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Summary Introduction Cyclical fluctuations in host immunity have been proposed as a driver of respiratory infection seasonality, however few studies have attempted to directly assess whether or not seasonal immune modulation occurs in humans. Materials and methods We reviewed studies assessing immune status at different times of the year, restricting our review to studies assessing any of the following three biomarkers: antibody responses following vaccination, delayed-type hypersensitivity responses following skin testing, and clinical responses following experimental infection. Results After systematic review and critical appraisal of the literature, six separate studies were available for final discussion. These results indicate that human immunity does vary by season. In the tropical setting of West Africa, both cell mediated and humoral immune responses appear to be reduced in children during the rainy season. In the tropical setting of Bangladesh, cell mediated immune responses also appear to be reduced in children during the rainy season. In the temperate setting of Russia, resistance to influenza infection appears to be reduced in young adults during winter. Conclusions Seasonal variation in immunity appears to occur in humans, and it is plausible that this variation may contribute to the seasonality of respiratory infections. Further research to assess the extent of seasonal immune modulation is required. We outline a number of recommendations to minimise bias in future studies.

The role of the environment in the spread of respiratory infections is poorly understood, and consequently probably underappreciated. To improve our understanding of the environmental drivers of respiratory syncytial virus (RSV) transmission, we examined RSV seasonality in two settings with unusual seasonal patterns: The Gambia (where RSV epidemics occur at different times of the year) and Southeast Florida (where RSV seasonality differs from the rest of mainland USA). We used published data to correlate the seasonality of RSV with rainfall and child nutrition in the Gambia, and with rainfall and temperature in Florida. In the Gambia, RSV incidence was more strongly and more consistently correlated with child nutrition (r = − 0.73 [95%CI − 0.90 to − 0.38]) than with rainfall (r = 0.37 [95%CI 0.20 to 0.52]). In Southeast Florida RSV incidence was strongly correlated with rainfall two months previously (r = 0.65 [95%CI 0.40 to 0.81]) compared to North Florida where RSV incidence was strongly correlated with temperature (r = − 0.75 [95%CI − 0.87 to − 0.56]). We propose that nutrition is the dominant environmental driver of RSV seasonality in the Gambia, while rainfall is the dominant driver of RSV seasonality in Southeast Florida. This reinforces the importance of an ecological scale understanding of disease transmission: only with such an evidence base can setting-specific recommendations be made for public health interventions that are targeted for maximum efficacy. Refereed/Peer-reviewed

Objective: Respiratory syncytial virus (RSV) is most common during the rainy season in a number of low- to middle-income tropical settings, a pattern driven by seasonal changes in climate and nutrition. We investigated the seasonality of RSV in the high-income tropical setting of North Queensland, Australia. Methods: We used RSV hospital admissions data from Cairns and Townsville to assess the seasonality of RSV. We examined the seasonal scale associations between selected meteorological exposures and RSV admissions using cross-correlation of weekly data. Results: In both Cairns and Townsville, RSV admissions were highest in the latter half of the rainy season. In Cairns, RSV admissions were most strongly correlated with rainfall four weeks previously. In Townsville, RSV admissions were most strongly correlated with rainfall six weeks previously. Conclusions: The seasonality of RSV in the tropical setting of North Queensland appears to be driven by seasonal variations in rainfall. Further research is needed to assess the impact of climate on RSV incidence in the tropics.

Background: Longitudinal information examining the effect of poor infant growth on respiratory syncytial virus (RSV) severity is limited. Children hospitalized with RSV lower respiratory infection represent those at the severe end of the disease spectrum. Conclusions: Poor infant growth increases the risk for severe RSV infection leading to hospitalization. Methods: We followed up a cohort of 12,191 infants enrolled in a previous pneumococcal vaccine trial in Bohol, Philippines. Exposure measures were weight for age z-score at the first vaccination visit (median age 1.8 months) as well as the growth (the difference in weight for age z-score) between the first and third vaccination visits. The outcome was hospitalization with RSV lower respiratory infection. Results: Children with a weight for age z-score ≤ −2 at their first vaccination visit had the highest rate of hospitalization with RSV lower respiratory infection, but this association was only evident in children whose mothers had >10 years of education (hazard ratio: 3.38; 95% confidence interval: 1.63-6.98). Children who had lower than median growth between their first and third vaccinations had a higher rate of RSV-associated hospitalization than those with growth above the median (hazard ratio: 1.34; 95% confidence interval: 1.02-1.76). Refereed/Peer-reviewed

Children with poor nutrition are at increased risk of pneumonia. In many tropical settings seasonal pneumonia epidemics occur during the rainy season, which is often a period of poor nutrition. We have investigated whether seasonal hunger may be a driver of seasonal pneumonia epidemics in children in the tropical setting of the Philippines. In individual level cohort analysis, infant size and growth were both associated with increased pneumonia admissions, consistent with findings from previous studies. A low weight for age z-score in early infancy was associated with an increased risk of pneumonia admission over the following 12 months (RR for infants in the lowest quartile of weight for age z-scores 1.28 [95% CI 1.08 to 1.51]). Poor growth in smaller than average infants was also associated with an increased risk of pneumonia (RR for those in the lowest quartile of growth in early infancy 1.31 [95%CI 1.02 to 1.68]). At a population level, we found that seasonal undernutrition preceded the seasonal increase in pneumonia and respiratory syncytial virus admissions by approximately 10 weeks (pairwise correlation at this lag was −0.41 [95%CI −0.53 to −0.27] for pneumonia admissions, and −0.63 [95%CI −0.72 to −0.51] for respiratory syncytial virus admissions). This lag appears biologically plausible. These results suggest that in addition to being an individual level risk factor for pneumonia, poor nutrition may act as a population level driver of seasonal pneumonia epidemics in the tropics. Further investigation of the seasonal level association, in particular the estimation of the expected lag between seasonal undernutrition and increased pneumonia incidence, is recommended. Refereed/Peer-reviewed

Well balanced ecosystems have an essential role in disease regulation, and consequently their correct functioning is increasingly recognised as imperative for maintaining human health. Disruptions to ecosystems have been found to increase the risk of several diseases, including Hantavirus, Lyme disease, Ross River virus, malaria and Ciguatera fish poisoning. Leptospirosis is a globally important emerging zoonosis, caused by spirochaete bacteria, borne by many mammalian hosts, and also transmitted environmentally. We propose that leptospirosis incidence in humans is also linked to ecosystem disruption, and that reduced biodiversity (the diversity of species within an ecological community) may be associated with increased leptospirosis incidence. To investigate this hypothesis, the relationship between biodiversity levels of island nations and their annual leptospirosis incidence rates (adjusted for GDP per capita) was examined by linear correlation and regression. Supportive, statistically significant negative associations were obtained between leptospirosis incidence and (a) total number of species (r2=0.69, p