Well I found the following two papers to be of interest. They are both available free on Pubmed so I don't know if people want the full-text in the library here or want to get it themselves. The first is an older paper with Susan Vernon and Bill Reeves about differential expression of some mitochondrial genes in CFS patients.
The second is a newer more technical paper I have yet to read entirely. I knew mitochondria were involved in energy production but I did not know they also played a major role in carefully programmed cell death = "apotosis". Cell death occurs all the time in our bodies and is a way to get rid of cancerous, non-functioning, infected, etc. cells the body does not want anymore. Since viruses depend on the cell machinery inside cells they infect to replicate and on cell death to release large bunches of new viruses, many, many viruses have proteins either stopping cell death (more time to replicate!) or promoting cell death (time to release viruses!).
These viruses often affect the mitochondria and I suppose as a byproduct disrupt other mitochondrial functions like energy production along the way. The long list in this article includes HIV and HTLV. It makes me wonder if this is also why people with influenza and hepatitis infections also feel tired (other than cytokine activation) and might have some version of PEM but on a shorter time scale (flu e.g.) or slightly different scale (hepatitis) but we don't hear about it as much because they are "recognized" illnesses and healthcare staff do not say push people to exercise when they have the flu.
1. Preliminary evidence of mitochondrial dysfunction associated with post-infective fatigue after acute infection with Epstein Barr Virus
Suzanne D Vernon1 , Toni Whistler1 , Barbara Cameron2 , Ian B Hickie3 , William C Reeves1 and Andrew Lloyd2
http://www.biomedcentral.com/1471-2334/6/15
2. PLoS Pathog. 2008 May 30;4(5):e1000018.
Viral control of mitochondrial apoptosis.
Galluzzi L, Brenner C, Morselli E, Touat Z, Kroemer G.
INSERM, U848, Villejuif, France.
Abstract
Throughout the process of pathogen-host co-evolution, viruses have developed a battery of distinct strategies to overcome biochemical and immunological defenses of the host. Thus, viruses have acquired the capacity to subvert host cell apoptosis, control inflammatory responses, and evade immune reactions. Since the elimination of infected cells via programmed cell death is one of the most ancestral defense mechanisms against infection, disabling host cell apoptosis might represent an almost obligate step in the viral life cycle. Conversely, viruses may take advantage of stimulating apoptosis, either to kill uninfected cells from the immune system, or to induce the breakdown of infected cells, thereby favoring viral dissemination. Several viral polypeptides are homologs of host-derived apoptosis-regulatory proteins, such as members of the Bcl-2 family. Moreover, viral factors with no homology to host proteins specifically target key components of the apoptotic machinery. Here, we summarize the current knowledge on the viral modulation of mitochondrial apoptosis, by focusing in particular on the mechanisms by which viral proteins control the host cell death apparatus.
PMID: 18516228 [PubMed - indexed for MEDLINE]PMCID: PMC2376094Free PMC Article