This is not just retroviruses (XMRV and HIV-1) but common viruses such as the rhinovirus, Epstein-Barr, influenza, herpes, papillomavirus, coronavirus and many more. This supports the idea, proposed over a century ago, by J.B.S.Haldane and Felix D'Herelle that viruses are responsible for the origin of life, and also the idea that viral inserts are responsible for evolutionary jumps.(the insertion of several viral genes, if passed on through the germ line, effectively creates a new being)
As if that were not interesting enough, here is the important factor , exemplified by Alzheimer's disease Bipolar disorder and schizophrenia. The insertion points of the viruses implicated as risk factors in any particular disease correspond to the locations of the genes implicated in the disease.
The more important the gene in Alzheimer's disease (and others), the more viral proteins it matches (and those of other pathogens).
These viral matches appear to cover the whole human genome, and every human protein is homologous to one virus or another.
In the human genome, these matches are characterised by millions of gapped consecutive and contiguous segments which translate into short contiguous peptide stretches (5-12 amino acids long).The older the viral insertion, the more fragmented the DNA, the shorter the protein matches,but the greater the number of human/viral homologues.
These human protein matches (vatches) are identical to those in the proteins expressed by the viruses implicated in the disease.
Because the viral protein is similar to human receptors, peptide ligands, enzymes, etc it can act as a dummy ligand or a decoy receptor, and also interfere with the interactome of its human counterpart. This is shown quite clearly in the DISC1/viral interactome
Upon infection, antibodies to the virus also risk targeting their human counterparts, which will in effect be knocked down when the antibody binds. The protein equivalent of gene knockouts. If the peptides are highly immunogenic, then cells containing the virus, or its human analogue will be targeted for destruction. This is exemplified by the fact that immunisation with tau in mice provokes the neurofibrillary tangle pathology seen in Alzheimer's disease.Tau is homologous to Herpes simplex and other viral proteins.
All of the diseases on the website pages Alzheimer's disease, Bipolar disorder, Schizophrenia, Chonic fatigue, and more, have an autoimmune component, pathogens are implicated in all, and the genes and pathogens fit together, hand in glove, for all (Bipolar disorder, Alzheimer's and schizophrenia).
Viruses (known and unsuspected culrits) are also homologous to the autoantigens in multiple sclerosis and to the mutant proteins in Huntington's disease and cystic fibrosis (see website)
This suggests that many human diseases work via this common mechanism, and therefore that most are preventable, by vaccination or elimination of the pathogen, and perhaps curable by immunosuppressant therapy.
Examples of how this works are here
A pdf of a prepublication is available at NaturePrecedings.
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