Does problem with intracellular calcium strengthen case that CFS is AIDS-related????
Novel identification and characterisation of Transient receptor potential melastatin 3 ion channels on Natural Killer cells and B lymphocytes: effects on cell signalling in Chronic fatigue syndrome/Myalgic encephalomyelitis patients
https://biolres.biomedcentral.com/articles/10.1186/s40659-016-0087-2
Changes in Blood Cell Membrane Properties in HIV Type1Infected Patients
Conclusions
Our novel discovery of TRPM3 on NK and B lymphocytes and their significantly reduced expression in CFS/ME patients, together with the preliminary discovery of impaired Ca2+ cytoplasmic concentration in these cells, suggests impaired Ca2+ metabolism may be implicated as a novel pathway for pathogenesis of CFS/ME. Further investigation may elucidate intracellular Ca2+ signalling pathways and the potential role this may play on transcriptional factors, such as NFκB and NFAT as both are activated by calcium through the calmodulin dependent protein kinases and phosphatases. Moreover, as TRPs are widely expressed on almost all human cells and tissues, this raises the question as to whether similar changes of TRPM3 expression or function of these receptors promotes more widespread disruption of intracellular signalling homeostasis in CFS/ME patients.
https://biolres.biomedcentral.com/articles/10.1186/s40659-016-0087-2
Changes in Blood Cell Membrane Properties in HIV Type1Infected Patients
Abstract
To evaluate the possible HIV-1 infection-induced changes in cell membrane properties and in calcium signaling, membrane fluidity, acetylcholinesterase (AChE, a glycosylphosphatidylinositol-anchored protein) activity, and intracellular calcium concentration ([Ca2(+)](int)) were evaluated in lymphocytes and erythrocytes of infected individuals, previous to their engagement in antiretroviral therapy. Membrane fluidity was assessed by fluorescence spectroscopy measurements, using the fluorescence probes 1,6-diphenyl-1,3,5-hexatriene (DPH) and 1-[4-(trimethylamino)-phenyl]-6-phenyl-1,3,5-hexatriene (TMA-DPH). AChE activity was determined by the colorimetric Ellman's method and [Ca2(+)](int) using the fluorescent fura-2 acetoxymethyl ester. When compared with the control group, lymphocytes of infected patients presented significantly decreased membrane fluidity, decreased AChE activity, and increased [Ca2(+)](int). Erythrocytes from HIV-infected patients presented decreased [Ca2(+)](int) when compared with the control group and decreased membrane fluidity near the lipid/water interface. Our data show that HIV-1 infection leads to biochemical and biophysical changes in the membrane itself and in membrane protein activity in lymphocytes (average of infected and noninfected subpopulations) and even in erythrocytes. The present observations are in agreement with a process of facilitated propagation of the infection to new cells, stimulation of virion production, and maintenance of a reservoir of erythrocyte-bound infectious virus.