Family-school connections and internalizing problems among children living with asthma in urban, low-income neighborhoods

Children with asthma living in urban environments are at risk for experiencing internalizing problems and difficulties at school due to social context and health-related stressors. Parent confidence and participation in the school and children’s attitudes about school were explored in association with children’s depressed mood and school anxiety. Forty-five parent—child dyads were recruited from urban community health centers. Most participants were members of ethnic minority groups. Hierarchical multiple regression analyses revealed that higher levels of parent confidence in the school were associated with fewer symptoms of school anxiety in children. Children’s attitudes toward school moderated the relation between parent participation in the school and children’s depressed mood. Specifically, lower levels of parent participation were associated with higher levels of depressed mood only for children with the least positive school attitudes. Although preliminary, these results suggest the importance of attending to family—school connections to optimize the school-related psychological functioning of children living with asthma in urban environments

Chimpanzee APOBEC3 proteins deter SIVs from any monkey business

Cross-species transmissions of viruses from animals to humans are at the origin of major human pathogenic viruses. While the role of ecological and epidemiological factors in the emergence of new pathogens is well documented, the importance of host factors is often unknown. Chimpanzees are the closest relatives of humans and the animal reservoir at the origin of the human AIDS pandemic. However, despite being regularly exposed to monkey lentiviruses through hunting, chimpanzees are naturally infected by only a single simian immunodeficiency virus, SIVcpz. Here, we asked why chimpanzees appear to be protected against the successful emergence of other SIVs. In particular, we investigated the role of the chimpanzee APOBEC3 genes in providing a barrier to infection by most monkey lentiviruses. We found that most SIV Vifs, including Vif from SIVwrc infecting western-red colobus, the chimpanzee's main monkey prey in West Africa, could not antagonize chimpanzee APOBEC3G. Moreover, chimpanzee APOBEC3D, as well as APOBEC3F and APOBEC3H, provided additional protection against SIV Vif antagonism. Consequently, lentiviral replication in primary chimpanzee CD4(+) T cells was dependent on the presence of a lentiviral vif gene that could antagonize chimpanzee APOBEC3s. Finally, by identifying and functionally characterizing several APOBEC3 gene polymorphisms in both common chimpanzees and bonobos, we found that these ape populations encode APOBEC3 proteins that are uniformly resistant to antagonism by monkey lentiviruses