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This paper suggests that, with two to three meters of meteorite material shielding them from radiation, a significant fraction of an intial spore population could still be viable after 25 million years in space. You're correct in thinking that naked spores don't live very long, though.

Interestingly, bacteria kinda anticipate that; the sporulation process contains some protections for DNA. Spores have some fairly sophisticated DNA repair machinery that begins operating very early in the germination process, and they use a lower water content and SASPs (small, acid-soluble proteins) to lock their DNA into a more A-like configuration during the sporulation process. A reasonably large population of bacterial spores can probably remain viable in outer space for a surprisingly long period of time. If you're interested in the subject, I recommend the paper "Resistance of Bacillus Endospore to Extreme Terrestrial and Extraterrestrial Environments" in Microbiology and Molecular Biology Reviews. This paper refers to meteor impacts rather than transfer via rocket components, though.

However, even if strains with mutant forms of M2 can be virulent and not be recognized by antigens resulting from this vaccine, the possibilities are probably going to be more limited than the eternally shuffled deck of HA and NA proteins. Hopefully. This doesn't sound too good, though:

There was almost no impact of the different M2 mutations on viral fitness, as assessed on the basis of the size of viral plaques generated in the absence of drug and of virus titers following MDBK infection at a low MOI (Fig. 1 and 2). These findings are in agreement with a previous report showing that influenza A/H3N2 recombinant viruses can undergo multiple cycles of replication without M2 ion channel activity (15). In that study, recombinants containing the M2 gene of A/Udorn/307/72 (H3N2) with V27T, A30P, and S31N mutations were found to replicate as efficiently as the recombinant WT in Madin-Darby canine kidney cells. Also, a recombinant mutant which had no detectable M2 ion channel activity due to a deletion in the transmembrane domain of the protein (M2-del29-31) exhibited replication efficiency in vitro similar to that of the WT virus (15).

But it's another story whether these strains would succeed in the wild.

By the way, the resistance of H5N1 to amantadine seems primarily due to China giving it to chickens. Wonderful. But the U.S. and Canada still give low-dose antibiotics in livestock feed, so I guess we don't have a drumstick to stand on.

Results from one of my papers: http://aem.asm.org/cgi/content/full/70/10/5980

This text had been classified as
AUTHENTIC
with a 95.2% chance of being an authentic paper

Whew!!, cool maybe I'll pass the turing test too.

Perhaps so, but these guys might be able to sell their domain name for a big ol' crapload of research funding!

Birth of a unique enzyme from an alternative reading frame of the preexisted, internally repetitious coding sequence says that the gene was generated by Flavobacterium.

Emergence of Nylon Oligomer Degradation Enzymes in Pseudomonas aeruginosa PAO through Experimental Evolution says that the gene was generated by Pseudomonas.

"A change is neither degenerative nor beneficial. It is just a change."

This is from the strange world of Darwinian genomics, which seeks to remove the idea of function from biology.

"Whether it is disadvantageous or beneficial depends upon environmental context, and the same alteration may be disadvantageous in one context and advantageous in another."

This is true to a degree. However, it also depends on whether or not the change makes sense in the context of the cell's own system. i.e. a change, in order to be beneficial, must maintain a semantic unity with the rest of the cell system.

The idea of directed mutation is that the class of changes which are most likely to generate beneficial mutations are directed by the cell itself in order to be adaptive. Darwinism holds that changes within the genome are not based on the needs of the organism, but just happenstance, and merely the good ones selected out. This has both experimental and theoretical problems.

Experimentally, more and more data is coming out showing that organisms _do_ change in specific ways in order to be more adaptive.

Theoretically, the search space for beneficial changes is so large, that without direction there would be no possibility of it occurring. See Dembski's Searching Large Spaces. And Dembski is not the only person to recognize the problem. This problem is also referenced in A Biochemical Mechanism for Nonrandom Mutations and Evolution.

"All of the difference between species observed to date are the result of multiple changes of the sort that arise by mutation."

You are confusing "mutation" with "random mutation". Also, this is not entirely true, as species can actually diverge without mutation just through mendellian mechanisms.

"There is no known or imaginable mechanism to prevent mutations from producing the kinds of genomic changes from occurring that have been shown to underlie all species differences"

I'm not sure what you are saying. I'm not saying that any specific mutation is _prevented_. However, many mutations are prevented from surviving, because, well, they would die.

The generative mechanism is cell-directed transcription (as shown in the paper linked above). Mobile elements also seem to be involved, although the exact mechanism triggering and placing them is not known. But, contrary to the neo-Darwinian view of "parasitic elements", mobile elements are highly adaptive in helping organisms cope with stress in specific ways, and can even help restructure genomes.

The advent of better genetic maps has allowed scientists to more accurately time the emergence of the delta32 CCR5 mutation. It now appears that this allele emerged earlier than previously thought and has not been strongly selected by plague. In other words, its frequency in Northern Europeans is explained by 'random', neutral selection and is not markedly different from other genes in the genome. (See here for more details)

Small molecule inhibitors that block the interaction between HIV and susceptible host cells show promise. Two huge concerns -- 1) HIV is not absolutely dependent on CCR5 usage. During chronic infection (presumably, when many CCR5+ cells have already been depleted), HIV can utilize an alternate coreceptor, CXCR4, to mediate entry into a cell. CXCR4-using viruses tend to be more aggressive than CCR5 viruses, and it is possible that CCR5 inhibitors would drive the more rapid emergence of these CXCR4-using strains. 2) Even though CCR5 inhibitors target a conserved, functionally essential target, HIV can still become resistant to these inhibitors.

Sure. See the following report for a further discussion:

http://www.asm.org/ASM/files/ccLibraryFiles/FILENA ME/000000001497/ASM-MicroTriggers.pdf

Considering the small amount of people involved with peacefull research of anthrax,...

...and the legitemate amount of the agent needed for same, the purchase and deployment of these amounts is rather suspicious.

(**For some mysterious reason the government-licensed test facilities want a big pile of money before they play with sarin gas or anthrax. And you generally don't get your equipment back afterwards, since it is now covered with a thin layer of Nasty Death.)

And anyway, anthrax production equipment is not even slightly suspicious. Commercial companies already make bioreactors to grow almost any microorganism you care to name, including bacillus thuringiensis, a very close relative of the anthrax organism b. anthracis. In fact, b. anthracis, b. thuringiensis, and the common soil bacterium b. cereus*** have been called strains of a single species.

(***B. thuringiensis is used commercially as a biowarfare agent against insects. It's basically anthrax for bugs. B. cereus is ubiquitous and can cause food poisoning.)

They have a relatively large circulation and a quite general coverrage. Specialized journals such as the Journal of Biological Chemistry http://www.jbc.org/ and Journal of Virology http://jvi.asm.org/ (two that I'm very familiar with) also add targeted advertising (just like google but without the guess work). I haven't read any journals targeted towards this audience, but my guess is there's advertising in those as well. These scientists must use some resources, whether it's software, raw materials for experimentation or equipment and likewise there are companies that must provide these materials. Perhaps it's not enough income to get a project like this off the ground, but it might be just enough to maintain it. In any event, I wouldn't discount the possibility of providing targeted advertising as a means of income to supplement costs of providing this service.

Well, it's documented in the literature, so you can make your own decision. I just mappened to be reading Ogasawara et al. which you can find here

Eventually, some script kiddie will come along and extrapolate from this paper. Containing the resulting outbreak, while not completely impossible will be most difficult

This work was published in the Journal of Virology, Sept 2003. Somewhat old news. Abstract follows. Full article in the following link http://jvi.asm.org/cgi/content/full/77/18/10028

Recent reports confirm that, due to the presence of long-lived, latently infected cell populations, eradication of human immunodeficiency virus type 1 (HIV-1) from infected patients by using antiretroviral drugs will be exceedingly difficult. An alternative to virus eradication may be to use gene therapy to induce a pseudo-latent state in virus-producing cells, thus transforming HIV-1 into a lifelong, but manageable, virus. Conditionally replicating HIV-1 (crHIV-1) gene therapy vectors provide an avenue for subduing HIV-1 expression in infected cells (by creating a parasite, crHIV-1, of the parasite HIV-1), potentially reducing the HIV-1 set point and delaying AIDS onset. Development of crHIV-1 vectors has proceeded in vitro, but the requirements for a crHIV-1 vector to proliferate and persist in vivo have not been explored. We expand a widely accepted mathematical model of HIV-1 in vivo dynamics to include a crHIV-1 gene therapy virus and derive a simple criterion for designing crHIV-1 viruses that will persist in vivo. The model introduces only two new parameters--HIV-1 inhibition and crHIV-1 production--and both can be experimentally engineered and controlled. Analysis demonstrates that crHIV-1 gene therapy can indefinitely reduce HIV-1 set point to levels comparable to those achieved with highly active antiretroviral therapy, provided crHIV-1 production is more efficient than HIV-1. Paradoxically, highly efficient therapeutic inhibition of HIV-1 was found to be disadvantageous. Thus, the field may benefit by shifting the search for more potent antiviral genes toward engineering optimized therapy viruses that package ultraefficiently while downregulating viral production moderately.

If the virus is nothing but the DNA and a protein coating around it, why are the people wanting it to be live?

Am I missing something? What am I missing?

As a card-carrying virologist let me give you a run down on the information you're missing. If you don't consider the type of nucleic acid (RNA or DNA), there are two types of viruses that infect mammalian cells - enveloped and non-enveloped. Enveloped viruses (such as smallpox) have an outer lipid bilayer (the envelope) that is studded with glycoproteins that need to bind specific molecules on the surface of mammalian cells to permit fusion between the viral envelope and the cell membrane. Fusion allows the virus' nucleic acid to enter the cell. The viral envelope is very fragile, and breaks down rapidly when dried. When the envelope breaks down, it spills the contents of the virus out -- i.e. the nucleic acid, which in the absence of the envelope doesn't have a means to specifically enter a cell. This is one reason why wiping surfaces with 100% ethanol (a dehydrating agent) is quite effective against enveloped viruses like HIV.

Even viruses that are not enveloped have protein coats that directly interact with cell surface molecules that act as receptors to mediate the entry of these viruses into cells. The proteins that make up these coats also denature (lose their proper shape) with time, although this is typically a slower process.

Finally, how stable is the viral nucleic acid? Viral nucleic acids are typically not present as naked RNA or DNA, but in a complex of DNA or RNA with proteins that coat them. These coated nucleic acids are quite stable. Nucleic acid from DNA viruses (like smallpox) is likely to be more stable than nucleic acid from RNA viruses, and I'm guessing that they should be able to do phylogenetic studies on the strain of smallpox present in those scabs after amplifying recovered DNA by PCR.

BTW, after many years of Slashdot lurking, a wee bit of horn tooting. My lab works on how the genome of EBV latches on to human chromosomes. Here's a pretty picture from our work that was on the cover of the Journal of Virology last month.

How do you simulate u-G?

You use a rotating test chamber as shown in a figure from the fulltext. By rotating the chamber, gavity never acts in the same direction for very long and nothing settles out of solution. A second rotating chamber is oriented to let gravity work, while duplicating the effects of spin.

Personally, I am skeptical that bacteria really experience gravity. Bacteria are too small -- at that scale most "fluids" are effectively the consistency of molasses in January. I wonder if something as simple as light impacted their experiment. We shall see.....

Gupta et al, J. Virology 2001 May; 75(10) 4649-54 is an article testing the same concept on mice, more wide-spread, and finding out that it works pretty well.

Jackson, R. J., A. J. Ramsay, C. D. Christensen, S. Beaton, D. F. Hall, and I. A. Ramshaw. 2001. Expression of mouse interleukin-4 by a recombinant ectromelia virus suppresses cytolytic lymphocyte responses and overcomes genetic resistance to mousepox. J. Virol. 75:1205-1210