Volume 12 · Issue 01 · 2023

Socioeconomic status (SES) inequity was recognized as a driver of some certain infectious diseases. However, few studies evaluated the association between SES and the burden of overall infections, and even fewer identified preventable mediators. This study aimed to assess the association between SES and overall infectious diseases burden, and the potential roles of factors including lifestyle, environmental pollution, chronic disease history.

We included 401,009 participants from the UK Biobank (UKB) and defined the infection status for each participant according to their diagnosis records. Latent class analysis (LCA) was used to define SES for each participant. We further defined healthy lifestyle score, environment pollution score (EPS) and four types of chronic comorbidities. We used multivariate logistic regression to test the associations between the four above covariates and infectious diseases. Then, we performed the mediation and interaction analysis to explain the relationships between SES and other variables on infectious diseases. Finally, we employed seven types of sensitivity analyses, including considering the Townsend deprivation index as an area level SES variable, repeating our main analysis for some individual or composite factors and in some subgroups, as well as in an external data from the US National Health and Nutrition Examination Survey, to verify the main results.

In UKB, 60,771 (15.2%) participants were diagnosed with infectious diseases during follow-up. Lower SES [odds ratio (OR) = 1.5570] were associated with higher risk of overall infections. Lifestyle score mediated 2.9% of effects from SES, which ranged from 2.9 to 4.0% in different infection subtypes, while cardiovascular disease (CVD) mediated a proportion of 6.2% with a range from 2.1 to 6.8%. In addition, SES showed significant negative interaction with lifestyle score (OR = 0.8650) and a history of cancer (OR = 0.9096), while a significant synergy interaction was observed between SES and EPS (OR = 1.0024). In subgroup analysis, we found that males and African (AFR) with lower SES showed much higher infection risk. Results from sensitivity and validation analyses showed relative consistent with the main analysis.

Low SES is shown to be an important risk factor for infectious disease, part of which may be mediated by poor lifestyle and chronic comorbidities. Efforts to enhance health education and improve the quality of living environment may help reduce burden of infectious disease, especially for people with low SES.

China is progressing towards the goal of schistosomiasis elimination, but there are still some problems, such as difficult management of infection source and snail control. This study aimed to develop deep learning models with high-resolution remote sensing images for recognizing and monitoring livestock bovine, which is an intermediate source of Schistosoma japonicum infection, and to evaluate the effectiveness of the models for real-world application.

The dataset of livestock bovine’s spatial distribution was collected from the Chinese National Platform for Common Geospatial Information Services. The high-resolution remote sensing images were further divided into training data, test data, and validation data for model development. Two recognition models based on deep learning methods (ENVINet5 and Mask R-CNN) were developed with reference to the training datasets. The performance of the developed models was evaluated by the performance metrics of precision, recall, and F1-score.

A total of 50 typical image areas were selected, 1125 bovine objectives were labeled by the ENVINet5 model and 1277 bovine objectives were labeled by the Mask R-CNN model. For the ENVINet5 model, a total of 1598 records of bovine distribution were recognized. The model precision and recall were 81.9% and 80.2%, respectively. The F1 score was 0.81. For the Mask R-CNN mode, 1679 records of bovine objectives were identified. The model precision and recall were 87.3% and 85.2%, respectively. The F1 score was 0.87. When applying the developed models to real-world schistosomiasis-endemic regions, there were 63 bovine objectives in the original image, 53 records were extracted using the ENVINet5 model, and 57 records were extracted using the Mask R-CNN model. The successful recognition ratios were 84.1% and 90.5% for the respectively developed models.

The ENVINet5 model is very feasible when the bovine distribution is low in structure with few samples. The Mask R-CNN model has a good framework design and runs highly efficiently. The livestock recognition models developed using deep learning methods with high-resolution remote sensing images accurately recognize the spatial distribution of livestock, which could enable precise control of schistosomiasis.

With the variability in emerging data, guidance on the isolation duration for patients with coronavirus disease 2019 (COVID-19) due to the Omicron variant is controversial. This study aimed to determine the predictors of prolonged viral RNA shedding in patients with non-severe COVID-19 and construct a nomogram to predict patients at risk of 14-day PCR conversion failure.

Adult patients with non-severe COVID-19 were enrolled from three hospitals of eastern China in Spring 2022. Viral shedding time (VST) was defined as either the day of the first positive test or the day of symptom onset, whichever was earlier, to the date of the first of two consecutively negative PCR tests. Patients from one hospital (Cohort I, n = 2033) were randomly grouped into training and internal validation sets. Predictors of 14-day PCR conversion failure were identified and a nomogram was developed by multivariable logistic regression using the training dataset. Two hospitals (Cohort II, n = 1596) were used as an external validation set to measure the performance of this nomogram.

Of the 2033 patients from Cohort I, the median VST was 13.0 (interquartile range: 10.0-16.0) days; 716 (35.2%) lasted > 14 days. In the training set, increased age [per 10 years, odds ratio (OR) = 1.29, 95% confidence interval (CI): 1.15-1.45, P < 0.001] and high Charlson comorbidity index (OR = 1.25, 95% CI: 1.08-1.46, P = 0.004) were independent risk factors for VST > 14 days, whereas full or boosted vaccination (OR = 0.63, 95% CI: 0.42-0.95, P = 0.028) and antiviral therapy (OR = 0.56, 95% CI: 0.31-0.96, P = 0.040) were protective factors. These predictors were used to develop a nomogram to predict VST > 14 days, with an area under the ROC curve (AUC) of 0.73 in the training set (AUC, 0.74 in internal validation set; 0.76 in external validation set).

Older age, increasing comorbidities, incomplete vaccinations, and lack of antiviral therapy are risk factors for persistent infection with Omicron variant for > 14 days. A nomogram based on these predictors could be used as a prediction tool to guide treatment and isolation strategies.

Cerebral malaria (CM) is a neuropathology which remains one of the deadliest forms of malaria among African children. The kinetics of the pathophysiological mechanisms leading to neuroinflammation and the death or survival of patients during CM are still poorly understood. The increasing production of cytokines, chemokines and other actors of the inflammatory and oxidative response by various local actors in response to neuroinflammation plays a major role during CM, participating in both the amplification of the neuroinflammation phenomenon and its resolution. In this study, we aimed to identify risk factors for CM death among specific variables of inflammatory and oxidative responses to improve our understanding of CM pathogenesis.

Children presenting with CM (n = 70) due to P. falciparum infection were included in southern Benin and divided according to the clinical outcome into 50 children who survived and 20 who died. Clinical examination was complemented by fundoscopic examination and extensive blood biochemical analysis associated with molecular diagnosis by multiplex PCR targeting 14 pathogens in the patients' cerebrospinal fluid to rule out coinfections. Luminex technology and enzyme immunoassay kits were used to measure 17 plasma and 7 urinary biomarker levels, respectively. Data were analysed by univariate analysis using the nonparametric Mann-Whitney U test and Pearson’s Chi2 test. Adjusted and multivariate analyses were conducted separately for plasma and urinary biomarkers to identify CM mortality risk factors.

Univariate analysis revealed higher plasma levels of tumour necrosis factor (TNF), interleukin-1beta (IL-1β), IL-10, IL-8, C-X-C motif chemokine ligand 9 (CXCL9), granzyme B, and angiopoietin-2 and lower urinary levels of prostanglandine E2 metabolite (PGEM) in children who died compared to those who survived CM (Mann-Whitney U-test, P-values between 0.03 and < 0.0001). The multivariate logistic analysis highlighted elevated plasma levels of IL-8 as the main risk factor for death during CM (adjusted odd ratio = 14.2, P-value = 0.002). Values obtained during follow-up at D3 and D30 revealed immune factors associated with disease resolution, including plasma CXCL5, C-C motif chemokine ligand 17 (CCL17), CCL22, and urinary 15-F2t-isoprostane.

The main risk factor of death during CM was thus elevated plasma levels of IL-8 at inclusion. Follow-up of patients until D30 revealed marker profiles of disease aggravation and resolution for markers implicated in neutrophil activation, endothelium activation and damage, inflammatory and oxidative response. These results provide important insight into our understanding of CM pathogenesis and clinical outcome and may have important therapeutic implications.

The Ibizan Hound is a canine breed native to the Mediterranean region, where leishmaniasis is an endemic zoonosis. Several studies indicate a low prevalence of this disease in Ibizan Hound dogs, whereas other canine breeds present a high prevalence. However, the underlying molecular mechanisms still remain unknown. The aim of this work is to analyse the relationship between serum levels of cytokines and the genomic profiles in two canine breeds, Ibizan Hound (resistant canine breed model) and Boxer (susceptible canine breed model).

In this study, we analyse the haplotypes of genes encoding cytokines related to immune response of Leishmania infantum infection in twenty-four Boxers and twenty-eight Ibizan Hounds apparently healthy using CanineHD DNA Analysis BeadChip including 165,480 mapped positions. The haplo.glm extension of haplo.score was used to perform a General Linear Model (GLM) regression to estimate the magnitude of individual haplotype effects within each cytokine.

Mean levels of interferon gamma (IFN-γ), interleukin 2 (IL-2) and IL-18 in Boxer dogs were 0.19 ± 0.05 ng/ml, 46.70 ± 4.54 ng/ml, and 36.37 ± 30.59 pg/ml, whereas Ibizan Hound dogs present 0.49 ± 0.05 ng/ml, 64.55 ± 4.54 ng/ml, and 492.10 ± 31.18 pg/ml, respectively. The GLM regression shows fifteen haplotypes with statistically significant effect on the cytokine serum levels (P < 0.05). The more relevant are IL6-CGAAG and IFNG-GCA haplotypes, which increase and decrease the IL-2, IL-8 and IFN-γ serum levels, respectively.

Haplotypes in the IFNG and IL6 genes have been correlated to serum levels of IFN-γ, IL-2 and IL-18, and a moderate effect has been found on IL8 haplotype correlated to IL-8 and IL-18 serum levels. The results indicate that the resistance to L. infantum infection could be a consequence of certain haplotypes with a high frequency in the Ibizan Hound dog breed, while susceptibility to the disease would be related to other specific haplotypes, with high frequency in Boxer. Future studies are needed to elucidate whether these differences and haplotypes are related to different phenotypes in immune response and expression gene regulation to L. infantum infections in dogs and their possible application in new treatments and vaccines.

Leprosy is an infectious disease caused by Mycobacterium leprae and remains a source of preventable disability if left undetected. Case detection delay is an important epidemiological indicator for progress in interrupting transmission and preventing disability in a community. However, no standard method exists to effectively analyse and interpret this type of data. In this study, we aim to evaluate the characteristics of leprosy case detection delay data and select an appropriate model for the variability of detection delays based on the best fitting distribution type.

Two sets of leprosy case detection delay data were evaluated: a cohort of 181 patients from the post exposure prophylaxis for leprosy (PEP4LEP) study in high endemic districts of Ethiopia, Mozambique, and Tanzania; and self-reported delays from 87 individuals in 8 low endemic countries collected as part of a systematic literature review. Bayesian models were fit to each dataset to assess which probability distribution (log-normal, gamma or Weibull) best describes variation in observed case detection delays using leave-one-out cross-validation, and to estimate the effects of individual factors.

For both datasets, detection delays were best described with a log-normal distribution combined with covariates age, sex and leprosy subtype [expected log predictive density (ELPD) for the joint model: -1123.9]. Patients with multibacillary (MB) leprosy experienced longer delays compared to paucibacillary (PB) leprosy, with a relative difference of 1.57 [95% Bayesian credible interval (BCI): 1.14-2.15]. Those in the PEP4LEP cohort had 1.51 (95% BCI: 1.08-2.13) times longer case detection delay compared to the self-reported patient delays in the systematic review.

The log-normal model presented here could be used to compare leprosy case detection delay datasets, including PEP4LEP where the primary outcome measure is reduction in case detection delay. We recommend the application of this modelling approach to test different probability distributions and covariate effects in studies with similar outcomes in the field of leprosy and other skin-NTDs.

The heterogeneity of COVID-19 spread dynamics is determined by complex spatiotemporal transmission patterns at a fine scale, especially in densely populated regions. In this study, we aim to discover such fine-scale transmission patterns via deep learning.

We introduce the notion of TransCode to characterize fine-scale spatiotemporal transmission patterns of COVID-19 caused by metapopulation mobility and contact behaviors. First, in Hong Kong, China, we construct the mobility trajectories of confirmed cases using their visiting records. Then we estimate the transmissibility of individual cases in different locations based on their temporal infectiousness distribution. Integrating the spatial and temporal information, we represent the TransCode via spatiotemporal transmission networks. Further, we propose a deep transfer learning model to adapt the TransCode of Hong Kong, China to achieve fine-scale transmission characterization and risk prediction in six densely populated metropolises: New York City, San Francisco, Toronto, London, Berlin, and Tokyo, where fine-scale data are limited. All the data used in this study are publicly available.

The TransCode of Hong Kong, China derived from the spatial transmission information and temporal infectiousness distribution of individual cases reveals the transmission patterns (e.g., the imported and exported transmission intensities) at the district and constituency levels during different COVID-19 outbreaks waves. By adapting the TransCode of Hong Kong, China to other data-limited densely populated metropolises, the proposed method outperforms other representative methods by more than 10% in terms of the prediction accuracy of the disease dynamics (i.e., the trend of case numbers), and the fine-scale spatiotemporal transmission patterns in these metropolises could also be well captured due to some shared intrinsically common patterns of human mobility and contact behaviors at the metapopulation level.

The fine-scale transmission patterns due to the metapopulation level mobility (e.g., travel across different districts) and contact behaviors (e.g., gathering in social-economic centers) are one of the main contributors to the rapid spread of the virus. Characterization of the fine-scale transmission patterns using the TransCode will facilitate the development of tailor-made intervention strategies to effectively contain disease transmission in the targeted regions.

The term virus 'spillover’ embodies a highly complex phenomenon and is often used to refer to viral transmission from a primary reservoir host to a new, naïve yet susceptible and permissive host species. Spillover transmission can result in a virus becoming pathogenic, causing disease and death to the new host if successful infection and transmission takes place.

The scientific literature across diverse disciplines has used the terms virus spillover, spillover transmission, cross-species transmission, and host shift almost indistinctly to imply the complex process of establishment of a virus from an original host (source/donor) to a naïve host (recipient), which have close or distant taxonomic or evolutionary ties. Spillover transmission may result in unsuccessful onward transmission, if the virus dies off before propagation. Alternatively, successful viral establishment in the new host can occur if subsequent secondary transmission among individuals of the same novel species and among other sympatric susceptible species occurred. As such, virus spillover transmission is a common yet highly complex phenomenon that encompasses multiple subtle stages that can be deconstructed to be studied separately to better understand the drivers of disease emergence. Rabies virus (RABV) is a well-documented viral pathogen which still inflicts heavy impact on humans, companion animals, wildlife, and livestock throughout Latin America due substantial spatial temporal and ecological—natural and expansional—overlap with several virus reservoir hosts. Thereby, the rabies disease system represents a robust avenue through which the drivers and uncertainties surrounding spillover transmission can be unravel at its different subtle stages to better understand how they may be affected by coarse, medium, and fine scale variables.

The continued study of viral spillover transmission necessitates the elucidation of its complexities to better assess the cross-scale impacts of ecological forces linked to the propensity of spillover success. Improving capacities to reconstruct and predict spillover transmission would prevent public health impacts on those most at risk populations across the globe.