore, this software can be extended to count any organisms moving across a camera including birds, mammals, fish or insects.

zoology↗

bioRxiv2022

A mouse model of human mitofusin 2-related lipodystrophy exhibits adipose-specific mitochondrial stress and reduced leptin secretion

Mitochondrial dysfunction has been reported in obesity and insulin resistance, but primary genetic mitochondrial dysfunction is generally not associated with these, arguing against a straightforward causal relationship. A rare exception, recently identified in humans, is a syndrome of lower body adipose loss, leptin-deficient severe upper body adipose overgrowth, and insulin resistance caused by the p.Arg707Trp mutation in MFN2, encoding mitofusin-2. How this selective perturbation of mitochondrial function leads to tissue- and adipose depot-specific growth abnormalities and systemic biochemical perturbation is unknown. To address this, Mfn2R707W/R707W knock-in mice were generated and phenotyped on chow and high fat diets. Electron microscopy revealed adipose-specific mitochondrial morphological abnormalities. Oxidative phosphorylation by isolated mitochondria was unperturbed, but the cellular integrated stress response was activated in adipose tissue. Fat mass and distribution, body weight, and systemic glucose and lipid metabolism were unchanged, however serum leptin and adiponectin concentrations, and their secretion from adipose explants were reduced. Pharmacological induction of the integrated stress response in wild-type adipocytes also reduced secretion of leptin and adiponectin, suggesting an explanation for the in vivo findings. These data suggest that the p.Arg707Trp MFN2 mutation perturbs mitochondrial morphology and activates the integrated stress response selectively in adipose tissue. In mice, this does not disrupt most adipocyte functions or systemic metabolism, whereas in humans it is associated with pathological adipose remodelling and metabolic disease. In both species, disproportionate effects on leptin secretion may relate to cell autonomous induction of the integrated stress response.

cell biology↗

bioRxiv2020

Fast and scalable lipid nanoparticle formulation of niclosamide (nano NCM) effectively inhibits SARS-CoV-2 replication in vitro

As exemplified by the COVID-19 pandemic, highly infective respiratory viruses can spread rapidly in the population because of lack of effective approaches to control viral replication and spread. Niclosamide (NCM) is an old anthelminthic drug (World Health Organization essential medicine list) with pleiotropic pharmacological activities. Several recent publications demonstrated that NCM has broad antiviral activities and potently inhibits viral replication, including replication of SARS-CoV-2, SARS-CoV, and dengue viruses. Unfortunately, NCM is almost completely insoluble in water, which limits its clinical use. We developed a highly scalable and cost-effective nanoparticle formulation of NCM (nano NCM) using only FDA-approved excipient and demonstrated potency against SARS-CoV-2 infection in cells (Vero E6 and ACE2-expressing lung epithelium cells). Our ultimate goal is to develop the nano NCM formulation for treatment of COVID-19 patients.

pharmacology and toxicology↗

bioRxiv2020

RLP/K enrichment sequencing; a novel method to identify receptor-like protein (RLP) and receptor-like kinase (RLK) genes

O_LIThe identification of immune receptors in crop plants is time-consuming but important for disease control. Previously, resistance gene enrichment sequencing (RenSeq) was developed to accelerate mapping of nucleotide-binding domain and leucine-rich repeat containing (NLR) genes. However, resistances mediated by pattern recognition receptors (PRRs) remain less utilised. C_LIO_LIHere, our pipeline shows accelerated mapping of PRRs. Effectoromics leads to precise identification of plants with target PRRs, and subsequent RLP/K enrichment sequencing (RLP/KSeq) leads to detection of informative SNPs that are linked to the trait. C_LIO_LIUsing Phytophthora infestans as a model, we identified Solanum microdontum plants that recognize the apoplastic effectors INF1 or SCR74. RLP/KSeq in a segregating Solanum population confirmed the localization of the INF1 receptor on chromosome 12, and lead to the rapid mapping of the response to SCR74 to chromosome 9. By using markers obtained from RLP/KSeq in conjunction with additional markers, we fine-mapped the SCR74 receptor to a 43-kbp G-LecRK locus. C_LIO_LIOur findings show that RLP/KSeq enables rapid mapping of PRRs and is especially beneficial for crop plants with large and complex genomes. This work will enable the elucidation and characterisation of the non-NLR plant immune receptors and ultimately facilitate informed resistance breeding. C_LI

plant biology↗

bioRxiv2019

The mitotic crosslinking protein PRC1 acts as a mechanical dashpot to resist microtubule sliding

Cell division in eukaryotes requires the regulated assembly of the spindle apparatus. The proper organization of microtubules within the spindle is driven by motor proteins that exert forces to push and slide filaments, while non-motor proteins can crosslink filaments into higher order motifs such as overlapping bundles. It has not been clear how active and passive forces are integrated to produce regulated mechanical outputs within spindles. Here we employ a combined optical tweezers and TIRF microscopy instrument to directly measure the resistive forces produced by the mitotic crosslinking protein PRC1. We observe that PRC1 generates frictional forces that resist microtubule sliding. These forces scale with microtubule sliding velocity and the number of PRC1 crosslinks, but do not depend on overlap length or PRC1 density within overlaps. Our results suggest that PRC1 ensembles act like a mechanical dashpot, producing significant resistance against fast motions, but minimal resistance against slow motions, allowing for the integration of diverse motor activities into a single mechanical outcome.

biophysics↗

bioRxiv2019

Targeting the resolvin E1 - eicosapentaenoic acid axis improves hyperinsulinemia and hyperglycemia in a host genetic dependent manner

ObjectiveEicosapentaenoic acid (EPA) has recently garnered strong attention given the success of the REDUCE-IT trial, which overturned previous conclusions on EPA and led to its FDA approval for lowering cardiovascular disease risk. Therefore, there is a need to study EPA for cardiometabolic risk factors. Here we focused on EPAs preventative role on hyperglycemia and hyperinsulinemia. MethodsC57BL/6J male mice were fed a high fat diet in the absence or presence of pure EPA. Mass spectrometry was used to identify how EPA prevents hyperinsulinemia and hyperglycemia that drove subsequent experiments with resolvin E1 (RvE1) across inbred and outbred models. ResultsAdministration of EPA to C57BL/6J mice prevented obesity-induced glucose intolerance, hyperinsulinemia, and hyperglycemia. Supporting analyses of National Health and Nutrition Examination Survey data showed fasting glucose levels of obese adults were inversely related to EPA intake in a sex-specific manner. We next investigated how EPA improved murine hyperinsulinemia and hyperglycemia. Mass spectrometry revealed EPA overturned the obesity-driven decrement in the concentration of 18-hydroxyeicosapentaenoic acid (18-HEPE) in white adipose tissue and liver. Treatment of obese mice with RvE1, the immunoresolvant metabolite of 18-HEPE, reversed hyperinsulinemia and hyperglycemia through the G-protein coupled receptor ERV1/ChemR23. RvE1s effects were not mediated by macrophage enrichment in white adipose tissue. Finally, we determined if the metabolic effects of RvE1 were dependent on host genetics. RvE1s effects on hyperinsulinemia and hyperglycemia were divergent in diversity outbred mice that model human genetic variation. Secondary SNP analyses further revealed extensive genetic variation in human RvE1- and EPA- metabolizing genes. ConclusionsThe data suggest EPA prevents hyperinsulinemia and hyperglycemia through the endogenous bioactive metabolite RvE1 that activates ERV1/ChemR23. Importantly, the studies reveal host genetics are an overlooked but critical factor in the metabolic response to RvE1. These results underscore the need for personalized administration of EPA-derived RvE1 based on genetic/metabolic enzyme profiles.

biochemistry↗

bioRxiv2019

Micro-scale fluid behavior during cryo-EM sample blotting

Blotting has been the standard technique for preparing aqueous samples for single-particle electron cryo-microscopy (cryo-EM) for over three decades. This technique removes excess solution from a TEM grid by pressing absorbent filter paper against the specimen prior to vitrification. However, this standard technique produces vitreous ice with inconsistent thickness from specimen to specimen and from region to region within the same specimen, the reasons for which are not understood. Here, high-speed interference-contrast microscopy is used to demonstrate that the irregular pattern of fibers in the filter paper imposes tortuous, highly variable boundaries during removal of excess liquid from a flat, hydrophilic surface. As a result, aqueous films of nonuniform thickness are formed while the filter paper is pressed against the substrate. This pattern of nonuniform liquid thickness changes again after the filter paper is pulled away, but the thickness still does not become completely uniform. We suggest that similar topological features of the liquid film are produced during the standard technique used to blot EM grids and that these manifest in nonuniform ice after vitrification. These observations suggest that alternative thinning techniques, which do not rely on direct contact between the filter paper and the grid, may result in more repeatable and uniform sample thicknesses.\n\nSTATEMENT OF SIGNIFICANCEMultiple imaging techniques are used to observe dynamic, micro-scale events as excess water is removed from a substrate by blotting with filter paper. As a result, new insight is gained about why the thickness values of remaining sample material are so variable across a single EM grid, as well as from one grid to the next. In addition, quantitative estimates are made of the shear forces to which macromolecular complexes can be exposed during blotting. The fact that sample thicknesses and flow rates are seen to be inherently under poor control during blotting suggests that other methods of removing excess water may be better suited for consistently achieving large sample areas that are suitable for use in electron cryo-microscopy.

biophysics↗

bioRxiv2018

How Public Transport affected the Propagation of Zika and Microcephaly within Rio de Janeiro early in 2015

From mid-2015 to the end of January 2016, 47 cases of microcephaly were observed in the city of Rio de Janeiro, that were not due to other viral infections (syphilis, toxoplasmosis, herpes & cytomegalovirus). These children were conceived from Dec 2014 to April 2015, far too early to be explained by the officially recorded cases from October 2015 onward. Zika must have been rampant in the city from late 2014 onward. In the first half of the paper we study how the geographic spread of microcephaly cases evolved from mid-2015 to January 2016 (and hence Zika 6-9 months earlier). Cases were not evenly spread in proportion to the number of births; they were preferentially located in the northern suburbs apparently following the public transport routes, with virtually no cases in favelas and none in the southern suburbs (Zona Sul). One key difference between the transport systems in the northern and southern suburbs is that the metro & rail system in the north is above ground in the north whereas in the southern part the metro is underground with air-conditioning in carriages and forced ventilation on the platforms. The train system does not extend to Zona Sul.\n\nIn the second half of the paper we postulate that the air-conditioning and ventilation prevent mosquitos from biting people who are waiting on platforms in Zona Sul. Agent-based simulations are used to test this hypothesis. After confirming this, we postulate that providing air-conditioning and/or forced ventilation on the rail-metro transport hub in the city center (Centro) would significantly delay the propagation of arboviruses in the city, possibly preventing epidemics. One advantage of this proposal is that it does not require the use of insecticides.

epidemiology↗

bioRxiv2017

Zika: An ongoing threat to women and infants

Recent data from Rio de Janeiro shows a sharp drop in the number of notified cases of Zika in the summer of 2016-17, compared to the previous summer. This is probably due to herd immunity built up after the previous year's epidemic. There is still a much higher incidence among women than men, almost certainly due to sexual transmission. An unexpected feature of the new data is that there are proportionally far more cases in children under 15 months than in older age classes. By comparing the incidence for 2016-17 with that of 2015-16, we can deduce the proportion of reported cases for men and women, and also verify that the disparity of incidence between them is still present. Women and children still represent risk groups with regard to Zika infection, even during a non-epidemic season.

epidemiology↗