I've been following a few threads over past weeks and trying to get up to speed with the sheer range of information and to try and tie all this stuff together. Sometimes its hard to see the wood for the trees. This includes (off the top of my head and obviously not exhaustive) : 1.The range of symptoms that we all know and love. No need to repeat them. 2.Many findings over the years of organic disease process(es) including : evidence of various specific infections, immune system dysregulation and/or damage; low blood volume, orthostatic hypotension, brain hypoperfusion, lesions, loss of grey matter, mitochondrial disorders, leaky gut etc. Various contributory factors have been proposed including viruses, bacteria, physical or psychological stress, environmental toxins, vaccines etc. None of these findings have fully explained the illness and none have been universally accepted. 3.Working back from 1 and 2 above, some researchers have tried to speculate on what pathogen could lead to the observed findings and have suggested that either a retrovirus or enterovirus might fit. 4.Dr Kerr's gene expression studies, which show some 80 plus genes either up or down regulated in ME patients compared to controls, suggesting an identifiable acquired ME genotype. The functions of most of these genes are identified and appear a close fit with the observed symptoms and disease processes : Genomic analysis revealed some common (neurological, haematological, cancer) and some distinct (metabolic, endocrine,cardiovascular, immunological, inflammatory) disease associations among the subtypes. Dr Kerr also states : It is intriguing that within our 88 gene signature, there are several genes with links to various aetiological triggering factors. For example, virus infection (EIF4G1, EBI2) and organophosphate exposure. 5.The WPI findings suggesting that 67% (or 95% unpublished) of a well specified ME cohort tested positive for the XMRV retrovirus. Three European studies have failed to find XMRV in either CFS patients or controls leading to much debate on cohorts, methodology, the original WPI findings and even the nature of the virus itself which appears to be 'hard to find'. 6.The recent virologists' findings that when monkeys were infected with XMRV, the virus didn't appear in the blood but was largely limited to CD4+ T cells in lymphoid organs -- spleen, lymph nodes, and GI tract -- as well as in reproductive organs, including prostate, testes, ovaries, vagina, and cervix. Despite the infection the animals 'appeared not to be' ill. Again the locations where the virus clusters appears consistent with the symptoms and findings of organic disease. While these are different approaches I don't see much evidence of incompatibility between them and indeed a lot of scope for a synthesis. The monkey studies and the European studies suggest that XMRV may be hard to detect, even in infected patients and that biopsy material may be more useful. There are obviously logistical and ethical issues with using biopsy material. One indirect route might be if Dr Kerr were to run his microassay tests on samples from the infected monkeys to see if the same gene expression patterns were seen. If positive, it would tie XMRV (or any other suggested pathogen) nicely to gene expression and the symptoms of ME. A negative result might suggest that there is no XMRV connection, or that something else is needed to make us and the monkeys ill. As for the negative XMRV findings, the ability to select between the infected monkey samples and controls might help determine if their methodology can detect XMRV or if the problem lies with cohorts or the absence or presence of XMRV in Europe.