A new laboratory study conducted in Viet Nam provides a sobering partial answer. Researchers used blood samples collected from thirteen dengue patients at the Hospital for Tropical Diseases in Ho Chi Minh City to feed colonies of wMel-infected Aedes aegypti, then compared how the mosquitoes fared when reared at different temperatures. The use of patient-derived viremic blood is a methodological strength, because it exposes mosquitoes to the genetically diverse, naturally circulating viruses that circulate in human populations rather than to a single laboratory-adapted strain. This design allowed the team to assess whether heat could compromise the protection that wMel affords under conditions that closely mimic natural transmission.

The central finding is that rearing temperature matters. Compared with wMel-infected mosquitoes maintained at 28 ± 4°C, those reared at 31 ± 4°C developed infectious saliva more frequently, meaning that virus reached the salivary glands and could be expectorated in a form capable of initiating a human infection. This is a critical endpoint in vector competence studies: a mosquito that never produces infectious saliva is, for practical purposes, a dead end for the virus. The elevated temperature regime therefore increased the frequency of what researchers call breakthrough infections, in which the Wolbachia-mediated block fails to prevent the virus from completing its journey through the mosquito.

Importantly, the protection was weakened but not abolished. Even at the higher rearing temperature, wMel-infected mosquitoes were still less likely to develop infectious saliva than wild-type mosquitoes exposed to the same conditions. The bacterium continued to provide a meaningful, if diminished, barrier to transmission. This distinction matters for public health planning, because it suggests that wMel deployments remain valuable even during hot periods, while also signaling that the margin of safety narrows when temperatures climb. The study thus reframes the conversation from whether Wolbachia works to under which thermal conditions it works best.

To understand the mechanism behind this temperature-dependent erosion of protection, the researchers examined Wolbachia densities in key mosquito tissues. Heat treatment reduced the density of wMel in all tissues tested, including the ovaries, midgut, and salivary glands. Wolbachia density is widely regarded as a key determinant of the strength of viral blocking, since the bacterium is thought to compete with viruses for intracellular resources and to prime antiviral immune pathways. A reduction in bacterial load in the midgut, the first site of viral amplification after a blood meal, and in the salivary glands, the final gateway to transmission, provides a plausible mechanistic explanation for the increased frequency of infectious saliva observed at higher temperatures.

The consequences for the virus itself were equally telling. Heat treatment significantly increased the amount of DENV-1 and DENV-4 replication in wMel-infected mosquitoes. In other words, the warmer conditions did not merely weaken the bacterium; they also created a more permissive environment for viral multiplication. Dengue viruses exist as four antigenically distinct serotypes, and the observation that both DENV-1 and DENV-4 replicated more abundantly under heat stress suggests that the effect is not limited to a single viral lineage. This convergence of reduced Wolbachia density and heightened viral replication paints a coherent picture of how elevated temperatures tip the balance within the mosquito toward successful transmission.

The team also looked for predictors of breakthrough at the level of individual mosquitoes. When comparing cohorts of wMel-infected mosquitoes that did or did not develop infectious saliva, the levels of dengue virus in the head and thorax were associated with increased odds of developing infectious saliva, whereas Wolbachia density itself was not statistically associated with that outcome. This finding is intriguing because it implies that once the virus has successfully disseminated beyond the midgut and established high titers in secondary tissues, the mosquito is likely to become salivary-gland infectious regardless of how much Wolbachia it carries. Dissemination, rather than bacterial load alone, may therefore be the pivotal bottleneck whose integrity is most vulnerable to heat.

These results build on earlier work showing that exposing wMel-infected Aedes aegypti to heat treatment, particularly during the larval stage, reduces wMel density in the ovaries, midgut, and salivary glands. They also echo a broader literature on the thermal biology of mosquito-borne transmission. Temperature shapes nearly every stage of the arbovirus transmission cycle, from mosquito development rates and blood-feeding frequency to viral replication kinetics within the vector. Laboratory studies with other systems have long suggested that heat stress can shorten the extrinsic incubation period of flaviviruses, and the present study extends this concern specifically to Wolbachia-based intervention strategies, which had sometimes been assumed to be relatively insensitive to environmental variation.

The authors conclude that elevated rearing temperatures increase the risk of patient-derived dengue breakthrough infections in wMel-infected Aedes aegypti, potentially because of increased viral replication within these mosquitoes. From this they draw a practical recommendation: it would be prudent to intensify surveillance in regions that rely on wMel for dengue control when daily mean temperatures remain above 30°C for multi-day periods. Such surveillance could include enhanced case detection, entomological monitoring, and, where feasible, molecular testing of mosquito samples to detect any decline in Wolbachia prevalence or density in the field. The recommendation acknowledges that the laboratory findings, while grounded in realistic patient-derived virus, will need to be reconciled with field observations across seasons and heat waves.

For the global dengue control community, the study arrives at a moment of both optimism and urgency. Wolbachia deployments have delivered striking public health gains, and no single laboratory result diminishes the value of that achievement. But the finding that sustained temperatures above 30°C can measurably weaken the wMel block underscores the need to plan for a warming world. Future work will likely focus on whether heat effects accumulate over multiple generations, whether thermotolerant Wolbachia strains can be selected or engineered, and how seasonal temperature profiles interact with mosquito population dynamics to shape transmission risk. In the meantime, the message for program managers is clear: the Wolbachia shield holds, but under a hot sun it must be watched more closely.

Subject of Research: Effect of rearing temperature on Wolbachia-mediated blocking of patient-derived dengue virus in Aedes aegypti mosquitoes

Article Title: Impact of temperature on patient-derived dengue virus breakthrough infections in w Mel-infected Aedes aegypti

Article References: da Silva Gonçalves, D., Thuy, V. T., Loterio, R. K., Tuyet, N. V., Xuan, T. H. T., Thi, G. N., Thi Thuy, V. H., LeDuyen, H., Thi, D. L., Vo, L. T., Huy, H. L. A., Thuy, N. T. V., Nguyen, P. T., Yacoub, S., Anders, K. L., Flores, H., Simmons, C. P., & Fraser, J. E. (2026). Impact of temperature on patient-derived dengue virus breakthrough infections in wMel-infected Aedes aegypti. PLOS Neglected Tropical Diseases, 20(10), e0014255. https://doi.org/10.1371/journal.pntd.0014255

Image Credits: AI Generated

DOI: 10.1371/journal.pntd.0014255

Keywords: Wolbachia, wMel, dengue virus, Aedes aegypti, temperature, vector competence, breakthrough infection, DENV-1, DENV-4, Ho Chi Minh City, salivary glands, mosquito-borne transmission

At the heart of the review is the idea that host seeking unfolds through overlapping phases: activation, orientation, approach, landing, probing, and feeding. Each phase depends on different cues with different reliability. Carbon dioxide exhaled by a vertebrate is a long-range signal that can activate a hungry female from tens of meters away, but it is not host-specific, since any breathing animal produces it. Skin odors carry the identity of a particular host but operate at shorter ranges. Heat and humidity become informative only at close quarters, and visual cues dominate in bright conditions. Because no single cue suffices across the entire journey, mosquitoes must stitch together fragments of information, and the authors emphasize that internal states such as hunger, mating status, and egg-development stage, along with learned associations, bridge the temporal gaps between cues encountered at different moments.

To explain how this stitching happens, the review outlines three sensory architectures that can contribute to host recognition. The first is feedforward multisensory integration, in which signals from different modalities converge in higher brain centers such as the antennal lobe, the lateral horn, and the mushroom body, producing a combined representation of the host. The second is cross-modal gating, in which one sensory channel modulates the sensitivity of another; the classic example is the way carbon dioxide primes the olfactory system to respond more strongly to skin odors. The third, and arguably the most conceptually important, is closed sensorimotor feedback: a mosquito’s own movements change the sensory input it encounters next, so flying upwind toward a plume, casting sideways when the plume is lost, and steering during landing are all acts of active sensing. The insect is not a passive receiver of stimuli but an agent that structures its own perceptual world through action.

This active-sensing perspective carries a technical implication that the authors highlight: host seeking cannot be fully understood by presenting mosquitoes with fixed stimuli in a wind tunnel and recording their choices. Behavior unfolds over seconds to minutes within a single host-seeking bout, and the trajectory of the insect determines which cues it samples and in what order. Sensorimotor dynamics therefore create a loop in which perception guides movement and movement reshapes perception. The review argues that future experiments should be designed to probe this loop directly, for example by tracking how mosquitoes modulate their flight patterns to resolve ambiguous plumes or how they adjust probing behavior on the skin in response to the thermal and chemical feedback they receive from each attempt.

The synthesis also examines how infection changes the picture. Pathogens such as dengue virus, Zika virus, and West Nile virus can modify the host-derived sensory signals that a mosquito encounters, and they can also alter the mosquito’s own responsiveness, probing behavior, feeding persistence, locomotion, and neuromodulation. The authors are careful to grade the evidence. Studies showing that infected hosts or infected mosquitoes differ in relevant traits provide association. Experiments that causally manipulate the pathogen or the mosquito’s physiology establish modulation. Only in a smaller subset of systems do the observed patterns fit what would be expected of adaptive manipulation, in which the pathogen benefits specifically from increased transmission. This tiered framing matters because claims of manipulation are easy to overstate, and the review provides a vocabulary for distinguishing strong from weak inference.

One of the most consequential findings the review consolidates is that infection can reshape the odor landscape itself. Work on dengue and Zika, for instance, has shown that infection can change the volatile chemicals emitted by host skin, making infected individuals more attractive to mosquitoes in ways that plausibly enhance transmission. Conversely, the mosquito’s own infection status can alter how its nervous system processes those cues. Because the extrinsic incubation period, the time a pathogen needs to become transmissible, must align with the mosquito’s blood-feeding schedule, even modest infection-associated shifts in host-seeking or feeding behavior can have disproportionate effects on epidemiological outcomes. The review stresses that these behavioral changes occur on timescales of seconds to minutes within a feeding bout, while transmission emerges over much longer timescales, and connecting the two levels remains an open challenge.

Redundancy emerges as a recurring theme with direct practical consequences. Because host recognition is multimodal, knocking out a single sensory pathway often fails to abolish host seeking. Mosquitoes with impaired carbon dioxide detection can still locate hosts using skin odors and heat; disrupting one family of odorant receptors does not silence the ionotropic receptor channel or the trigeminal-like pathways that detect thermal and humidity cues. This sensory compensation explains why many laboratory interventions, including repellents such as DEET and IR3535 and genetic manipulations of receptor co-receptors such as Orco, show reduced or context-dependent performance in the field. The review argues that intervention studies should evaluate whole-animal phenotypes and mosquito-human contact rates, not just responses at the receptor level, because the intact animal can route around a blocked pathway.

Ecological context is the second major caveat the authors raise for control strategies. Field studies consistently show that the effectiveness of attractant-baited traps, spatial repellents, and odor-based interventions depends on the local environment, the composition of competing host odors, wind conditions, and the species and physiological state of the local mosquito population. A lure that outperforms a human in a semi-field enclosure may fail in a village where natural host cues are abundant and varied. The review therefore proposes a tiered evaluation framework spanning receptor-level mechanisms, whole-animal behavior, effects on mosquito-human contact, and ultimately transmission or disease endpoints, and it warns that laboratory results should not be extrapolated to field performance without explicit testing across contexts.

The microbiome adds yet another layer of complexity. Skin microbiota shape the volatile profile that makes one human more attractive to mosquitoes than another, and the mosquito’s own microbial community can influence its olfactory sensitivity and feeding behavior. The review integrates this evidence into the multimodal framework, suggesting that microbiome-mediated variation in host odors and vector competence represents a modifiable component of the transmission cycle. Combined with the growing recognition that learning allows mosquitoes to adjust their host preferences based on experience, the picture that emerges is of a vector whose host-seeking behavior is plastic at multiple levels: neural, microbial, and experiential.

The review closes by generating testable predictions for active sensing, sensory compensation, infection-associated modulation, and the persistence of intervention effects across laboratory and field settings, and it identifies unresolved sites of neural convergence in the mosquito brain as priorities for future research. For a field in which mosquito-borne diseases such as malaria, dengue, and West Nile fever continue to impose enormous burdens, the message is clear: durable transmission control will come not from blocking a single cue but from understanding the full sensorimotor loop that connects a flying insect to its next blood meal. By mapping that loop, from plume-following flight to the final probing of the skin, and by specifying where pathogens intervene within it, the authors offer both a conceptual framework and a practical roadmap for the next generation of vector-control research.

Subject of Research: Multimodal sensory integration and active sensing in mosquito host recognition and its implications for pathogen transmission control

Article Title: Multimodal host recognition in mosquitoes: sensory integration, active sensing, and transmission control

Article References: Liu, Z., Shu, Z., Bai, Y., Zhang, T., Shi, H., Zhang, D., Liu, G., & Jin, Y. (2026). Multimodal host recognition in mosquitoes: sensory integration, active sensing, and transmission control. Parasites & Vectors. https://doi.org/10.1186/s13071-026-07702-9

Image Credits: AI Generated

DOI: 10.1186/s13071-026-07702-9

Keywords: mosquitoes, host seeking, multisensory integration, active sensing, carbon dioxide, odorant receptors, dengue virus, Zika virus, West Nile virus, pathogen-vector interactions, vector control, sensory neurobiology

The patient, who had been working in Malaysia, first fell ill with intermittent fever during his period of immigration there. Screening at that stage returned a positive result for dengue, a diagnosis that seemed unremarkable in a region where the dengue virus circulates intensely. Yet the fever refused to settle. Dengue is typically a self-limited, mosquitoborne viral illness in which the nonstructural protein 1, or NS1, antigen circulates in blood during the acute phase and clears within days to a couple of weeks as the immune response takes hold. In this patient, however, the fever persisted long enough that he was forced to return to Nepal, carrying with him a dengue label that would shape every subsequent clinical decision.

Back in South Asia, the diagnostic journey grew more tangled rather than less. During evaluation in India, clinicians confronting the patient’s prolonged febrile illness and laboratory abnormalities turned their suspicion toward a hematological malignancy, an understandable but ultimately erroneous interpretation. Visceral leishmaniasis, caused by the protozoan parasite Leishmania donovani and transmitted by phlebotomine sand flies, is famous for mimicking other conditions: it produces splenomegaly, hepatomegaly, pancytopenia, weight loss, and relentless fever, a constellation that can indeed resemble lymphoma or leukemia on superficial review. The misdirection meant that the true diagnosis remained unmade while the underlying parasitic infection continued its indolent destruction of the patient’s immune defenses.

It was only after a third discrete febrile episode that visceral leishmaniasis was finally identified. By that point, however, the case had acquired another layer of complexity: the dengue NS1 antigen was still detectable, a strikingly prolonged persistence for a protein that normally vanishes as acute infection resolves. The reporting team argues that the concomitant infections appear to have driven this prolonged persistence of dengue features and, in parallel, may have propelled a previously asymptomatic Leishmania infection into symptomatic, life-threatening visceral disease. The immunology of such an interaction is plausible if speculative: dengue and Leishmania both manipulate mononuclear phagocytes, and the profound cell-mediated immunosuppression of active visceral leishmaniasis could plausibly impair clearance of viral antigens, while the viral insult could tip a controlled parasitic infection toward clinical manifestness.

Treatment brought the next setback. The patient received liposomal amphotericin B, or LAMB, the recommended first-line therapy for visceral leishmaniasis in many endemic settings, prized for its potency against Leishmania parasites sequestered in the spleen, liver, and bone marrow. Six doses were administered, yet the patient demonstrated no adequate response. Relapse followed the initial course, an outcome that forced the clinical team to reconsider both the diagnosis and the therapeutic strategy. Drug failure in visceral leishmaniasis can arise from host immunosuppression, parasite resistance, inadequate drug exposure, or an incorrect initial diagnosis, and in a patient whose dengue serology remained abnormal, every one of those possibilities demanded attention.

The decisive moment in the odyssey arrived through careful serial testing. When repeat assays for dengue NS1 antigen, dengue-specific IgM, and dengue-specific IgG all finally returned negative results, the diagnostic fog began to lift. With the dengue infection definitively behind him and active visceral leishmaniasis confirmed as the driver of his ongoing febrile illness, the clinicians turned to miltefosine, an oral alkylphosphocholine originally developed as an anticancer agent and later repurposed as a leishmanicidal drug. The intervention proved highly effective: the patient’s visceral leishmaniasis resolved, closing a clinical narrative that had spanned Malaysia, India, and Nepal and involved misdiagnosis, failed therapy, and relapse along the way.

The case carries technical lessons that extend well beyond one patient. Rapid diagnostic tests for dengue, including NS1 antigen detection and IgM/IgG antibody assays, are cornerstones of febrile illness triage in low- and middle-income countries, but their performance assumes a typical immunocompetent, monoinfected host. When a second pathogen remodels the immune landscape, antigen clearance kinetics can change in ways that no single test anticipates. Conversely, the rK39 rapid diagnostic test for visceral leishmaniasis, which the authors highlight among their keywords, detects antibodies that may be absent early or inconsistent across the disease course. A febrile traveler or migrant whose work history spans multiple endemic regions therefore represents a diagnostic worst case for panel-based, single-pathogen thinking, and the authors argue that the case demonstrates a clear need for better diagnostic tools and management strategies specifically designed for coinfections.

Epidemiologically, the report sits at the intersection of two burdens of the same geography. Visceral leishmaniasis remains endemic in the lowland plains of Nepal, India, and Bangladesh, where elimination programs have driven incidence down but not to zero, and dengue has expanded dramatically across the same territories in recent decades, with Nepal experiencing increasingly large seasonal epidemics. Migrant workers such as this patient, who move between endemic countries for employment, occupy a distinctive risk niche: they may acquire one infection in one country, carry it across borders, and have it diagnosed or misdiagnosed in another, fragmenting the clinical record that any single physician depends upon. The three-country trajectory recorded in this report illustrates how health systems that do not share records can each hold a partial truth about the same patient.

The authors caution, appropriately, that a single case report cannot establish the mechanism by which dengue and Leishmania interacted in this individual, only that the association coincided with atypical antigen persistence, disease progression, and treatment failure. Still, the therapeutic implication is concrete: in patients with visceral leishmaniasis who fail liposomal amphotericin B, especially those with concurrent or recent viral infections, clinicians should consider rescue therapy with miltefosine and should pursue serial virological testing to clarify what is resolving and what is not. The patient’s consent, anonymization of identifying details, ethical approval from the Nepal Health Research Council, and adherence to the Declaration of Helsinki documented in the report reflect the care taken to convert one man’s prolonged illness into a lesson for the clinics of the tropical world.

Subject of Research: Leishmania-dengue virus coinfection with persistent NS1 antigenemia complicating visceral leishmaniasis diagnosis and treatment

Article Title: Persistent dengue NS1 antigen in a patient with visceral leishmaniasis: A diagnostic and therapeutic odyssey

Article References: Chalise, B. S., Shrestha, S., Sapkota, A. S., Bajracharya, M., Basaula, Y. N., Bras‑Goncalves, R., & Manandhar, K. D. (2026). Persistent dengue NS1 antigen in a patient with visceral leishmaniasis: A diagnostic and therapeutic odyssey. BMC Infectious Diseases. https://doi.org/10.1186/s12879-026-14469-y

Image Credits: AI Generated

DOI: 10.1186/s12879-026-14469-y

Keywords: visceral leishmaniasis, dengue virus, NS1 antigen, coinfection, miltefosine, liposomal amphotericin B, rK39 RDT, neglected tropical diseases, Nepal, migrant workers, case report, diagnostic challenges

The investigation began with a deceptively simple behavioral question: given a choice, do mosquitoes prefer well-fed or undernourished hosts? Using controlled dietary restriction in laboratory mice, the researchers ran paired preference assays with multiple medically important mosquito species and found a consistent and striking result. Female mosquitoes preferentially oriented toward and fed on the undernourished animals. Because host-seeking in mosquitoes is governed by a layered integration of sensory cues, including carbon dioxide, heat, humidity, vision, and above all odor, the team reasoned that nutritional status might be altering the volatile chemical signature that hosts emit into the air. Behavioral experiments in which cues were selectively masked or manipulated confirmed that the differential attraction was olfactory in nature, pointing the investigators toward the skin surface as the source of the signal.

Gas chromatography-mass spectrometry analysis of volatile emissions from the skin of undernourished mice revealed a specific chemical culprit: elevated levels of volatile aldehydes. When these aldehydes were presented to mosquitoes in isolation or applied to otherwise unattractive hosts, they acted as potent attractants, reproducing the preference pattern observed with live undernourished animals. The aldehydes were not produced by the hosts themselves. Instead, they emerged from an unexpected intermediate player, the community of commensal bacteria that colonizes the skin. Sequencing and culture-based analyses showed that undernutrition was associated with a marked dysbiosis of the skin microbiota, with certain bacterial taxa proliferating to excessive densities and shifting their metabolic output toward aldehyde production. In effect, the mosquito-attractive odor was a microbial byproduct, released in greater quantities whenever the host’s nutritional state deteriorated.

The next question was mechanistic: why would a poor diet destabilize the skin microbiome in the first place? The answer lay in the dermal sebaceous glands, the microscopic structures that secrete sebum, a lipid-rich film coating the outer skin. The researchers found that undernutrition impaired the secretion of free fatty acids from these glands. Free fatty acids are not merely structural components of the skin barrier; they possess well-documented antimicrobial activity, suppressing the overgrowth of bacteria on the surface. With fatty acid output diminished, this chemical shield weakened, and commensal skin bacteria expanded unchecked. The team demonstrated this causal chain experimentally: restoring antimicrobial fatty acids, or reducing bacterial loads with antibiotics, both reversed the microbiota expansion and abolished the excess aldehyde emissions, thereby eliminating the heightened attractiveness of undernourished mice to mosquitoes.

To rule out confounding factors such as fur and general husbandry, the researchers extended their experiments to SKH1 hairless mice, in which skin surface chemistry can be sampled directly. The same pattern held. Undernutrition drove sebaceous dysfunction, skin bacterial overgrowth, dysbiosis, elevated aldehyde production, and increased mosquito attraction, providing a clean replication of the mechanism in a model system where the skin itself is fully accessible to analysis. The authors also showed that the effect operates in both directions of the transmission cycle. Undernourished mice were not only more likely to be bitten; they were also more susceptible to infection with dengue virus (DENV), developing higher viral loads. When mosquitoes fed on these viremic, undernourished hosts, the insects acquired virus more efficiently, and when infected mosquitoes subsequently fed, transmission onward was enhanced.

This dual effect, increasing both the probability that a host infects a mosquito and the probability that an infected mosquito infects a host, is what gives the finding its epidemiological weight. Vector-borne pathogens depend on a chain of events, each of which carries a probability, and interventions that raise or lower any single link can have outsized effects on the reproduction of an epidemic. By strengthening two links at once, host attractiveness and host infectivity, undernutrition may function as a critical modulator of transmission efficacy at the population level. The researchers present a model in which the prevalence of undernourished individuals within a community critically shapes the intensity of arbovirus circulation, a proposition with obvious implications for the geography of disease burden.

The human relevance of the mechanism was tested directly. In a cohort of undernourished human subjects, the team documented skin microbiota alterations mirroring those seen in mice, alongside elevated emission of volatile aldehydes from the skin. In behavioral assays, undernourished participants were more attractive to mosquitoes than their well-nourished counterparts. These converging lines of evidence, spanning rodent models, chemical analytics, microbiology, and human physiology, elevate the study beyond a correlation and support a coherent biological narrative: caloric and nutritional insufficiency suppresses sebaceous antimicrobial output, permits bacterial overgrowth, changes the skin’s volatile signature, and rewires the chemical conversation between humans and mosquitoes.

The broader context is sobering. Undernutrition and mosquito-borne disease overlap extensively across the tropics and subtropics, where food insecurity, poverty, and endemic dengue, malaria, Zika, and other arboviruses co-occur. Earlier work from the same field had established that host nutritional status can influence arbovirus virulence and evolution, and that host serum iron modulates dengue virus acquisition by mosquitoes, indicating that diet intersects with vector-borne transmission at multiple physiological levels. The new study adds skin chemistry and microbiota to this list and identifies a targetable axis. If aldehyde emissions and bacterial overgrowth mediate the effect, then interventions that restore sebaceous antimicrobial lipids, modulate the skin microbiome, or neutralize aldehyde cues could, in principle, reduce the excess bite risk borne by malnourished individuals, complementing bed nets, repellents, and vaccines.

For public health planners, the message is that nutritional support programs may double as disease control programs. Addressing undernutrition in regions where mosquito-borne pathogens are endemic would not only alleviate the direct morbidity and mortality of deficiency itself, but could also dampen the transmission cycles that keep those pathogens circulating. The authors argue that undernutrition should be recognized as a key driver of mosquito-borne disease transmission in nature, a reframing that places nutrition squarely within the toolkit of vector-borne disease control. As climate change expands the range of Aedes and Anopheles vectors and as food insecurity persists or worsens in many endemic regions, understanding and disrupting the metabolic link between diet, skin microbiota, and mosquito behavior may prove essential to bending the curves of some of the world’s most persistent epidemics.

Subject of Research: How undernutrition increases host attractiveness to mosquitoes and promotes the transmission of mosquito-borne diseases through skin microbiota changes.

Article Title: Undernutrition enhances host attractiveness to mosquitoes and transmission of mosquito-borne diseases

Article References: Wang, M., Song, X., Zhu, Y., Niu, J., Wang, G., Wang, Y., Xiao, H., Lei, D., Wu, T., Liu, L., Wang, P., Wang, J., & Cheng, G. (2026). Undernutrition enhances host attractiveness to mosquitoes and transmission of mosquito-borne diseases. Cell Research. https://doi.org/10.1038/s41422-026-01291-z

Image Credits: AI Generated

DOI: 10.1038/s41422-026-01291-z

Keywords: undernutrition, mosquito-borne diseases, dengue virus, skin microbiota, volatile aldehydes, sebaceous glands, fatty acids, host-seeking behavior, arboviruses, vector biology, malnutrition, disease transmission