The Influence of Meteorology on the Spread of Influenza: Survival Analysis of an Equine Influenza (A/H3N8) Outbreak

The influences of relative humidity and ambient temperature on the transmission of influenza A viruses have recently been established under controlled laboratory conditions. The interplay of meteorological factors during an actual influenza epidemic is less clear, and research into the contribution of wind to epidemic spread is scarce. By applying geostatistics and survival analysis to data from a large outbreak of equine influenza (A/H3N8), we quantified the association between hazard of infection and air temperature, relative humidity, rainfall, and wind velocity, whilst controlling for premises-level covariates. The pattern of disease spread in space and time was described using extraction mapping and instantaneous hazard curves. Meteorological conditions at each premises location were estimated by kriging daily meteorological data and analysed as time-lagged time-varying predictors using generalised Cox regression. Meteorological covariates time-lagged by three days were strongly associated with hazard of influenza infection, corresponding closely with the incubation period of equine influenza. Hazard of equine influenza infection was higher when relative humidity was <60% and lowest on days when daily maximum air temperature was 20–25°C. Wind speeds >30 km hour−1 from the direction of nearby infected premises were associated with increased hazard of infection. Through combining detailed influenza outbreak and meteorological data, we provide empirical evidence for the underlying environmental mechanisms that influenced the local spread of an outbreak of influenza A. Our analysis supports, and extends, the findings of studies into influenza A transmission conducted under laboratory conditions. The relationships described are of direct importance for managing disease risk during influenza outbreaks in horses, and more generally, advance our understanding of the transmission of influenza A viruses under field conditions

A Human Lung Xenograft Mouse Model of Nipah Virus Infection

Nipah virus (NiV) is a member of the genus Henipavirus (family Paramyxoviridae) that causes severe and often lethal respiratory illness and encephalitis in humans with high mortality rates (up to 92%). NiV can cause Acute Lung Injury (ALI) in humans, and human-to-human transmission has been observed in recent outbreaks of NiV. While the exact route of transmission to humans is not known, we have previously shown that NiV can efficiently infect human respiratory epithelial cells. The molecu

Epidemic curve and hazard function for occurrence of clinical equine influenza in a closed population of horses at a 3-day event in Southern Queensland, Australia, 2007

The risk of individuals becoming infected during an epidemic of infectious disease can vary as the disease progresses. Monitoring this risk may provide information about the dynamics of transmission. This study describes the epidemic curve for an epidemic of equine influenza (EI) in a closed population of horses predominantly immunologically naïve to EI at a 3-day event at Morgan Park in southern Queensland, Australia. The hazard function suggested that a subset of horses were at reduced risk of becoming infected. This highlights the importance, when modelling infectious disease in populations, of considering possible differences in the risk of infection among subgroups in the population

Clinical signs of equine influenza in a closed population of horses at a 3-day event in Southern Queensland, Australia

This report describes the clinical signs of equine influenza (EI) during an epidemic in a closed, predominantly immunologically naïve population of horses. It included 254 study horses, few of which exhibited all three signs of pyrexia, nasal discharge and cough simultaneously. We conclude that although the majority of affected horses exhibit temperature patterns resembling those most often described in the published literature, clinicians should be aware that other profiles are quite common

Subclinical infection without encephalitis in mice following intranasal exposure to Nipah virus-Malaysia and Nipah virus-Bangladesh

10.1186/1743-422X-11-102Virology Journal11110

Identification of Risk Factors for African Swine Fever: A Systematic Review

African swine fever (ASF) is an internationally-spreading viral pig disease that severely damages agricultural pork production and trade economy as well as social welfare in disease-affected regions. A comprehensive understanding of ASF risk factors is imperative for efficient disease control. As the absence of effective ASF vaccines limits disease management options, the identification and minimisation of ASF-associated risk factors is critical to preventing ASF outbreaks. Here, we compile currently known potential ASF risk factors identified through a systematic literature review. We found 154 observation-based and 1239 potential ASF risk factors, which we were able to group into the following defined risk categories: ‘ASF-virus’, ‘Biosecurity’, ‘Disease control’, ‘Environment’, ‘Husbandry’, ‘Movement’, ‘Network’, ‘Pig’, ‘Society’ and ‘Surveillance’. Throughout the epidemiological history of ASF there have been similar risk categories, such as ‘Environment’-related risk factors, predominantly reported in the literature irrespective of the ASF situation at the time. While ASF risk factor reporting has markedly increased since 2010, the majority of identified risk factors overall have referred to domestic pigs. The reporting of risk factors for ASF in wild boar mostly commenced from 2016 onwards. The compendium of ASF risk factors presented herein defines our current knowledge of ASF risk factors, and critically informs ASF-related problem solving

T-dependent B cell responses to <i>Plasmodium</i> induce antibodies that form a high-avidity multivalent complex with the circumsporozoite protein

<div><p>The repeat region of the <i>Plasmodium falciparum</i> circumsporozoite protein (CSP) is a major vaccine antigen because it can be targeted by parasite neutralizing antibodies; however, little is known about this interaction. We used isothermal titration calorimetry, X-ray crystallography and mutagenesis-validated modeling to analyze the binding of a murine neutralizing antibody to <i>Plasmodium falciparum</i> CSP. Strikingly, we found that the repeat region of CSP is bound by multiple antibodies. This repeating pattern allows multiple weak interactions of single F_AB domains to accumulate and yield a complex with a dissociation constant in the low nM range. Because the CSP protein can potentially cross-link multiple B cell receptors (BCRs) we hypothesized that the B cell response might be T cell independent. However, while there was a modest response in mice deficient in T cell help, the bulk of the response was T cell dependent. By sequencing the BCRs of CSP-repeat specific B cells in inbred mice we found that these cells underwent somatic hypermutation and affinity maturation indicative of a T-dependent response. Last, we found that the BCR repertoire of responding B cells was limited suggesting that the structural simplicity of the repeat may limit the breadth of the immune response.</p></div

The multivalency of the NANP repeat region of the CSP protein.

<p>(A) An (NANP)₆ peptide results in the presentation of two symmetrical epitopes, formed by alternating repeats (cyan and magenta), allowing binding by two F_AB domains, in keeping with the stoichiometry observed by ITC. (B) The full 27-mer repeat region results in the presentation of at least 10 separate epitopes and the twist of the helix results in displacement along the length of the repeat region, which allows binding of up to 10 separate F_AB fragments, consistent with 4 antibodies bound by both F_AB domains, and two bound by a single F_AB domain.</p

ITC data for interactions between 2A10 F_AB and antigens.

<p>(A) Titration of 2A10 F_AB with (NANP)₆. (B) Titration of 2A10 F_AB with rCSP. (C) Titration of 2A10 (complete antibody) with rCSP. The upper panels represent baseline-corrected power traces. By convention, negative power corresponds to exothermic binding. The lower panels represent the integrated heat data fitted to the independent binding sites model.</p