What could be the mechanism behind virus latency?

Martin Lerner MD proposed that the reason why patients could have negative blood tests for virus yet still be infected was because the virus(es) that infected them became abortive and therefore unable to reproduce. What could cause this change?

 

When you have develop an environment custom-tailored for defending against bacteria (increased sanitation, frequent antibiotic use) then you lose the ability for native viral control. There is only a finite amount of the immune system, you just exchange acute fatal risk for a small chance of chronic illness.

Also, viral illnesses can cause permanent neuron death, so latency does not particularly matter. Unlike somatic cells, neurons are not synthesized as quickly or efficiently.

 

Everyone of us harbor latent viruses, even healthy persons. For example herpesviruses stay latent in the body, forever, once you are infected. Medicine in general has done a poor job at explaining how pathogens work, at least from my experience, since even the medicine students I have talked with are often surprised when I point out that many pathogens stay in the body forever once you catch them.

This is easy to understand so far. The idea about an abortive infection is more complicated and isn't simply just a latent infection, but one where a virus continues to make viral proteins inside the cell which, according to this idea, causes cellular dysfunction. To understand this complex hypothesis more in detail you should read the relevant papers.

 

https://en.wikipedia.org/wiki/Virus_latency

The short story is that they either

-integrate their viral genome into the host DNA.

-leave their genome floating around the host cell in a protected state.

 

Sorry, I confused latency with abortive. I meant to say what mechanisms cause abortive viral infections.

 

As far as I remember this is just a speculation by Lerner without any substantive evidence.
Cells have a variety f mechanisms for disrupting different phases of viral replication. There might be a way to produce an 'abortive' state but I don't think we have any evidence it occurs in any known clinical situation.

 

I think it's a good hypothesis considering that EBV is very common. Two different herpes viruses could very well interfere with each other's replication because of similar but incompatible molecular RNA. Sort of a Frankenstein's monster creation with broken virions that are sterile.

Another consideration is superinfection due to lack of antibody generation from high nagalase disabling GcMAF. This could allow viruses to spread to tissues they normally couldn't invade.

 

Everyone has EBV replicating at low level, but what has that got to do with 'abortive' colonisation? I don't really see why this idea is at all likely - just because a physician has dreamt it up at some point. I have not heard of viruses competing in the way you suggest.

Again, this sounds pure speculation. I spent my life studying antibody regulation and I cannot see nagalase being important.

All the evidence we have is that PWME do not have persistent viruses any more than other people - and to me that makes sense clinically. These virus theories by and large do not come from immunologists but from individual cphysicians with pet theories.

 

Not pure speculation.

-Buller, 1981. https://jvi.asm.org/content/jvi/40/1/241.full.pdf

In EBV and HIV coinfection:

-Sehrawat, 2018. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5981231/

Let's say you are right and there is no interaction. Another hypothesis would be that coinfection allowing viral penetration into abnormal cell types could itself be the cause of the abortive infection and you don't need the different products to compete. This is supported by Smith et al.

-Smith, 1982. https://link.springer.com/article/10.1007/BF01314164

As for nagalase I don't think CFS nagalase level has ever been explored.

-Yamamoto N. and Urade M. Pathogenic significance of alpha-N-acetylgalactosaminidase activity found in the hemagglutinin of influenza virus..Microbes Infect 2005 Apr;7(4):674-81. Epub 2005 Mar 22.
-Yamamoto N. Pathogenic significance of alpha-N-acetylgalactosaminidase activity found in the envelope glycoprotein gp160 of human immunodeficiency virus Type 1. AIDS Res Hum Retroviruses. 2006 Mar;22(3):262-71.

 

Yes, there are a scattering of odd results from a few researchers with pet ideas - but there always are.

Why bother theorising about viruses anyway? If the problem was really persistent virus there would be some well-documented cases where that got out of control and overt. My thought is to look for new explanations rather than raking over again and again ideas from isolated physicians from thirty years ago.

 

It has been something I have been exploring in my own history. I've had bizarre results like being EBV+ in 2007 with acute mono-nucleosis then having it go negative after HSV6 infection. I also have had success triggering apoptosis using blockers of viral apoptosis inhibition and this has greatly decreased ME associated muscle pain, weakness, Raynaud's disease and periostitis.

 

It's a proof of concept for the theory. If ME is a coinfection due to abortive viruses then allowing the infected cells to die should improve the disease.

Apoptosis occurs when the cells undergo automatic death. Normally this is blocked from inhibition by the viruses. For example, epstein barr virus upregulates Nf-kb which is proinflammatory and blocks caspase 3. HSV6 blocks caspase 8.

A treatment has to find a way around the blocks to trigger cell death.

Apoptosis feels like a localized burning pain then the area goes numb, becomes hypersensitive and twitchy, has localized skin itching then normalizes. Brain fog lessens. Muscles get more exercise tolerance. Localized pain stops.

The reason why ME patients have lots of muscle fasciculation early on that wanes is a symptom of their bodies fighting through apoptosis. However, with increasing viral load the response is overcome and they are stuck with chronic inflammation of all the infected tissue (cold, painful muscles, tendons, fascia and nerves).

 

You'd think, but maybe not. Definitions and thresholds can form built-in impediments which only autopsies may overcome - and even then you'd have to be deliberately searching for the right agent with the right tools. Certainly this has been the case with Lyme disease; it's dragged down, in part, by a hidden history characterized by post-mortem case studies which identified viable spirochetes after the patients death, but defied diagnoses while the patients lived due in large part to crappy metrics and myopic clinicians.

 

I don't see a mechanism for an abortive infection becoming more virulent during a period of low immunity like you do with Herpes Zoster or EBV solo infections. Since that is the basis of viral infection recurrences it explains why we don't see them with ME.

 

I think this is a relevant question. The whole point about apoptosis is that it is silent, without any irritant response. Every day the bone marrow hosts a shedload of apoptotic red cells 'dying' and the rest of the body hosts a shed load of apoptotic white cells 'dying' and for those lucky enough not to have ME (or in my case sciatica) there is not a trace of a symptom.

 

When red cells die at abnormal rates, we feel the very real downstream effects as anemia.

 

Surely you realise that is completely non sequitur?
You get the same symptoms by bleeding 3 pints, with no apoptosis at all.

 

My point is that we do in fact at times feel the effects of cell die off, irrespective of leeching.