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This acquired immunodeficiency could also justify the lytic or abortive reactivation of this and other latent pathogens, such as other herpesviruses and Parvovirus B19, that occurs in patients with ME/CFS [9, 10, 15, 17, 34, 361–363] and could generate, on the one hand, the production of transient autoantibodies such as ANCAs, ANAs, or antiphospholipid antibodies (such as anticardiolipin) [71, 360], causing exacerbation of symptoms, and on the other hand, the increased release of viral dUTPases that increase neurological symptoms [10, 11, 26], generating more inflammation and disease flares