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Fibromyalgia Syndrome: Canadian Clinical Working Case Definition, Diagnostic and Treatment Protocols–A Consensus Document
Published in I. Jon Russell, The Fibromyalgia Syndrome: A Clinical Case Definition for Practitioners, 2020
Anil Kumar Jain, Bruce M. Carruthers, Maijorie I. van de Sande, Stephen R. Barron, C. C. Stuart Donaldson, James V. Dunne, Emerson Gingrich, Dan S. Heffez, Y.-K. Frances Leung, Daniel G. Malone, Thomas J. Romano, I. Jon Russell, David Saul, Donald G. Seibel
Another important difference between FMS and ME/CFS is in the response to exercise. Patients with mild FMS may be better able to tolerate exercise whereas it aggravates the symptoms in ME/CFS and severely afflicted FMS patients, who need alternate forms of exercise and a gentler progression. Patients with ME/ CFS can be distinguished from healthy controls and FMS patients by determining the ratio of normal 80 kilodalton [kDa] ribonuclease L [RNase L] to the low molecular weight 37 kDa RNase L found in ME/CFS patients (44), but not characteristic of FMS. [See also Appendix 5, p. 82.] A clear diagnosis often has a considerable therapeutic benefit as it reduces uncertainty and orients therapy, both specific and nonspecific.... Dr. Bruce Carruthers, Canada
Transport of mRNA into the Cytoplasm
Published in Alvaro Macieira-Coelho, Molecular Basis of Aging, 2017
Werner E. G. Müller, Paul S. Agutter, Heinz C. Schröder
The 2′,3′-exoribonuclease is able to degrade 2′,5′-oligoadenylates (2-5As) as well as poly(A), and age-related changes in the activity of this enzyme have been shown to be one causative factor in the age-dependent reduction in efficiency of the antiviral 2′,5′-oligoadenylate synthetase/ribonuclease L-system.102
Fatigue in ANCA-associated vasculitis (AAV) and systemic sclerosis (SSc): similarities with Myalgic encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). A critical review of the literature
Published in Expert Review of Clinical Immunology, 2022
Charmaine van Eeden, Mohammed S. Osman, Jan Willem Cohen Tervaert
Other important impaired immunoregulatory cells in ME/CFS, AAV, and SSc include natural killer (NK) cells. In particular, NK cell cytotoxicity is significantly reduced in ME/CFS patients [40–44] – suggested the NK cells may be activated but are incapable of eliminating the target [41]. Like other leukocytes, NK cell functions are regulated by the balance of activating and inhibitor receptors [45]. Hence, increases in KIR3DL1, an NK cell inhibitory receptor which has been observed in ME/CFS [43], may promote NK cell functional attenuation. Further to this, a reduction in NK cell cytotoxicity has been observed in both SSc and AAV [46], with a reduction in the expression of various activating receptors including, NKG2D suggested to be associated with SSc [47,48]. Antiviral defense mechanisms may also attenuate NK cell functions [49,50]. Hence, increased ribonuclease L/2-5A synthetase (RNase L) activity and RNase L proteolysis may further promote this as suggested in patients with ME/CFS [49,50].
Exploring the rationale for thermotherapy in COVID-19
Published in International Journal of Hyperthermia, 2021
Javier Mancilla-Galindo, Norma Galindo-Sevilla
Most respiratory viruses are particularly heat-sensitive and have greater replication and infectivity at the colder temperatures found in the upper respiratory tract as compared to the lower respiratory tract (i.e., 33 °C versus 37 °C) [17,18]. This is seemingly the case for SARS-CoV-2, which replicates more efficiently at 33 °C compared to 37 °C in human airway epithelial cells (AECs) [19]. For instance, incorporation of the SARS-CoV-2 S protein into pseudoviral particles is diminished at 37 °C with respect to 33 °C [20]. Increased temperature is known to suppress rhinovirus replication through increased expression of antiviral defense response genes in AECs and higher levels of type I and III interferons (IFN) [17], and through IFN-independent mechanisms relying on viral double-stranded RNA (dsRNA) intermediates inducing earlier apoptosis of infected cells and enhanced ribonuclease L (RNAseL) activity (independent of its known increased expression by IFN) [21]. RNA interference (RNAi) could be a third dsRNA-dependent mechanism being enhanced at higher temperatures, which is both IFN and non-IFN dependent, and possibly relevant for SARS-CoV-2 infection; we discuss on this in a different subheading.
Chikungunya Virus Infection Outcome: A Systematic Review of Host Genetics
Published in Immunological Investigations, 2021
Jean Moisés Ferreira, Leandro Douglas Silva Santos, Susana Paiva Oliveira, Bárbara Rayssa Correia dos Santos, Ana Caroline Melo dos Santos, Edilson Leite de Moura, Elaine Virginia Martins de Souza, José Luiz de Lima Filho
OAS families are formed by homologous enzymes that are encoded by IFN-stimulated genes. The 2ʹ-5ʹ-oligoadenylate synthetase (OAS)/ribonuclease L (RNase L) system is an innate immunity pathway that responds to pathogens and is associated with the induction of viral and cellular RNAs degradation, thereby, blocks viral infections (Silverman 2007). The OAS genes encode the critical effector enzyme 2ʹ,5ʹ-oligoadenylate synthetase (Bonnevie-Nielsen et al. 2005). Polymorphisms in the genes encoding OAS enzymes are known to influence susceptibility and severity of viral diseases (Alagarasu et al. 2013).