it doesn’t have to line up exactly if what matters is some developmental change that influences some EBV-related response. The unlucky early peak might be people on the tail end of one developmental change and on the start of the EBV spike. In MS we know the relevance of EBV because people who miraculously managed to avoid EBV are strongly protected from the disease. We’d just need to check if there’s a similar tendency in ME/CFS
okay, so it doesn’t need to be an auto reactive B cell. Just one that can wreak a lot of damage when it ends up in the wrong place. And EBV might facilitate getting into the wrong place. None of what I’m saying hinges on the auto reactivity.
Maybe, but not necessarily. In the mouse paper they showed that one face of the endothelial cells bound to circulating IFN, and the cell started dumping out CXCL10 into the parenchyma through its other face. Most neuron types seem to have receptors for CXCL10, and I’ve shared some ex vivo studies showing that it can affect firing rate of e.g. hippocampal neurons. So maybe you get sickness behavior if CXCL10 reaches some hypothalamic neurons, or maybe CXCL10 directly touches lots of different parts of the brain to create symptoms.
Out of curiosity -- by face do you mean one side of the cell, or does it have a specific meaning?
One side of the cell, endothelial cells are barrier cells so one side will be structurally different than the other in various ways
EBV test result negative here. I am moderate. Mild symptoms appeared well before the first age-related peak, and aggravate right in the second (age 41).
Do you know if it was IgG or IgM and what antigen?
I’ll let you know as soon as possible.
No worries it’s not super important, was just curious because some tests only come back positive if you’re actively in the acute phase of infection