Modelling sexually transmitted infections: the effect of partnership activity and number of partners on R0

We model a sexually transmitted infection in a network population where individuals have different numbers of partners, separated into steady and casual partnerships, where the risk of transmission is higher in steady partnerships. An individual's number of partners of the two types defines its degree, and the degrees in the community specify the degree distribution. For this structured network population a simple model for disease transmission is defined and the basic reproduction number R0 is derived, R0 being a size-biased (i.e. biasing individuals with many partners) average number of new infections caused by individuals during the early stages of the epidemic. First a homosexual population is considered and then a heterosexual population. The heterosexual model is fitted to data from a census survey on sexual activity from the Swedish island of Gotland. The main empirical finding is that, for relevant transmission rates, the effect that so-called superspreaders have on R0 is over-estimated when not admitting for different types of partnerships.     

Endemic persistence or disease extinction: The effect of separation into sub-communities

Consider an infectious disease which is endemic in a population divided into several large sub-communities that interact. Our aim is to understand how the time to extinction is affected by the level of interaction between communities. We present two approximations of the expected time to extinction in a population consisting of a small number of large sub-communities. These approximations are described for an SIR epidemic model, with focus on diseases with short infectious period in relation to life length, such as childhood diseases. Both approximations are based on Markov jump processes. Simulations indicate that the time to extinction is increasing in the degree of interaction between communities. This behaviour can also be seen in our approximations in relevant regions of the parameter space.     

SOS induction in a subpopulation of structural maintenance of chromosome (Smc) mutant cells in Bacillus subtilis

The structural maintenance of chromosome (Smc) protein is highly conserved and involved in chromosome compaction, cohesion, and other DNA-related processes. In Bacillus subtilis, smc null mutations cause defects in DNA supercoiling, chromosome compaction, and chromosome partitioning. We investigated the effects of smc mutations on global gene expression in B. subtilis using DNA microarrays. We found that an smc null mutation caused partial induction of the SOS response, including induction of the defective prophage PBSX. Analysis of SOS and phage gene expression in single cells indicated that approximately 1% of smc mutants have fully induced SOS and PBSX gene expression while the other 99% of cells appear to have little or no expression. We found that induction of PBSX was not responsible for the chromosome partitioning or compaction defects of smc mutants. Similar inductions of the SOS response and PBSX were observed in cells depleted of topoisomerase I, an enzyme that relaxes negatively supercoiled DNA.     

RNA interference in parasitic nematodes of animals: a reality check?

RNA interference (RNAi) is widely used in Caenorhabditis elegans to identify gene function and has been adapted as a high-throughput screening method to identify genes involved in essential processes. The technique has been applied to parasitic nematodes with variable success and we believe that inconsistent outcomes preclude its use as a robust screen with which to identify potential control targets. In this article, key issues that require clarification are discussed, including the mode of delivery of double-stranded RNA to the parasite, the developmental stage targeted and, perhaps of most importance, whether the RNAi pathway (as defined by studies in C. elegans) is fully functional in some parasitic nematodes.     

Dietary contributions of the alien zebra mussel Dreissena polymorpha in British freshwater fish suggest low biological resistance to their invasion

Hydrobiologia - Native communities can resist the establishment and invasion of alien species through consumptive and/or competitive interactions. The extent of consumptive resistance from...     

Coronavirus nsp6 proteins generate autophagosomes from the endoplasmic reticulum via an omegasome intermediate

Autophagy is a cellular response to starvation which generates autophagosomes to carry cellular organelles and long-lived proteins to lysosomes for degradation. Degradation through autophagy can provide an innate defence against virus infection, or conversely autophagosomes can promote infection by facilitating assembly of replicase proteins. We demonstrate that the avian coronavirus, Infectious Bronchitis Virus (IBV) activates autophagy. A screen of individual IBV non-structural proteins (nsps) showed that autophagy was activated by IBV nsp6. This property was shared with nsp6 of mammalian coronaviruses Mouse Hepatitis Virus, and Severe Acute Respiratory Syndrome Virus, and the equivalent nsp5-7 of the arterivirus Porcine Reproductive and Respiratory Syndrome Virus. These multiple-spanning transmembrane proteins located to the endoplasmic reticulum (ER) where they generated Atg5 and LC3II-positive vesicles, and vesicle formation was dependent on Atg5 and class III PI3 kinase. The vesicles recruited double FYVE-domain containing protein (DFCP) indicating localised concentration of phosphatidylinositol 3 phosphate, and therefore shared many features with omegasomes formed from the ER in response to starvation. Omegasomes induced by viral nsp6 matured into autophagosomes that delivered LC3 to lysosomes and therefore recruited and recycled the proteins needed for autophagosome nucleation, expansion, cellular trafficking and delivery of cargo to lysosomes. The coronavirus nsp6 proteins activated omegasome and autophagosome formation independently of starvation, but activation did not involve direct inhibition of mTOR signalling, activation of sirtuin1 or induction of ER stress.     

Identification, replication, and fine-mapping of Loci associated with adult height in individuals of african ancestry

Adult height is a classic polygenic trait of high heritability (h ² ∼0.8). More than 180 single nucleotide polymorphisms (SNPs), identified mostly in populations of European descent, are associated with height. These variants convey modest effects and explain ∼10% of the variance in height. Discovery efforts in other populations, while limited, have revealed loci for height not previously implicated in individuals of European ancestry. Here, we performed a meta-analysis of genome-wide association (GWA) results for adult height in 20,427 individuals of African ancestry with replication in up to 16,436 African Americans. We found two novel height loci (Xp22-rs12393627, P = 3.4×10⁻¹² and 2p14-rs4315565, P = 1.2×10⁻⁸). As a group, height associations discovered in European-ancestry samples replicate in individuals of African ancestry (P = 1.7×10⁻⁴ for overall replication). Fine-mapping of the European height loci in African-ancestry individuals showed an enrichment of SNPs that are associated with expression of nearby genes when compared to the index European height SNPs (P<0.01). Our results highlight the utility of genetic studies in non-European populations to understand the etiology of complex human diseases and traits.