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Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of and finding treatments for complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia (FM), long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.
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There appear to be many flaws in Huber's work but the 'master flaw', I believe, from which all erroneous conclusions will arise is the absence of a group with mono but without ME.
As a result of this design, we have no way of knowing whether the activation pattern of the HERV in question in patients with ME is any different from its activation pattern in people with a mono infection who do not have ME.
She should also be aware that HERVs are part of the intrisic immune system and are activated as a result of any viral infection, particularily if that virus is a retrovirus. She, therefore, should have checked the activity level of other HERVS.
It is a shame that she missed two glaring opportunities to test her hypothesis. She has, however, provided the information which will enable that hypothesis to be tested by others.
Why is it that so many scientists fail to design solid studies into ME? What am I missing here?
How come Huber, like you say Fred, did not test mono without ME? She can not be that bad a researcher, so do I go with Flex's assessment or can someone offer another opinion.
Are studies into any disease always this weak, or is it that they rush through to get any result, and drag out these important questions?