Persistent infection hypothesis
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The persistent infection hypothesis or persistent viral infection theory is the hypothesis that myalgic encephalomyelitis is triggered and/or maintained by one or more persistent viruses or infections. This is in contrast to the "hit and run" hypothesis, which is that the infection triggers a disease process that continues long after the immune system has eradicated the initial infection.
Theory[edit | edit source]
Evidence[edit | edit source]
Treatment[edit | edit source]
Notable studies[edit | edit source]
- 1992, Epstein-Barr Virus-Related Persistent Erythema Multiforme in Chronic Fatigue Syndrome[1] - (Abstract)
- 1993, Persistence of enterovirus RNA in muscle biopsy samples suggests that some cases of chronic fatigue syndrome result from a previous, inflammatory viral myopathy[2] - (Abstract)
- 1999, Persistence of enteroviral RNA in chronic fatigue syndrome is associated with the abnormal production of equal amounts of positive and negative strands of enteroviral RNA[3] - (Full text)
- 2010, Acute enterovirus infection followed by myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and viral persistence[4] - (Full text)
- 2012, Can persistent Epstein-Barr virus infection induce chronic fatigue syndrome as a Pavlov reflex of the immune response?[5] - (Full text)
- 2016, Type I and Type II Interferon Coordinately Regulate Suppressive Dendritic Cell Fate and Function during Viral Persistence[6] - (Full text)
- 2018, Myalgic Encephalomyelitis/Chronic Fatigue Syndrome in the era of the human microbiome: persistent pathogens drive chronic symptoms by interfering with host metabolism, gene expression and immunity[7] - (Full text)
See also[edit | edit source]
Learn more[edit | edit source]
References[edit | edit source]
- ↑ Rebora, Alfredo; Loi, Anna; Romagnoli, Marina; Drago, Francesco (February 1, 1992). "Epstein-Barr Virus-Related Persistent Erythema Multiforme in Chronic Fatigue Syndrome". Archives of Dermatology. 128 (2): 217–222. doi:10.1001/archderm.1992.01680120089009. ISSN 0003-987X.
- ↑ Bowles, N. E.; Bayston, T.A.; Zhang, H.Y.; Doyle, D.; Lane, R.J.; Cunningham, L.; Archard, L.C. (1993). "Persistence of enterovirus RNA in muscle biopsy samples suggests that some cases of chronic fatigue syndrome result from a previous, inflammatory viral myopathy". Journal of Medicine. 24 (2–3): 145–160. ISSN 0025-7850. PMID 8409778.
- ↑ Cunningham, Louise; Bowles, N.E.; Lane, R. J.M.; Dubowitz, V.; Archard, L.C. (1990). "Persistence of enteroviral RNA in chronic fatigue syndrome is associated with the abnormal production of equal amounts of positive and negative strands of enteroviral RNA". Journal of General Virology. 71 (6): 1399–1402. doi:10.1099/0022-1317-71-6-1399.
- ↑ Chang, R.; Lee, T.; Voeller, M.; Chia, A.; Chia, J. (February 1, 2010). "Acute enterovirus infection followed by myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and viral persistence". Journal of Clinical Pathology. 63 (2): 165–168. doi:10.1136/jcp.2009.070466. ISSN 0021-9746. PMID 19828908.
- ↑ Agliari, Elena; Barra, Adriano; Vidal, Kristian Gervasi; Guerra, Francesco (March 1, 2012). "Can persistent Epstein–Barr virus infection induce chronic fatigue syndrome as a Pavlov reflex of the immune response?". Journal of Biological Dynamics. 6 (2): 740–762. doi:10.1080/17513758.2012.704083. ISSN 1751-3758. PMID 22873615.
- ↑ Brooks, David G.; Smale, Stephen T.; Bensinger, Steven J.; Horwitz, Marcus A.; Kitchen, Scott G.; Torre, Juan Carlos de la; Wilson, Elizabeth B.; Snell, Laura M.; Elsaesser, Heidi (January 25, 2016). "Type I and Type II Interferon Coordinately Regulate Suppressive Dendritic Cell Fate and Function during Viral Persistence". PLOS Pathogens. 12 (1): e1005356. doi:10.1371/journal.ppat.1005356. ISSN 1553-7374. PMC 4726812. PMID 26808628.
- ↑ Proal, Amy; Marshall, Trevor (November 2018). "Myalgic Encephalomyelitis/Chronic Fatigue Syndrome in the era of the human microbiome: persistent pathogens drive chronic symptoms by interfering with host metabolism, gene expression and immunity". Frontiers in Pediatrics. doi:10.3389/fped.2018.00373.
