Goals: During disease pathogens cause a series of changes in systemic metabolism and behaviour which we call sickness behaviour. One of the systems impacted by these changes is the endocrine system that controls energy homeostasis. I have noticed that strong viral infection, but not normal level of infection, causes a drop in blood glucose levels that I have termed relative hypoglycaemia (RHG). The goal of this research was to determine how and why RHG appears. I wanted to elucidate the mechanisms by which strong infection causes a drop in glucose levels, and whether that is the result of virus or our systemic response to infection. Furthermore, I wanted to determine whether RHG has an impact on the progression of infection and by which mechanisms and pathways. Materials and methods: To study the effects of the different glucose levels on the progression of viral infection in vitro I have used the methods of cell culture using primary and immortalized cell lines and infection in vitro. To monitor the progress of infection I have used plaque assay or viruses that express fluorescent protein which enabled me to visualize infected cells using flow cytometry or confocal microscopy. To study the effects of low glucose levels on infection rate I have used cell media with varying levels of glucose or those with added key metabolites which take parti n energy metabolism of the cell. To determine the levels of various biomarkers and molecules I have used various methods including colorimetric assays, ELISA, and Western blot. To track the infection in vitro I have used an array of genetically modified mice. They were infected with different viruses (MCMV, LCMV, influenza, etc.) in varying concentrations, then I was tracking their fasting blood glucose levels or other metabolites. To determine the viral load in tissues I have used qPCR or plaque assay. To determine the level of liver glycogen I have used colorimetric assay and histology slides of the liver. Results: I have shown that strong viral infection causes a drop in blood glucose levels, and that lower blood glucose levels during viral infection have a protective effect. Strong infection induces hyperinsulinemia via its effect on  T cells and production of cytokines IFN and IL-1. This results in a decreased glycogen utilization in liver which leads to relative hypoglycemia (RHG). Low glucose levels then lead to an increase in type I interferon production via changes in cell lactate production which affects signaling pathways that promote the secretion of type I interferons. Conclusions: Strong viral infection causes a drop in blood glucose levels (RHG) due to temporary hyperinsulinemia caused by immune system activation and secretion of IFN and IL-1. RHG promotes immune response via type I interferons and that has a protective antiviral effect. This discovery offers a new insight in the interactions between immune and endocrine system, giving weight to changes in energy metabolism during infection. Considering that an increasing part of global population suffers from (pre)diabetes which causes aberrations in blood glucose level management and the increase in infections persistence in that group, this research can help with medicinal practices in regard to treatment during strong viral infections.