A common, seemingly benign human virus can trigger an immune response that leads to celiac disease in a mouse model, researchers show.
Editor’s summary: Viruses compound dietary pathology
Reoviruses commonly infect humans and mice asymptomatically. Bouziat et al. found that immune responses to two gut-infecting reoviruses take different paths in mice (see the Perspective by Verdu and Caminero). Both reoviruses invoked protective immune responses, but for one reovirus, when infection happened in the presence of a dietary antigen (such as gluten or ovalbumin), tolerance to the dietary antigen was lost. This was because this strain prevented the formation of tolerogenic T cells. Instead, it promoted T helper 1 immunity to the dietary antigen through interferon regulatory factor 1 signaling. Celiac disease patients also exhibited elevated levels of antibodies against reovirus.
Virus-driven energy theft causes the degradation of messenger RNA in organized genomes, which links mutations to all pathology in all living genera. The energy theft can be viewed in the context of bacteria that become archaea, or in the context of the transgenerational epigenetic inheritance of Zika virus-damaged DNA.
Zika virus-damaged DNA is the obvious link from bacteriophages in gut bacteria to celiac disease. That fact has been placed into the context of nutrient-energy dependent endogenous RNA interference and pheromone-controlled chromosomal inheritance.
Pheromones control the physiology of food energy-dependent reproduction that links the anti-entropic virucidal effects of sunlight to all biophysically constrained biologically-based diversity in all organisms that have not evolved into other species. For example, 1) octopuses, 2) nematodes, and 3) humans.
1) Trade-off between Transcriptome Plasticity and Genome Evolution in Cephalopods
2) Endogenous RNAi Pathways Are Required in Neurons for Dauer Formation in Caenorhabditis elegans
3) RNA-Guided Human Genome Engineering
See also: Virus-driven dietary pathology (2)