Indonesia Discussion (Alternative to Venting Category)

[Shannon Bennett]

Re: Indonesia Discussion (Alternative to Venting Category)

Sorry, dh came home for lunch. LOL
Mellie, ask her about raised ph values in locals. Ask about flu infections. Are there fewer? Fewer complications or secondary infections in victims? Do people tend to get well faster?
The water tastes pretty good I doubt many would purchase bottled water. But Hailey might have a different social background than does Fairfield. By that I mean farmers versus dot-commers that got out early and bought property at Sun Valley. One segment might buy bottled water in the perception it was better for them. Anyway, see what kind of information you can get that might be relevant. My profoundest appreciation goes out to you.

[Laidback Al]

Re: Indonesia Discussion (Alternative to Venting Category)

. . . Is there a database that would have incidence of flu for the area of Idaho?

I checked Idaho for regular influenza data. All I found was this chart, but not by area.

http://www.healthandwelfare.idaho.go...ersion=Staging

Main Idaho health and welfare page (reporting "no activity") is:

http://www.healthandwelfare.idaho.go...9/default.aspx

and they don't appear to have an archive listing for influenza like Utah.

For Utah: http://health.utah.gov/epi/diseases/.../p_archive.htm

[Shannon Bennett]

Re: Indonesia Discussion (Alternative to Venting Category)

Thanks Al.
Mellie, perhaps your contact can find the data for her area by going to the state health person. Someone has to gather the information perhaps she/he still has records by region. We might not be able to get it but a doctor might have access.

[Theresa42]

Re: Indonesia Discussion (Alternative to Venting Category)

IMHO infection is just a case of viral load and luck (or lack there of).

I suggested genetic variablity (in humans not H5N1) after looking at the family relationships in the Turkish cluster....

I think there's probably a lot to the genetic variability in the host (us!) theory -- although viral load and luck clearly have a lot to do with it as well. Personally, I would bet that there are pretty significant differences between natural 'immunity' (or whatever the correct word is) between different populations of humans. I would think that if historically influenzas have arisen in Asia, then genes protecting people from influenza infections would be more common in that area of the world. This is purely speculation on my part, though.

Here's an article about genomes and viruses you might find interesting. The article has to do with retroviruses, but I don't see why it couldn't apply to other types of viruses as well.:

Learning To Ignore Your Viruses
March 31, 2006

A couple weeks ago I wrote about the 98,000 viruses that have permanently pasted their genes into our genome over the past 60 million years. What makes these viruses doubly fascinating is that scientists are making new discoveries about them all the time. Over at the open-access journal PLOS Pathogens, two new papers add some pieces to the puzzle of how these viruses get into our genomes, and how they affect our health along the way.

(...)

HIV is also a retrovirus, meaning that it inserts its genes into our own. But it is not a live-in virus. It primarily infects one class of white blood cells, and then spreads to other people through shared needles, sex, and other forms of contact. HIV leads to the collapse of the immune system, otherwise known as AIDS. Growing evidence suggests that it does so not by killing cells directly, as once thought, but by chronically overactivating the immune system. As the immune cells divide madly, they eventually start malfunctioning and even committing suicide.

In an opinion piece in PLOS Pathogens, Viktor Muller and Rob J. De Boer point out that most of HIV's cousins, which infect other primates, don't do anything of the sort. I've reproduced a tree they put together, showing the relationship of HIV-like viruses in apes and monkeys. (Go here for a closer view.) HIV, marked in red, is not a single lineage of viruses. One form, HIV-2, jumped from sooty mangabey monkeys into people several times. The more common form, HIV-1, descends from chimpanzee viruses, which have moved into humans many more times. As the tree shows, lots of primates get infected by their own HIV relatives, and this appears to have been going on for millions of years. But if you look at sooty mangabeys or some other monkey, you generally find abundant amounts of the virus without any sign of an overactive immune system. It's not that the virus carried by sooty mangabeys is weak. Scientists have injected it into other monkeys, and it has triggered a strong immune response. The blue arrows on the tree mark the rise of new virus strains in macaques that came from sooty mangabeys. This shift appears to have happened at primate research centers in the past few decades. In their new hosts, these viruses cause lots of nasty symptoms.

Muller and De Boer propose an intriguing hypothesis to explain all of this: perhaps apes and monkeys don't suffer ill effects from these viruses because they carry copies of the viruses in their own genome. After all, the authors point out, HIV's genes have been isolated in human sperm DNA, so these viruses clearly have the potential to make their way into a host genome. Muller and De Boer suggest that primate viruses got into their hosts' genome. The young primates then began making proteins from the virus, which their developing immune system recognized as part of their "self." When the primates then got infected with new copies of the virus, they didn't mount an attack or become overstimulated. The viruses infected the primate's immune cells, but they were only a minor burden to the primates compared to a collapsed immune system. Natural selection would have favored the primates who carried these in-house viruses, as those without them died from viral infections.

Muller and De Boer point out that scientists have created a similar kind of tolerance by injecting viruses into mice -- specifically into the thymus, the finishing school for immune cells. It would be nice if Muller and De Boer could also point to the DNA of HIV-like viruses sitting in the genomes of primates. They did look at the published sequences and came up dry. But the absence of evidence in this case definitely does not mean the evidence of absence. Only a couple primate genomes have been sequenced so far, and it is possible that simple searches may miss virus genes that have become fragments and have acquired a lot of mutations. Muller and De Boer propose that scientists should closely examine the genes that are expressed in developing immune cells in a wide range of primates. Some of these genes may turn out to be similar to the genes of the HIV-like viruses that infect their species. Another way to the test the hypothesis is to run an experiment in which the tolerance to the virus is blocked. Theoretically, these harmless viruses should become as vicious as HIV.

It's cool but a little frightening to imagine if Muller and De Boer are on to something. It would mean that primates have not survived their own HIV epidemics by destroying the virus. Nor would it mean that the virus had become more benevolent, in order to spare its host. It would mean that they simply evolved to ignore the virus altogether. I'm not sure I would agree to gene therapy to insert HIV genes into the genome of my children to protect them from HIV. But it might turn out to be the best way to come to an evolutionary truce with the viruses.

http://loom.corante.com/archives/2006/03/31/learning_to_ignore_your_viruses.php