anciendaze
Senior Member
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I've just skimmed this thread, and might have missed something, but I think there is another way this tricky rascal of a virus can operate which causes endless confusion. Consider this a conspiracy theory which blames the virus for deliberately misleading both immune system and doctors.
First, there is plenty of reason to believe XMRV is active at some times and not others in infected people. There are also stages to the trainwreck of immune problems. I have not had a fever in about 15 years, where these were common at the beginning.
The most important characteristic I've gleaned from information about the virus itself is the connection with the RNase-L 2,5A pathway. This has a very specific function in controlling latent viral infections, where infected cells cannot be eliminated, but the virus can be destroyed, when it reappears, by an enzyme cleaving RNA. Clearly, inhibiting this helps an RNA virus like XMRV survive and propagate.
Aside from inserting genes and making copies of itself, at a low rate, and protecting itself, there doesn't seem to be much that XMRV by itself actually does. For survival it is best not to draw much attention to itself. Because the genes have been completely sequenced, we know there is not a lot of extra functionality hiding inside its genome.
The confusion I suspect in different kinds of onset comes from two sources. One is that this, like many, many infectious diseases, produces a spectrum of illness. At one extreme, we have people infected, but completely asymptomatic. (They may outnumber people with symptoms.) At the other extreme, we have people felled quickly by "the worst flu of my life" who know the day their illness began. In between we can expect to have a continuum of responses.
The second source of confusion is that the illness which catches our attention may not be the original XMRV infection. We may start out asymptomatic, then develop symptoms when a different infection stresses the specifically weakened immune pathways activated to fight it.
My own suspicion here is that this is the connection with vaccination. I tend to doubt the vaccine itself carries the virus. There are already too many available routes of transmission to require that assumption, and the times when people are vaccinated tend to occur when exposure to those is greatest. What I'm guessing is that the immunization exposes a defect previously introduced by XMRV.
Finally, here is something which might be more original, the infection which catches our attention could easily be an earlier viral infection which was driven into latency by a healthy immune system, then reactivated when XMRV crippled defense against latent viruses.
My own experience involved quarantine because of an outbreak of German measles. I was diagnosed as having this because of the classic signs of disease, plus the fact I had had a solid case of ordinary measles as a child. Textbooks say one such case confers life-long immunity.
The catch here is that part of the differential diagnosis of ordinary measles (rubeola) vs. German measles (rubella) is sensitivity to light (photophobia). I definitely had that while quarantined. This leads to two possibilities: my original case of measles as a child was misdiagnosed; the case of German measles was misdiagnosed, and my original latent measles infection was reactivated. Until I read about XMRV, that episode was an unexplainable anomaly.
If that could happen in one case, there is room for enormous confusion in others. This would be part of the reason few seem to agree about the relation to infectious disease.
First, there is plenty of reason to believe XMRV is active at some times and not others in infected people. There are also stages to the trainwreck of immune problems. I have not had a fever in about 15 years, where these were common at the beginning.
The most important characteristic I've gleaned from information about the virus itself is the connection with the RNase-L 2,5A pathway. This has a very specific function in controlling latent viral infections, where infected cells cannot be eliminated, but the virus can be destroyed, when it reappears, by an enzyme cleaving RNA. Clearly, inhibiting this helps an RNA virus like XMRV survive and propagate.
Aside from inserting genes and making copies of itself, at a low rate, and protecting itself, there doesn't seem to be much that XMRV by itself actually does. For survival it is best not to draw much attention to itself. Because the genes have been completely sequenced, we know there is not a lot of extra functionality hiding inside its genome.
The confusion I suspect in different kinds of onset comes from two sources. One is that this, like many, many infectious diseases, produces a spectrum of illness. At one extreme, we have people infected, but completely asymptomatic. (They may outnumber people with symptoms.) At the other extreme, we have people felled quickly by "the worst flu of my life" who know the day their illness began. In between we can expect to have a continuum of responses.
The second source of confusion is that the illness which catches our attention may not be the original XMRV infection. We may start out asymptomatic, then develop symptoms when a different infection stresses the specifically weakened immune pathways activated to fight it.
My own suspicion here is that this is the connection with vaccination. I tend to doubt the vaccine itself carries the virus. There are already too many available routes of transmission to require that assumption, and the times when people are vaccinated tend to occur when exposure to those is greatest. What I'm guessing is that the immunization exposes a defect previously introduced by XMRV.
Finally, here is something which might be more original, the infection which catches our attention could easily be an earlier viral infection which was driven into latency by a healthy immune system, then reactivated when XMRV crippled defense against latent viruses.
My own experience involved quarantine because of an outbreak of German measles. I was diagnosed as having this because of the classic signs of disease, plus the fact I had had a solid case of ordinary measles as a child. Textbooks say one such case confers life-long immunity.
The catch here is that part of the differential diagnosis of ordinary measles (rubeola) vs. German measles (rubella) is sensitivity to light (photophobia). I definitely had that while quarantined. This leads to two possibilities: my original case of measles as a child was misdiagnosed; the case of German measles was misdiagnosed, and my original latent measles infection was reactivated. Until I read about XMRV, that episode was an unexplainable anomaly.
If that could happen in one case, there is room for enormous confusion in others. This would be part of the reason few seem to agree about the relation to infectious disease.
