...Am I missing something here?
I don't totally understand it... Are they saying that HHMMTV is primarily an endogenous or an exogenous virus? And if it is both, then what are the implications?
I don't totally understand it because it looks like HHMMTV might be both endogenous and exogenous...
So is it another HERV (human endogenous retrovirus) that expresses itself fully to form an exogenous virus, which I didn't think was possible for HERV's, or is it a new exogenous human retrovirus?
Has anyone got any insight into this?
A lot of research seems to end up quietly disappearing after it can't be replicated, so maybe it is one of those studies... I haven't looked up any further research studies on the subject yet.
This is indeed an example which is used when researchers like Weiss talk about 'rumor viruses'. The problem is that nobody ever seems to get to the bottom of the subject; all they do is falsify some simple hypothesis without enlightening us further. The idea that breast cancer is the result of an exogenous virus may be one of these.
There is a rule of thumb here that ERVs entered the germ line over many, many years, perhaps even millions of years, and no longer cause disease in species that carry them. For the majority of individuals in a species this seems to be true. However, there is a big catch in this reasoning when you are dealing with a single interconnected human population of billions: there are more possibilities in that population than you can ever test in controlled experiments with any laboratory animal; the sheer scale defeats you.
Another rule of thumb is that ERV sequences in the genomes have been mutated to the point they are not competent to reproduce functional virions. This says even when you see particles in a host they are not signs of disease. These things do turn up, and when they do they are disregarded.
Now we have a new generation of researchers with new tools and the persistence to keep looking. One discovery is that a retrovirus like HIV can sometimes activate genes in HERVs. This does not create a new virus, it simply allows that gene to participate in the infectious disease. Other researchers are finding extensive evidence of recombination of sequences in retroviruses. These sequences may come from host sequences, including possible ERVs, or they may come from other infections in the same host.
A chronic disease need not behave like the familiar model of infectious disease with a simple etiology. When it comes to pathological processes which take place over some 30 years, we have no reliable animal models to study. Even if we did have such models, it is easy to miss the one case in 1000 which would mean millions of human victims.
From a standpoint of sociology of science, you can see that the first discoveries in a field are likely to be the easy ones. Researchers who make a string of discoveries by following a few simple rules become objects of emulation. Their rules of thumb which led them to the easy discoveries become enshrined in textbooks as principles, often without mention of the problems in applying them. Nature does not read textbooks, and is under no obligation to obey these rules.
We are at a time when the simple pat answers are no longer enough. To follow the trail further it is necessary to consider things previously ruled out. Interaction between endogenous and exogenous virus, or between distinct exogenous viruses, is a major complication which will have to be considered. Limited progress in treatment of HIV infection may be the result of ignoring such interactions. A disease which requires transfer of significant quantities of fluids for contagion could easily involve more than one infectious agent.
