Activation of human herpesviruses 6 and 7 in patients with chronic fatigue syndrome

Chapenko, Svetlana; Krūmiņa, Angelika; Kozireva, Svetlana; Nora, Z.; Sultanova, Alina; Vīksna, Ludmila; Murovska, Modra

doi:10.1016/s1386-6532(06)70011-7

Cited by 62 publications

(58 citation statements)

References 27 publications

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“…Chapenko et al [17] recently found a significantly higher prevalence of persistent/latent HHV-6 infections and dual HHV-6 and HHV-7 infections among patients with CFS. The study compared levels and characteristics of viral infection using nested polymerase chain reaction, restriction endonuclease analysis, and flow cytometry in 17 patients with CFS, 12 patients with unexplained chronic fatigue, and 20 healthy controls.…”

Section: Viral Reactivationmentioning

confidence: 97%

“…Researchers found active HHV-6 and dual HHV-6 and HHV-7 infections only in CFS patients, and these infections were present in 40% of those tested. Based on these findings, the researchers concluded that HHV-6 and HHV-7 may be involved in the pathogenesis of CFS and that reactivation of both viruses could cause changes in circulating lymphocytes and a state of chronic immune activation [17].…”

Section: Viral Reactivationmentioning

confidence: 99%

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Chronic fatigue syndrome: Inflammation, immune function, and neuroendocrine interactions

Klimas

Koneru²

2007

Curr Rheumatol Rep

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Investigations into the underlying cause of chronic fatigue syndrome have advanced the field considerably in the past year. Gene microarray data have led to a better understanding of pathogenesis. Recent research has evaluated genetic signatures, described biologic subgroups, and suggested potential targeted treatments. Acute viral infection studies found that initial infection severity was the single best predictor of persistent fatigue. Genomic studies showed that persistent cases express Epstein Barr virus-specific genes and demonstrate abnormalities of mitochondrial function. Studies of immune dysfunction extended observations of natural killer cytotoxic cell dysfunction of the cytotoxic T cell through quantitative evaluation of intracellular perforins and granzymes. Other research has focused on a subgroup of patients with reactivated viral infection. These advances should result in targeted therapies that impact immune function, hypothalamic-pituitary-adrenal axis regulation, and persistent viral reactivation.

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Section: Viral Reactivationmentioning

confidence: 97%

Section: Viral Reactivationmentioning

confidence: 99%

Chronic fatigue syndrome: Inflammation, immune function, and neuroendocrine interactions

Klimas

Koneru²

2007

Curr Rheumatol Rep

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“…Assays of blood in some patients indicate altered T helper (Th)1 and Th2 cytokine profiles, natural killer cell function and activation of the 2-5A synthetase/ RNase L antiviral pathway. [1][2][3] Infection has been reported with a wide range of viruses and bacteria, 4 including Epstein-Barr virus, [5][6][7][8] human herpes viruses 6 and 7, [9][10][11] enteroviruses, 7,12 cytomegalovirus 13,14 and lentiviruses, 15 as well as chlamydia, 7 mycoplasma 16 and borrelia species. 17 An association of ME/CFS with central nervous system (CNS) dysfunction is supported by imaging studies documenting cerebral hypoperfusion and increased white matter T2 signal consistent with chronic inflammation 18 in addition to regional differences in gray 19 and/ or white matter.…”

Section: Introductionmentioning

confidence: 99%

Cytokine network analysis of cerebrospinal fluid in myalgic encephalomyelitis/chronic fatigue syndrome

et al. 2015

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Myalgic encephalomyelitis/chronic fatigue syndrome is an unexplained debilitating disorder that is frequently associated with cognitive and motor dysfunction. We analyzed cerebrospinal fluid from 32 cases, 40 subjects with multiple sclerosis and 19 normal subjects frequency-matched for age and sex using a 51-plex cytokine assay. Group-specific differences were found for the majority of analytes with an increase in cases of CCL11 (eotaxin), a chemokine involved in eosinophil recruitment. Network analysis revealed an inverse relationship between interleukin 1 receptor antagonist and colony-stimulating factor 1, colony-stimulating factor 2 and interleukin 17F, without effects on interleukin 1α or interleukin 1β, suggesting a disturbance in interleukin 1 signaling. Our results indicate a markedly disturbed immune signature in the cerebrospinal fluid of cases that is consistent with immune activation in the central nervous system, and a shift toward an allergic or T helper type-2 pattern associated with autoimmunity.

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“…These approaches consisted primarily of serological studies using many different virus proteins as antigens; some that are expressed early during the replication cycle of the virus and others that are expressed late. Since the antibody pattern against a virus early protein would not be the same as the antibody pattern against a virus late protein, serology studies using different virus proteins (early vs. late) as antigens could lead to variable results [81,82,83,84,85,86,87,88,89,90,91]. Other studies have employed culture methods and polymerase chain reaction (PCR) methods to determine increased viral load when compared to controls [64,81].…”

Section: Herpesviruses Dutpases and Human Diseasementioning

confidence: 99%

Herpesviruses dUTPases: A New Family of Pathogen-Associated Molecular Pattern (PAMP) Proteins with Implications for Human Disease

2016

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The human herpesviruses are ubiquitous viruses and have a prevalence of over 90% in the adult population. Following a primary infection they establish latency and can be reactivated over a person’s lifetime. While it is well accepted that human herpesviruses are implicated in numerous diseases ranging from dermatological and autoimmune disease to cancer, the role of lytic proteins in the pathophysiology of herpesvirus-associated diseases remains largely understudies. Only recently have we begun to appreciate the importance of lytic proteins produced during reactivation of the virus, in particular the deoxyuridine triphosphate nucleotidohydrolases (dUTPase), as key modulators of the host innate and adaptive immune responses. In this review, we provide evidence from animal and human studies of the Epstein–Barr virus as a prototype, supporting the notion that herpesviruses dUTPases are a family of proteins with unique immunoregulatory functions that can alter the inflammatory microenvironment and thus exacerbate the immune pathology of herpesvirus-related diseases including myalgic encephalomyelitis/chronic fatigue syndrome, autoimmune diseases, and cancer.

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Activation of human herpesviruses 6 and 7 in patients with chronic fatigue syndrome

Cited by 62 publications

References 27 publications

Chronic fatigue syndrome: Inflammation, immune function, and neuroendocrine interactions

Chronic fatigue syndrome: Inflammation, immune function, and neuroendocrine interactions

Cytokine network analysis of cerebrospinal fluid in myalgic encephalomyelitis/chronic fatigue syndrome

Herpesviruses dUTPases: A New Family of Pathogen-Associated Molecular Pattern (PAMP) Proteins with Implications for Human Disease

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