Abstract

Japanese encephalitis virus causes epidemics of encephalitis throughout southeast Asia. It is a single-stranded, positive sense RNA virus with non-coding regions at both the 3′ and 5′ ends. In their work “La Protein Can Simultaneously Bind to Both 3′- and 5′-Noncoding Regions of Japanese Encephalitis Virus Genome,” Vashist and colleagues demonstrated that La protein binds to both ends of the viral genome and suggested that this interaction between host protein and viral RNA may aid transcription and translation of the virus. Another human pathogen is the focus of work by Gong et al. The replicative intermediate of hepatitis B virus is organized into minichromosomes by histones and non-histone proteins. Gong and colleagues investigated histone modification during viral replication in their work “Chromosome Remodeling Related to HBV Replication in HepG2 Cells.”
Viral infection is a source of morbidity and mortality in animals as well as humans. Porcine reproductive and respiratory syndrome virus is economically important to swine production causing reproductive failure in sows along with lack of growth and predisposition to secondary infection in piglets. Shortly after viral infection, the animals mount an interferon β response, which triggers viral expression of nsp1. The mechanism of nsp1 action is not known. However, Shi and colleagues demonstrated that protease activity of nsp1α is required to inhibit interferon β production in their work “The Nonstructural Protein 1 α Papain-like Cysteine Protease was Necessary for Porcine Reproductive and Respiratory Syndrome Virus Nonstructural Protein 1 to Inhibit Interferon- β Induction.”
The study of disease is continually progressing; new techniques and investigations raise as many questions as they answer. Large-scale projects such as sequencing the human microbiome highlight the interactions among human genetics, microbial communities, and environmental factors. DNA and Cell Biology has a tradition of publishing research focused on the development of cutting-edge methods in molecular biology and mechanistic studies in molecular medicine. Thus, we are inviting submission of mechanistic studies exploring human genetics and microbe–host interactions for our new section “Molecular Mechanisms of Disease.” These papers will join a wide array of clinical studies concerning the role of human genetic diversity in disease susceptibility and severity published in the journal. Our hope is that by combining molecular and clinical studies in a single journal, we can facilitate communication among varied biological sub-disciplines. For more information, please contact the editorial office (
