It is an interesting finding since some treatments for ER stress exist and are worth testing. It's also somewhat linked to the Itaconate shunt theory that Robert Phair at Stanford has been investigating for the past year.
It is an interesting finding since some treatments for ER stress exist and are worth testing. It's also somewhat linked to the Itaconate shunt theory that Robert Phair at Stanford has been investigating for the past year.
* Virus' have a high failure rate - many infected cells never go on to multiply.
* However, those infected cells may also not still perform correctly.
* If you have a good chunk of your cells in your body no longer performing their function, yet not dying and making way for replacements either, everything isn't going to work as well.
That would explain why it is a wide range of viruses that can all cause fatigue symptoms, and also why parasitic and bacterial infections rarely cause the same.
Technical term: Virus-induced senescence
In this hypothesis, what would be a solution?
Best I can think of is Chemo-therapy, to kill of the bad cells. But that feels incredibly heavy handed, as well as liable to do more damage.
And time.
Prolonged fasting is known to clear away senescent cells. So that is the intervention which seems most promising here. Intermittent fasting can help the gut by giving it time to rest between meals, and it can improve insulin sensitivity because the body spends more time in a low insulin state. Maybe there are longer chains of mechanism there, but at first glance, they don't seem quite as relevant.
* person gets infected
* enyzmes needed to fight infection are used more
* these enzymes need cofactors like manganese, zinc and iron
* Patient becomes depleted in Manganese, zinc and iron.
* since these cofactors are needed to control oxidative stress in the mitochondria there is more oxidative stress in the mitochondria
* fatigue
https://onlinelibrary.wiley.com/doi/10.1016/j.cdtm.2020.11.0...
How would you look for DNA alteration, generally?
However, this is likely to be a fool's errand in this case, because this kind of sequencing normally assumes that we can take a sample of many cells from the body, and that all those cells have the exact same DNA changes. If you have a mutation that is induced in a parent or the single-figure-cell stage of embryo development then that will be true, but for DNA modification by a virus in an adult it will not be. Each cell will have a different insertion. Now, there are some techniques that can sequence the DNA from a single cell, but they don't give quite as good quality data, and because you'd be wanting to sample a good number of cells to see what the distribution of insertions is, it will likely also be very expensive.
It totally could be. Viral persistence is a strong suspect. HIV hides in "sanctuary" tissues. Other viruses and bacteria probably can evade the immune system in certain types of tissue.