As the world starts to reel from the devastating effects of the COVID-19 pandemic, there is an increasingly urgent demand for vaccines and new therapeutics to combat the virus. HMT offers collaborative support to scientists and clinicians working to develop these drugs and vaccines. With our metabolomics technology, we can help to identify biomarkers and novel drug targets, as well as time-dependent metabolic changes and characteristics that are able to predict the drug and vaccine effectiveness and/or toxicity. Here, we propose some ideas on how metabolomics can be extremely useful for pre-clinical and clinical studies.
HMT recently caught up with Dr Chan, the lead author of the paper “Metabolic perturbations and cellular stress underpin susceptibility to symptomatic live-attenuated yellow fever infection”, which includes key findings based on HMT’s metabolome analysis, and was published in top biomedical journal Nature Medicine last August. Dr. Chan’s team focused on the differences in blood profiles of symptomatic and asymptomatic individuals before and after inoculation with live yellow fever viral vaccine. Transcriptome analysis and metabolome analysis performed on blood specimens revealed that individuals with endoplasmic reticulum (ER) stress and reduced tricarboxylic acid (TCA) cycle activity have increased susceptibility to symptomatic outcomes after inoculation with the vaccine.
HMT had the opportunity to ask Dr. Chan via e-mail about examples of metabolome analysis in his research, and the significance and prospects of using metabolomics in infectious diseases research. Read his interview HERE
Metabolic perturbations and cellular stress underpin susceptibility to symptomatic live-attenuated yellow fever infection
Prevalence of Slow-Growth Vancomycin Nonsusceptibility in Methicillin-Resistant Staphylococcus aureus
Prominent Steatosis with Hypermetabolism of the Cell Line Permissive for Years of Infection with Hepatitis C Virus
Hepatitis C Virus Infection Promotes Hepatic Gluconeogenesis through an NS5A-Mediated, FoxO1-Dependent Pathway