I'm not sure whether this is what you're referring to, but I attempted to summarise Dr Bansal's presentation at this year's Invest in ME conference here
The part of my article that seems relevant is the proposed explanation of a vicious cycle involving B cell production - specifically, defective B-cell gating which causes the production of low avidity B cells, which in turn may then mount autoimmune attacks on the very cells which caused the defects in B-cell gating.
Yes, things are complicated but this is roughly the idea. In the version that Jo Cambridge and I work with it is not so much that anything mounts an attack on gating cells, and T cells do not really come in to this part of the story (we think they are really just innocent dupes in all this) but the cycling idea is on the right lines.
So, if we ask 'why are the B cells dysfunctional?' the answer may be because B cells are dysfunctional - or to be a bit clearer B cells coming along today will be dysfunctional because yesterdays B cells were dysfunctional. If B cells are not right at the transitional stage the problem must be in bone marrow. What looks tricky about bone marrow is that not only does it grow up young B cells but it is the permanent residence of the fully mature plasma cells that actually make most of the antibodies - cells that a while back were themselves transitional cells coming out of bone marrow.
For this reason I would actually disagree with Amolak Bansal - in a friendly debating way - and say that it is far from clear that we need to get rid of any viruses, which are probably endemic anyway and would cause no trouble if the immune system was working smoothly. If the reason the B cells are misbehaving is because B cells are misbehaving then all we need to do is deal with misbehaving B cells.
But, as people have mentioned, this may need a bit of organising. I tend to think of B cells as a bit like Samurai cadets at the Kyoto Bone Marrow School of Martial Arts. (B cells themselves make hardly any antibody, they are learner cells; it is the plasma cells they turn into that make the antibodies.) They are supposed to learn the art of killing enemies by throwing enemy shaped knives into the Japanese circulation. They are taught their art by venerable plasma cell masters who give them bits of enemy with knives in to practice on. (In order to start making antibodies B cells rely heavily on other B cells having made antibodies before. For babies it is mother's antibodies from the placenta and in milk. If a B cell is shown a protein that already has an antibody attached to it, together with complement, it will start making antibodies. If it is shown a protein without antibody attached it tends to roll over and die.) It is a tough school, because any cadet that has not been given a bit of enemy that fits their knives to practice on after a week is taken by matron to the kitchen, put through the mincer and served up for dinner.
Unfortunately autoimmunity has set in and some master plasma cells are going around killing innocent citizens of Kyoto. Worse, they are handing bits of citizen to cadets with citizen shaped knives so that these are no longer put in matron's mincer. What can be done? Nobody can kill a schoolmaster Samurai, they are too clever, and they can live for ten years. Fortunately, it seems that most of the killing in town is being done by newly trained plasma cells, who, unlike the masters that live in the Bone Marrow School, live in the crowded Spleen camp and mostly only survive for a few months. So if we prevent any new cadets arriving at the School for six months by removing B cells for that time most of the carnage will settle down. The trouble is if we then reopen the doors the rogue masters will get up to their tricks again. We have been waiting for a safe effective anti-plasma cell drug for fifteen years now, although using one would require care, because we don't really want to get rid of all the masters.
Of course if it was only some plasma cells in Spleen that were leading new recruits astray on field days, as might be true of immune thrombocytopenia, then closing the School for six months would do the trick. The problem is that now we have studied this for ten years we have come to realise how hideously complicated the detail is. For almost every rule there is a group of B cells that is exempt. General patterns emerge but there are exceptions.
A key point of this story is that there need be no mention of infections at all. The problem starts with a B cell getting away with making an autoantibody that, by definition, it will have generated at random, and, once it has become a plasma cell, teaching other B cells to follow suit. The epidemiology of autoimmune disease is actually very against any infective trigger. Lots of doctors still just talk of genetic and environmental factors in disease and forget that the epidemiology textbooks mention another class of factor - stochastic or random. Antibody generation is entirely random. But for ME it does look as if, at least in one form, infection is a trigger. That need not mean that it matters much which infection it is. The idea that there is a cross reactivity between a microbe and a self protein has never had much evidence to support it. But it might mean that viruses need to be thought about. The only thing is that the one virus that one would obviously suspect is EBV and rituximab clears away the EBV with the B cells.
I hope that makes some sense.