bioRxiv ScienceSearch

bioRxiv · 10.1101/2021.01.22.427761

Forecasting the future risk of dengue epidemics facing climate change in New Caledonia, South Pacific.

Abstract

BackgroundDengue dynamics result from the complex interaction between the virus, the host and the vector, all being under the influence of the environment. Several studies have explored the link between climate and dengue outbreaks in New Caledonia. None of them have explored the evolution of the dengue outbreak risk facing climate change. Methodology/Principal FindingsIn this study we chose the threshold time dependent reproduction number (Rt) as the modeling target to focus on time frames suitable for outbreak growths. A weekly statistical model of dengue outbreak risk (i.e. dengue outbreak probability) based on climate variables was developed using support vector machines (SVM) and then used in combination with CMIP5 projections of rainfall and temperature to estimate the future evolution of seasonal weekly risk and the inter-annual yearly risk of dengue outbreak up to the year 2100. The weekly risk of dengue outbreak is estimated using the number of days with maximal temperature exceeding 30.8{degrees}C during 80 days preceding the predicted week and the mean of precipitation during 60 days preceding the predicted week. According to the SVM model and to the worst greenhouse gas emission scenario projection (RCP8.5), the time frame suitable for epidemic growth will gain one month starting in November instead of December and the yearly risk of dengue outbreak occurrence increases regularly up to 2100 and reach a probability of 1 around 2080, making the dynamic of dengue fever endemic in New Caledonia. Conclusions/SignificanceA complete method to assess seasonal and inter annual variability of the risk of dengue outbreaks with respect to climate change is proposed. We conclude that climate change is likely to increase the risk of dengue in New-Caledonia (the other non climatic parameters remaining constant) in terms of both frequency of outbreak and temporal spread of the outbreak. Author summaryDengue virus is transmitted to human through the bite of an Aedes mosquito vector. Dengue fever is a worldwide public health concern, especially on tropical and subtropical countries. Over the last decade, the toll of dengue fever has increased in New Caledonia, raising questions about the future of the disease in this French island territory located in the South Pacific. Climate has a strong influence on dengue through its influence on the ecology of the vector and the viral cycle. Several studies have explored the link between climate and dengue in New Caledonia, with the aim of explaining and predicting dengue outbreaks. None of these studies have explored the possible outcome climate change will have on the risk of dengue fever in New Caledonia. This is the goal of this study, through projections of rainfall and temperature and the selection of an appropriate prediction target for our statistical model, we assess the climate-induced risk of dengue outbreaks up to the 2100 horizon. We prove that the inter-annual risk of dengue outbreaks in New Caledonia will raise, according to all the greenhouse gas emission scenarios and according to the high emission scenario, dengue fever will become an endemic disease in New Caledonia.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

OCHIDA, N., Mangeas, M., Myrielle, D.-R., Dutheil, C., Forfait, C., Pelletier, A., Descloux, E., Menkes, C.. 2021-01-22. Forecasting the future risk of dengue epidemics facing climate change in New Caledonia, South Pacific.. https://doi.org/10.1101/2021.01.22.427761

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

A conserved cysteine-histidine-glutamate metal site identifies DUF501 (Rv1025), an essential uncharacterised protein family of Mycobacterium tuberculosis, as a candidate metalloenzyme and drug target

A substantial fraction of the Mycobacterium tuberculosis proteome remains functionally uncharacterised. Rv1025, a 155-residue protein carrying the domain of unknown function DUF501 (Pfam PF04417), is essential by transposon mutagenesis and vulnerable by CRISPR interference, an attractive but neglected drug target, yet has never been functionally described. The family (4,370 proteins, no Gene Ontology term, no solved structure) is uncharacterised across all organisms and essential in three Actinobacterial genera. A Foldseek search of the AlphaFold model against complete structural databases finds no significant homolog, indicating a novel fold. The operon eno-divIC-Rv1025-ppx2 is conserved across the Actinobacteria phylum, yet AlphaFold-Multimer finds no direct complex between Rv1025 and its neighbour DivIC. Instead, conservation across 8,700 homologous sequences reveals a near-invariant Cys113-His115-Glu59 cluster forming a pocket. Holo AlphaFold3 predictions with Zn, Fe and Mn confidently place a divalent metal on this triad at 2.25-2.47 A; mutating the triad relocates the metal, and an independent backbone-geometry predictor recovers the same site, confirming specificity. The triad is universal across the family: present in all 1,472 near-complete bacterial sequences of the Pfam alignment, with no non-conservative substitution among the 2,228 sequences examined, a defining feature of bacterial DUF501 rather than a mycobacterial peculiarity. We propose that DUF501 is a metal-binding protein and candidate metalloenzyme, the first functional hypothesis for this family, whose conserved, essential metal pocket is a promising drug target. As the predictions build on a conservation-defined site within a fully computational study, they are supportive rather than proof of metal occupancy and warrant experimental validation.

microbiology

Mycoplasmal endosymbionts of Trichomonas vaginalis are associated with reduced risk for Chlamydia trachomatis endometrial infection in asymptomatic, coinfected, women.

Trichomonas vaginalis is a protozoan parasite that causes trichomoniasis, the most common curable non-viral sexually transmitted infection, and Chlamydia trachomatis is a bacterial pathogen that can ascend to the upper genital tract and cause pelvic inflammatory disease, infertility, and ectopic pregnancy. T. vaginalis harbors bacterial endosymbionts, including Candidatus Malacoplasma girerdii, an obligate symbiont, and Metamycoplasma hominis, which can live freely or symbiotically. In a 16S rRNA sequencing study of the cervicovaginal microbiome of women at high risk for chlamydial infection, Ca. M. girerdii abundance was one of 13 features predicting lack of chlamydial spread to the endometrium, despite no direct association between T. vaginalis infection and reduced chlamydial ascension. Investigating the relationship between these microorganisms further, we found that T. vaginalis vaginal abundance correlated positively with chlamydial burden in women whose infection was confined to the cervix, while a nonsignificant inverse relationship was seen in women with endometrial spread. Among participants with high chlamydial burden, Ca. M. girerdii was detected exclusively in women without endometrial infection. Both endosymbionts trended toward more frequent detection, and higher abundance, in coinfected women without endometrial spread, while M. hominis abundance correlated strongly with T. vaginalis burden in this group. These findings suggest that mycoplasmal endosymbionts of T. vaginalis, rather than T. vaginalis itself, are microbial factors limiting chlamydial ascension, and point to a three-way interaction between parasite, endosymbiont, and bacterial pathogen that shapes upper genital tract C. trachomatis infection risk.

microbiology

Understanding the physiological alterations of Vibrio cholerae upon exposure to L-ascorbic acid

The scourge of cholera remains a major global public health threat. It affects up to 4 million people worldwide and causes tens of thousands of deaths each year. The disease is experiencing a concerning resurgence in many parts of Africa, the Middle East, and Asia. To effectively tackle cholera and circumvent rising antimicrobial resistance, targeted biological and preventive approaches, complementing traditional rehydration, are urgently needed. In this regard, our group has demonstrated the efficacy of L-ascorbic acid in controlling the growth and pathogenesis of Vibrio cholerae in vitro. The present work further provides a mechanistic elucidation of the L-ascorbic acid-mediated physiological changes in V. cholerae and also bolsters such a non-antibiotic approach to control cholera.

microbiology