This article shows that mitochondrial fragmentation benefits the body by preventing the spread of HHV6 so it looks like it's a protective mechanism with that infection. If you disable it then the HHV6 spreads.
https://www.immunohorizons.org/content/4/4/201
That is a very interesting paper by Bhupesh Prusty, Robert Naviaux, Carmen Scheibenboge and others. I had not seen that before.
The quoted passages from the paper below indicate that Prusty et al are saying
HHV-6 might be inducing mitochondrial fragmentation (mitochondrial fission) in order
to thwart the innate immune response.
From what I can make out, this Prusty paper suggests there is a possibility mitochondrial fission benefits HHV-6, protecting this virus from the innate immune system.
Thus if we can promote the opposite of fission, mitochondrial fusion, by means of stearic acid or other interventions, may help the immune system to clear HHV-6, as well as help clear coxsackievirus B.
We have recently shown that HHV-6A reactivation induces mitochondrial fragmentation
HHV-6A might also have evolved a mechanism to induce mitochondrial fission. Mitochondrial fission reduces the cell’s ability to mount innate immune response (reviewed in Ref. 24).
mitochondrial fragmentation might be an adaptation by the virus to avoid innate immune response at the time of viral reactivation
The next quote is interesting, as it says mitochondria fissions thwarts MAVS, and MAVS is a critical immune pathway necessary for mounting an interferon response against coxsackievirus B (ref:
here). So here is another way that mitochondrial fission may benefit coxsackievirus B infection.
Fragmented mitochondria are inefficient in providing strong innate immune response, as they prevent interaction between mitochondrial antiviral signaling protein (MAVS) and stimulator of IFN genes (STING)
Thus, our results show that partial reactivation of HHV-6A is enough to induce mitochondrial fragmentation that leads to lower ATP content in the cells accompanied by lower innate immune response.
The final two quotes below may refer to that "something in the serum" found in ME/CFS patients' blood serum which affects cells and their energy metabolism.
The Prusty paper refers to a "transferrable factor" created in HHV-6A–reactivated cells, which when it arrives at adjacent uninfected cells, puts them into a hypo-metabolic state with reduced ATP production:
These results suggested that an unknown and IFN-independent transferrable factor from HHV-6A–reactivated cells can induce a hypometabolic, fragmented mitochondrial phenotype in responder cells.
we showed that serum from ME/CFS patients contained an activity that produced mitochondrial fragmentation, decreased mitochondrial ATP production, and induced a powerful antiviral state.
What is not quite clear is why HHV-6 infection in cells seems to induce mitochondria fission, and Prusty suggests this fission may protect the virus from the immune response.
But then this "something in the serum" transferrable factor created in HHV-6-infected cells seems to induced a powerful antiviral state when it arrives at adjacent cells (so presumably this factor is created by the host immune system to prevent viral spread to nearby cells, by putting uninfected cells adjacent to the infected cell on antiviral alert).
However, in spite of placing the adjacent cells on antiviral alert, the transferrable factor also fragments mitochondria of these adjacent cells, which Prusty thinks may actually benefit the HHV-6 virus.
So on the one hand the transferrable factor makes it harder for HHV-6 to infect adjacent cells (by putting cells into an antiviral alert state), which makes sense; but on the other hand this factor also does something to make it easier for HHV-6 to infect the nearly cells (fragments the mitochondria), which on first analysis does not quite make sense.
However, perhaps the fragmentation triggered by the transferrable factor might be explained by the fact that in viral infection, apoptosis (destruction of an infected cell by the immune system) is the final step if all other means to clear the virus from the cell have failed. And in order for apoptosis to take place, mitochondrial fragmentation is necessary. So perhaps this transferrable factor is just preparing adjacent uninfected cells for possible apoptosis, should they get infected and should apoptosis become necessary.
