Genetic modification for the control of mosquitoes is frequently touted as a solution for a variety of vector-borne diseases. There has been some success using non-insecticidal methods like sterile or incompatible insect techniques to control arbovirus diseases. However, control by genetic modifications to reduce mosquito populations or create mosquitoes that are refractory to infection with pathogens are less developed. The advent of CRISPR-Cas9-mediated gene drives may advance this mechanism of control. In this review, use and progress of gene drives for vector control, particularly for malaria, is discussed. A brief history of population suppression and replacement gene drives in mosquitoes, rapid advancement of the field over the last decade and how genetic modification fits into the current scope of vector control are described. Mechanisms of alternative vector control by genetic modification to modulate mosquitoes’ immune responses and anti-parasite effector molecules as part of a combinational strategy to combat malaria are considered. Finally, the limitations and ethics of using gene drives for mosquito control are discussed.
Despite being vaccine-preventable, hepatitis B virus (HBV) infection remains the seventh leading cause of mortality in the world. In South Africa (SA), over 1.9 million people are chronically infected with HBV, and 70% of all Black chronic carriers are infected with HBV subgenotype A1. The virus remains a significant burden on public health in SA despite the introduction of an infant immunization program implemented in 1995 and the availability of effective treatment for chronic HBV infection. In addition, the high prevalence of HIV infection amplifies HBV replication, predisposes patients to chronicity, and complicates management of the infection. HBV research has made significant progress leading to better understanding of HBV epidemiology and management challenges in the SA context. This has led to recent revision of the national HBV infection management guidelines. Research on developing new vaccines and therapies is underway and progress has been made with designing potentially curative gene therapies against HBV. This review summarizes research carried out in SA on HBV molecular biology, epidemiology, treatment, and vaccination strategies.
1 November 2013 in Biochimica et Biophysica Acta (BBA) - General Subjects
Each year, approximately 1.2 million new cases of hepatitis B are recorded globally, caused by the hepatitis B virus (HBV). This underscores the persistent transmission of the disease despite widespread availability of an effective vaccine. Although current drugs can reduce the chances of severe disease, they are not curative. Physiologically relevant in vitro models of HBV infection are essential to understand the biology of HBV and to develop strategies to target the virus. Until recently, only primary human hepatocytes could be infected with HBV. The discovery of the HBV receptor, the sodium taurocholate co-transporting polypeptide, resulted in the development of several immortalised cell lines that are infectable by HBV. These have made significant contributions to hepatitis B research. However, 2-D cell culture models fail to fully capture the complexity of the liver and HBV infection. The recent development of 3-D culture technologies offers new possibilities for modelling all the steps of HBV replication in cell culture and mimicking the liver microenvironment. This review discusses recent progress in developing models of HBV infection in 3-D cell culture and their contributions to HBV biology research and novel drug development.