I find the observation that cell function seems to improve after a bacterial infection is very interesting, and I hear this occasionally from patients. Hypothesis and test is one phase of a larger cycle. Focusing on one step limits the effectiveness of science. Showing the severity of ME/CFS is much worse than a range of other severe diseases is helpful, but its not necessarily objective. Aside from a few patients, ME/CFS patients have less viral load than healthy controls. RNA viruses have not been properly tested yet. They are also exploring exhaustive genetic sequencing looking for unknown viruses. They are working on a general parasite test. Sleeping sickness not only has a nearly identical gene match to ME/CFS, but it has almost identical sickness. The one that amazed me, and I missed in my own review many years ago, was that its less about sleeping too much than about having an inverted circadian rhythm, sleeping during the day and not at night. I have discussed this with many patients and seems to be common in patients sick longer than three years, including me and several of my ME friends. So one hypothesis being tested is that African Sleeping Sickness IS CFS. Many nutritional metals, used in detox, are very low. They are planning to compare our metabolimics to gene changes, looking for a metabolic trap. Hypothetically this means the onset can be very sudden, within hours. I was involved in metabolic regulation for ME in 1993, as a patient and giving some very limited analytic advice. They should hopefully know in months to a year. Treatment under this hypothesis might be easy, fast and cheap, once we know exactly what is going wrong. A lot of the glucose we have is shunted to fat synthesis. Suramin might be available by the end of the year, and he pointed out its also used for Sleeping Sickness. I was hoping someone would look into this, and it looks like it will happen maybe next year.