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Earlier I discussed some parallels between Mason-Pfizer Monkey Virus MPMV and beta retroviruses which cause mammary tumors in other species in my post Curse of the Monkey God?. In the post titled The Purloined Virus I mentioned a delta retrovirus commonly infecting domesticated cattle and found in unpasteurized milk, thus hiding in plain sight. I've also mentioned Equine Infectious Anemia Virus (EIAV) in passing, an example of a lentivirus still quite active in a domesticated animal found throughout human civilizations today. This stops far short of exhausting even the subject of active retroviral infections in domesticated animals. As my title suggests, we are a wee bit late in planning to deal with the consequences.

This post deals with more recent research on endogenous retroviruses in birds, and what this tells us about recent activity of retroviruses. It turns out not all these viruses are quite as ancient and inactive as typically assumed. The paper in question is titled Unexpected Diversity and Expression of Avian Endogenous Retroviruses.

One finding is pretty clear, alpha retroviruses appear to have evolved in birds from beta retroviruses, and to have left a long trail of viral fragments in bird genomes. There is even an intermediate stage of alphabeta retroviral fragments in birds which has not turned up in any other genomes. The alpha retroviruses seem to have discarded unused parts of their genomes as they became better adapted, which suggests they are not much of a risk to other animals in different taxonomic classes. This kind of sweeping change really looks like the result of evolution in bird hosts over a very long time.

While some gamma retroviral fragments in birds may be extremely old, others may be the result of recent infections by exogenous retroviruses. Avian Reticuloendotheliosis Virus (REV) is still quite active, and is of economic importance to poultry farming. It is also very peculiar in its apparent close relation to mammalian retroviruses like murine leukemia virus (MLV). Generally speaking, viruses, including retroviruses, rarely jump between animals in different taxonomic classes.

We now come across evidence of extremely strange evolutionary events strongly suggesting human involvement. This is described in a paper titled The Extraordinary Evolutionary History of the Reticuloendotheliosis Viruses. Here's a readable discussion of the findings.

Some sequences within avian REV closely resemble sequences from retroviruses found in the echidna (an egg-laying mammal) and in mongoose species found in Madagascar. These animals would essentially never come in contact with domesticated fowl found in North America, yet that is where current evidence shows the origin of avian REV. This evidence is always subject to revision.

Evidence presented in the above paper shows a connection with research on malaria, for which there was no convenient animal model at a time (WWII) when research on a vaccine for malaria became extremely important. The earlier discovery in Sri Lanka of an avian disease resembling malaria suggested this might serve as a model, but import of a new disease which could infect commercial poultry was forbidden. Researchers then examined previously imported fowl to see if a similar disease was already in the U.S. This turned up a parasite named plasmodium lophurae in the crested fireback pheasant imported earlier from Borneo. This could be transmitted to very young chicks.

This parasite was cultured into a form convenient for laboratory work by serial passage through chicken, duck and turkey chicks. What no one realized at that time was that the parasite was already contaminated with a virus. Reports suggesting that a very similar disease could persist even in the absence of detectable parasites then gave clues to the existence of a second infectious agent, other than the parasite. The same problem showed up in a renewed epidemic of Marek's disease, caused by a herpes-type virus (MDV or GaHV2).

Even though Borneo is somewhat close to the range of the echidna, which can be found in New Guinea as well as Australia, there are still problems for a theory concerning wild transmission to that pheasant. The above authors suggest that transmission took place at the New York Zoological Park where exotic wildlife, including those pheasants and echidnas, were housed close together. (Both fare best in tropical conditions, and need protection from New York winters.)

At this point I feel the need to remind readers that none of the people involved in this could have been prepared to deal with a retrovirus because these were unknown except as tumor viruses of chickens and mice. Small viruses like these could not even be imaged at the time the pheasants were first imported because that requires an electron microscope. (Even for those who could afford them, commercial electron microscopes were not available until 1939. Other events of that year distracted people from virological research, and diverted funds to military development.) Those retroviruses then known were also significantly different from REV. Researchers couldn't check for DNA sequences because the discovery that genetic information was carried by DNA lay in the future.

Even after discovery of the significance of DNA there was a long period when reverse transcription was discounted as a possibility by researchers pursuing the more common transcription of genes into RNA and proteins. The original statement of the Central Dogma of Molecular Biology seemed to rule out reverse transcription.

At this point we cross the trail of two other viruses causing two diseases in fowl with serious economic impact: fowlpox and Marek's Disease. (Both diseases were well documented before the events described in the paper on evolution of REV.)

Both of these are caused by DNA viruses, quite different from retroviruses. Marek's Disease Virus (MDV) is also called Gallid Herpes Virus 2 (GaHV2 or GHV2) in research literature. Both DNA viruses are much larger and have much larger genomes than REV (185 kbp vs. 8.7 kpb). There is even room within the genomes of fowlpox virus and GaHV2 for a retrovirus to insert its entire genome. This seems to have happened early during work on vaccines for these two diseases, though the details of exactly where and how are obscure.

Reports of REV genomes inside fowlpox genomes have been around for some years. This was originally thought to come from wild-type fowlpox virus because it was possible to isolate similar chimeric viruses from birds which had not been vaccinated. Later work also found retroviral insertions in MDV/GaHV2. This facilitated the spread of REV into many other birds. It is only now, with detailed analysis of genomes and ERVs from many species, that we can see the clear evidence for recent appearance of REV from a common source which would be very unlikely to arise in natural evolution.

The discovery of this mode of transmission, via a retroviral genome inside a DNA virus, is very troubling. Such a virus would not be easily distinguished from one without retroelements unless the retrovirus were active. The pattern of discovery here via the persistence of disease even after the apparent elimination of the suspected pathogen also raises questions about chronic human diseases which can continue after standard treatment for known pathogens.

Other work shows that retroviral insertions can increase virulence of existing diseases or add new pathological consequences even if there is no complete retrovirus within the DNA virus. These insertions can enhance replication of the DNA virus even if they consist of nothing but LTRs.

Before you blame 20th-century scientists too much, I'd like to say that a great deal of cross-species transmission is much older than these examples. If there is a species of domesticated animal completely free of active retroviral infections, I have to admit I can't think of it. Some diseases caused by viruses in domesticated animals can jump to humans, as apparently happened many years ago with the herpes virus causing chickenpox and shingles (VZV), though that is not a retrovirus.

Domesticated animals are often far more vulnerable to infectious agents than their wild cousins. Anyone who has worked on a farm should be able to confirm the danger of epidemics in dense populations of domesticated animals. Their unnatural environment also increases the chance that highly-contagious pathogens will evolve. In low-density populations, a virulent pathogen which rapidly kills hosts before it is passed on becomes extinct. This biases evolution toward slow or non-lethal diseases. Just as analysis of host genomes shows dramatic changes in domesticated host animals, so too there are dramatic changes in host pathogens which can be traced to the time of domestication. Infectious agents are also more likely to jump between species kept together in groups you would not find in the wild. Many such problems started a long time ago when people were completely ignorant about any microbes.

We don't really have the option of going back to a state of nature before we started domesticating animals, and I doubt many people would choose to do so if given the choice. Civilization, which you might consider the domestication of humans, is as unnatural a phenomenon as the domestication of cattle. When it comes to infectious disease civilization is also an unstable equilibrium which can only be maintained by constant intervention in epidemic processes which would destroy it, as nearly happened on a number of occasions in history.

Our distant ancestors started us on this path, without knowing the consequences. Neither continued ignorance nor inaction are viable options.


Anciendaze every single post of yours is absolutely brilliant, I'm in awe of your research and writing capacity!
You must come from another planet or maybe you are a retrovirus ;).
Just want to add that the interactions between REV and MDV described in the hypothesis of that paper violate Koch's postulates about a single pathogens which can be isolated and observed separately. Unthinking reliance on these in cases where they may not apply could be responsible for the slow recognition of the situation.

The relevance to ME/CFS is that we need to keep in mind that the either/or distinction between a single cause by a DNA virus like EBV or a single retrovirus like MLV is artificial. No natural law rules out the interactions described above.
Incidentally, I notice that the places where Burkitt's lymphoma is most common are also hotbeds of malaria infection. Burkitt's lymphoma is said to be caused by EBV, but it was virtually non-existent in the U.S. before HIV hit us, even though EBV is found at similar incidence in the U.S. One big difference between the U.S. and much of Africa is the way mosquito control has stopped malaria epidemics here. In Africa the parasite which causes the worst malaria is plasmodium falciparum. Plasmodium lophurae is quite similar. Non-human primates with gamma retroviral infections are fairly common in the region where Burkitt's lymphoma has been common. A second parallel is the existence of herpes viruses in both humans and primates which might carry retroviral insertions.

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