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Human movement drives spatial transmission patterns of infectious diseases. Population-level mobility patterns are often quantified using aggregated data sets, such as census migration surveys or mobile phone data. These data are often unable to quantify individual-level travel patterns and lack the information needed to discern how mobility varies by demographic groups. Individual-level datasets can capture additional, more precise, aspects of mobility that may impact disease risk or transmission patterns and determine how mobility differs across cohorts; however, these data are rare, particularly in locations such as sub-Saharan Africa.
The intensity of transmission of Aedes-borne viruses is heterogeneous, and multiple factors can contribute to variation at small spatial scales. Illuminating drivers of heterogeneity in prevalence over time and space would provide information for public health authorities. The objective of this study is to detect the spatiotemporal clusters and determine the risk factors of three major Aedes-borne diseases, Chikungunya virus, Dengue virus, and Zika virus clusters in Mexico.
Multiple sclerosis is associated with Epstein–Barr virus (EBV) infection, B-cell dysfunction, gut dysbiosis, and environmental and genetic risk factors, including female sex.
We have demonstrated that a single dose of a closely related commensal can delay onset of NTHi otitis media in vivo
Active vaccine safety surveillance leading to rapid detection of a safety signal would likely have resulted in earlier suspension of Fluvax from the vaccination programme
Inappropriate antimicrobial prescribing in children was linked to specific risk factors, presenting opportunities for targeted interventions to improve prescribing
Review and highlight of the significant advances made towards vaccine development and understanding of the immunology of otitis media
We found a numerically higher rate of preterm births among women who received 23vPPV in pregnancy compared to unvaccinated pregnant women
A review of cases informed a change from a "3 + 0" infant schedule to a "2 + 1" schedule
An optimized, rapid method for creating markerless isogenic mutations that combines Gibson assembly cloning with a new temperature-sensitive plasmid, pLZts