Phylogenic evidence suggests that the strain of Zika virus causing an unprecedented outbreak of disease in the Americas had its origin in Southeast Asia, where reports of isolated cases of Zika virus infection have occurred since 2010. Why there has been no large outbreak of Zika infection in Southeast Asia remains unclear and whether such an outbreak will occur in the future is a question of significant concern. This review looks at Zika virus from a Southeast Asian perspective and highlights some of the possible scenarios with regards to Zika virus in this part of the world as well as highlighting some of the research questions that need to be urgently addressed.

Objective: To identify immunological evidence of Zika virus transmission in Thailand. Methods: To undertake a preliminary serosurvey of possible exposure to Zika virus, 21 serum samples from cohort of acute undifferentiated fever patients were examined for immunoreactivity to Zika, Dengue, Japanese encephalitis and Chikungunya envelope antigens by Western blot analysis. Results: Twenty of the 21 serum samples showed immunoreactivity to at least one of the antigens, with seven samples showing immunoreactivity to all antigens. Of particular note, two serum samples showed immunoreactivity only to Zika envelope antigen, with no immunoreactivity to other envelope antigens. Conclusions: This study presents the first evidence of Zika virus transmission in Thailand, although as yet the relationship between transmission and possible cases of Zika fever in Thailand requires further investigation.

Iron deficiency anemia and iron overload conditions affect more than one billion people worldwide. Iron homeostasis involves the regulation of cells that export iron into the plasma and cells that utilize or store iron. The cellular iron balance in humans is primarily mediated by the hepcidin–ferroportin axis. Ferroportin is the sole cellular iron export protein, and its expression is regulated transcriptionally, post-transcriptionally and post-translationally. Hepcidin, a hormone produced by liver cells, post-translationally regulates ferroportin expression on iron exporting cells by binding with ferroportin and promoting its internalization by endocytosis and subsequent degradation by lysosomes. Dysregulation of iron homeostasis leading to iron deposition in vital organs is the main cause of death in beta-thalassemia patients. Beta-thalassemia patients show marked hepcidin suppression, ineffective erythropoiesis, anemia and iron overload. Beta-thalassemia is common in the Mediterranean region, Southeast Asia and the Indian subcontinent, and the focus of this review is to provide an update on the factors mediating hepcidin related iron dysregulation in beta-thalassemia disease. Understanding this process may pave the way for new treatments to ameliorate iron overloading and improve the long term prognosis of these patients.

Objective To investigate the impact of the endogamous marriage culture on the prevalence of the hemoglobin E (HbE) recessive variant. Methods The prevalence of the hemoglobin E (HbE) recessive variant was determined by dot-blot hybridization in 4 endogamous villages (1 Mlabri and 3 Htin ethnic groups) in comparison with 9 other nearby non-endogamous populations. Results Although the overall HbE prevalence in the population studied (8.44%, 33/391) was not significantly different from that of the general southeast Asian population, a high prevalence and individuals with homozygous HbE were observed in two villages, the Mlabri from Wiang Sa district and the Htin from Thung Chang district of Nan province (26.3% and 26.9%, respectively). The low HbE allelic frequency noticed in some endogamous populations suggests that not only endogamy but also other evolutionary forces, such as founder effect and HbE/β-thalassemia negative selection may have an effect on the distribution of the HbE trait. Conclusion Our study strongly documents that cultural impact has to be considered in the extensive prevalence studies for genetic disorders in the ethnic groups of northern Thailand.

Objective To generate insights into the mechanism of NVP induced hepatotoxicity. Methods Liver (HepG2) cells were cultured with various concentrations of NVP. This cell line was chosen because it has low expression of cytochrome P450, allowing evaluation of the effects of NVP rather than specific metabolites. Cytotoxicity was determined using a proliferation assay and cell numbers were monitored using trypan blue exclusion assay for long term culture experiments and apoptosis induction was determined by morphological and biochemical investigation. Results HepG2 cells treated with the highest concentration of NVP tested (819 μM) initially showed a rounded morphology and all cells had died by week three of exposure. Nuclear condensation and fragmentation, increased Annexin V/propidium iodide staining and caspase 9 activation all supported the induction of apoptosis in HepG2 cells in response to NVP treatment. Conclusions There is a clear induction of apoptosis in response to NVP which suggests that NVP has significant cytotoxicity, over and above any cytotoxicity of metabolites and may contribute directly to patient hepatotoxicity.