Free fulltext: https://apcz.umk.pl/QS/article/view/52946 BIEŃKOWSKI, Kuba, BIELASKA, Albert, WESOŁEK-BIELASKA, Ewelina, KOŁODZIEJ, Wojciech, GAŁĄZKA, Jakub Krzysztof and GRESZTA, Magdalena. Chronic fatigue syndrome related to herpes simplex viruses infection – a narrative review. Quality in Sport. Online. 21 July 2024. Vol. 17, p. 52946. [Accessed 24 July 2024]. DOI 10.12775/QS.2024.17.52946. Chronic fatigue syndrome related to herpes simplex viruses infection – a narrative review Authors Kuba Bieńkowski Medical University of Lublin https://orcid.org/0009-0007-0589-2035 Albert Bielaska Medical University of Lublin https://orcid.org/0009-0000-0976-1445 Ewelina Wesołek-BielaskaMedical University of Lublin https://orcid.org/0000-0001-7819-2661 Wojciech Kołodziej Medical University of Lublin https://orcid.org/0009-0003-4752-387X Jakub Krzysztof Gałązka Medical University of Lublin https://orcid.org/0000-0003-3128-773X Magdalena Greszta Catholic University of Lublin John Paul II https://orcid.org/0000-0002-0874-4704 DOI: https://doi.org/10.12775/QS.2024.17.52946 Keywords chronic fatigue syndrome, herpes simples viruses, neurology, infectious diseases, neuroinflammatory Abstract This article reviews the potential impact of herpes simplex viruses (HSV) on chronic fatigue syndrome (CFS). HSV-1 and HSV-2 are prevalent pathogens, with HSV-1 acquired early in life and HSV-2 typically transmitted sexually. Studies have shown an association between HSV and CFS, with HSV-1 detected in saliva and cerebrospinal fluid of CFS patients and elevated HSV-2 antibodies found in CFS patients. Immunological abnormalities, including increased pro-inflammatory cytokines and chemokines, suggest immune dysregulation in CFS patients infected with HSV. HSV infections can also disrupt the hypothalamic-pituitary-adrenal axis and autonomic nervous system, impacting energy metabolism regulation and contributing to CFS fatigue. Neuroinflammation, indicated by increased translocator protein binding in CFS patients' brains, may play a role in CFS symptoms. However, the mechanisms linking HSV to CFS and the contribution of viral-induced neuroinflammation are still unclear. Despite the evidence, understanding the complex interactions between HSV, immune responses, and other factors in CFS remains challenging. In conclusion, HSV, particularly HSV-1 and HSV-2, may contribute to CFS development. Further research is needed to unravel the mechanisms involved and identify potential therapeutic interventions.