Phage , the virus that cures

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jagec

Lifer
Apr 30, 2004
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Cool indeed.

Gene therapy is very promising. But in my opinion should be limited in use until it is actually known how life works. These are dangerous grounds to play on if you can not see the whole playing field. We are constantly invested by bacteria and viruses and recombining of dna happens often. Maybe i am over cautious.

FWIW, the only human gene therapy trials are done in cases where the disease itself is definitively worse than the cure, even if things go wrong.

For example, there was a French study where they used an integrating virus to deliver a corrected copy of a gene that was defective in children with SCID (Severe Combined ImmunoDeficiency, think "bubble boy syndrome"). Random integration is dangerous, and indeed some of the kids got cancer later, but having an immune system beats not having cancer, and cancer is treatable in many cases. So, a net win..but the initial disease was pretty terrible.

More modern ideas/approaches are being pursued for site-specific gene repair, but nothing has been conclusively demonstrated in humans.
 
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FWIW, the only human gene therapy trials are done in cases where the disease itself is definitively worse than the cure, even if things go wrong.

For example, there was a French study where they used an integrating virus to deliver a corrected copy of a gene that was defective in children with SCID (Severe Combined ImmunoDeficiency, think "bubble boy syndrome"). Random integration is dangerous, and indeed some of the kids got cancer later, but having an immune system beats not having cancer, and cancer is treatable in many cases. So, a net win..but the initial disease was pretty terrible.

More modern ideas/approaches are being pursued for site-specific gene repair, but nothing has been conclusively demonstrated in humans.


Not so long ago i read an article about that genes from genetic modified mais and other crops are found in mais that used to be "natural". I worry for such scenario's. I am all for gene manipulation and stemcell research to remove physical and / or mental suffering. But i fear for abuse of the technology. And for people neglecting serious issues for money and fame.
 
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In large part, yes. It's not really the codons that are preferred, it's the amino acids they code for. You can take these mutant p53s and compare their properties to wild type p53 and demonstrate biochemical differences. i.e. wild type binds DNA, mutant doesn't.

As for benzopyrene, after some metabolic processing, it covalently attaches to a base in the double helix. If nothing else, this makes it difficult to impossible for DNA polymerase to copy faithfully. (see pic, notice how the opposing bases don't pair up correctly).
http://en.wikipedia.org/wiki/File:Benzopyrene_DNA_adduct_1JDG.png

I see, thank you.

Finally, I'd bet a reproductive organ that superatoms have nothing whatsoever to do with any of this.

I am sure that in this specific scenario it is not used.
But It's the principle that i find interesting.
And it just does not let me go that it could be or is used in some chemical process.
 
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FWIW, the only human gene therapy trials are done in cases where the disease itself is definitively worse than the cure, even if things go wrong.

For example, there was a French study where they used an integrating virus to deliver a corrected copy of a gene that was defective in children with SCID (Severe Combined ImmunoDeficiency, think "bubble boy syndrome"). Random integration is dangerous, and indeed some of the kids got cancer later, but having an immune system beats not having cancer, and cancer is treatable in many cases. So, a net win..but the initial disease was pretty terrible.

More modern ideas/approaches are being pursued for site-specific gene repair, but nothing has been conclusively demonstrated in humans.


I assume there is now much more (thanks to ever improving technology, but in all honesty i do not know how these techologies works) testing done on contamination and scenario's where unforeseen consequences can arise. Back in the 1960's , Salk and others used monkey tissue cells to produce a polio vaccine. A polio vaccine given to millions of people around the world. Little did they know that these vaccines where contaminated with numerous monkey viruses. One of those viruses is the now well known SV40 virus. A virus that can cause cancer.

http://www.sv40foundation.org/

http://en.wikipedia.org/wiki/SV40

In my opinion though, genetic variance plays a role where SV40 becomes lethal . Or perhaps a combination of pathogens are needed.

But what i am writing is that when scientists overlook something they might create something devastating without intent. Knowing only of what they have done after the effects become apparent. This is what fears me, scientists are human too and can make mistakes too you know...
But i hope that since many of these events occurred , there is now a strict regulation system prevent serious errors...

EDIT :

Some more examples form the past ?

The cutter incident : a paralyzing polio vaccine.

http://en.wikipedia.org/wiki/Cutter_Laboratories


In 1955 Cutter Laboratories was one of several companies licensed by the United States government to produce Salk polio vaccine. In what came to be known as the Cutter Incident, a production error caused some lots of the Cutter vaccine to be tainted with live polio virus.The problem had not only been the carelessness of the Cutter company , but the lack of scrutiny from the Agency ( and its excessive trust in the polio foundation reports ) Ed. Shorter , The Health Century.

The Cutter incident was one of the worst pharmaceutical disasters in U.S. history and caused several thousand children to be exposed to live polio virus upon vaccination.[1] . It should be noted that NIH's Laboratory of Biologics Control ,which had certified the Salk vaccine, had received advance warnings of problems : in 1954 , one of its staff member, Dr Bernice Eddy had reported to her superiors that some of the inoculated monkeys were getting paralysed ( pictures were sent as well). William Sebrell,the director of NIH wouldn't hear of such a thing...Ed.


This is just 30 years ago...


In the 1980s Cutter Laboratories produced unsafe blood products to treat hemophilia. The pharmaceutical product, which was produced from blood given by donors all across the US, was contaminated with HIV. These problems were the subject of lawsuits over the next twenty years.[3].

A recent German documentary called "Toedlicher Ausverkauf: Wie BAYER AIDS nach Asien importierte" (Deadly Sale: How Bayer imported AIDS into Asia) researched the Koate product sold by Cutter Laboratories under full knowledge of its HIV contamination. Cutter ex-manager Merill Boyce expressed that the company should be made responsible and pay damages. Another ex-manager John H Hink, who was also in the responsible team for marketing Koate to Asia, express regret in the documentary, that management required that old stock should be sold despite the HIV contamination. Lexi J Hazan and Charles A Kozak are attorneys representing victims against Bayer AG in the Koate cases. Thomas C Drees is a consultant that researched the Koate Cutter case.
 
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This article also mentions just like Bonnie Bassler did in the video linked in another post in this thread below( or above) that the amount of microbial genes outnumber our own genes.


Two excerpts...

The thousands of bacteria, fungi and other microbes that live in our gut are essential contributors to our good health. They break down toxins, manufacture some vitamins and essential amino acids, and form a barrier against invaders. A study published in Nature shows that, at 3.3 million, microbial genes in our gut outnumber previous estimates for the whole of the human body.

From a bacterium's point of view, the human gut is not the best place to set up home, with low pH and little oxygen or light. Thus, bacteria have had to evolve means of surviving in this challenging environment, which this study now begins to unveil. The scientists identified the genes that each individual bacterium needs to survive in the human gut, as well as those that have to be present for the community to thrive, but not necessarily in all individuals, since if one species produces a necessary compound, others may not have to. This could explain another of the scientists' findings, namely that the gut microbiomes of individual humans are more similar than previously thought: there appears to be a common set of genes which are present in different humans, probably because they ensure that crucial functions are carried out. In the future, the scientists would like to investigate whether the same or different species of bacteria contribute those genes in different humans.

http://www.sciencedaily.com/releases/2010/03/100304075703.htm

EDIT :

http://www.ted.com/index.php/talks/bonnie_bassler_on_how_bacteria_communicate.html
 
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beginner99

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Jun 2, 2009
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My Opinion is that through vertical gene transfers (aka offspring through sexual reproduction) and evolution a complex lifeform can loose genes. But with horizontal gene transfers a complex lifeform can gain genetic code. And not just a few basepairs but an entire sequence.

Don't really get what you mean. That you can only gain by horizontal transfer?

What is a complex lifeform exactly in this context (in your statement)?


Of course you can "gain dna" both ways if something goes wrong in Meiosis. (eg building of eggs or sperms) and the horizontal way.
(Down-syndrome, 3 versions of chromosome 21). -> more dna.

That you can get new genes by horizontal transfer is especially in bacteria nothing else but normal. Easy seen with antibiotic resistance that usually passes different bacteria species.

Also bacterial genomes can be full of latent phages, eg phages that don't replicate but just integrate into the genome. Over time they can become part of the bacteria.
 
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Don't really get what you mean. That you can only gain by horizontal transfer?

What is a complex lifeform exactly in this context (in your statement)?


Of course you can "gain dna" both ways if something goes wrong in Meiosis. (eg building of eggs or sperms) and the horizontal way.
(Down-syndrome, 3 versions of chromosome 21). -> more dna.

That you can get new genes by horizontal transfer is especially in bacteria nothing else but normal. Easy seen with antibiotic resistance that usually passes different bacteria species.

Also bacterial genomes can be full of latent phages, eg phages that don't replicate but just integrate into the genome. Over time they can become part of the bacteria.


Well, i meant gaining fresh genes just like bacteria do it. But normally i doubt complex lifeforms as multicellular lifeforms would allow this to happen that easy. We have way to much protection in our cells to make sure dna does not alter. That is if everything works properly. Now if this alteration indeed would happen in sperm or an egg, it would have to be critical or the error detection and error correction of the cell must not work properly.

And it is the case to get different strands of dna from the mother and the father. If i remember correctly and i am right we get al our mitochondrial dna from the mother and most of the dna is a mix of a single dna strand from the mother and a single dna strand of the father ? Because i remember where a mutation on the dna of the father on the same location causes a different genetic disease then when the mutation is located on the same location but from the mother. .

That is very interesting what you mentioned about the phages. quite interesting indeed. I assumed these phages would destroy the bacteria but afcourse it is an endless war.
How to let evolution make a new bacteria ? Add some phages. But what would happen if we or any other lifeform would get infected by a bacteria that is filled with phages. Is it the phages that infect host cells and not the bacteria itself ? Or is the bacteria bursting open because of the phages and releasing its inner machinery into the cell where it interferes with the cell machinery ?
 
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beginner99

Diamond Member
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I actually studied microbiology but it's few years ago and i work in very different field (Chemistry - IT related). So what I say may not be 100 % even though but is sure is not far fetched either.

Human cells or any mammalian cells can take up dna just like bacteria. Still if this dna encodes one or many genes it's not sure they are actually expressed becase of many reasons like regulation of expression.

Our cells also contain alot of so called junk dna (= no function whatsoever based on current knowledge). Inserting new dna in these regions can't destroy any exisiting genes. Contrary to that bacteria contain more or less 0 junk dna. so any insertion might cause troubles.
So there is no reason why it should not work in humans. Already read something about gene therapy.

The reason is too simple you didn't see it. Bacteria are single-celled, you are not. If your livercells get new genes your children won't have them because they are made from sperms. So only "alterations" to sperms or eggs are transmitted to the offspring everything else is lost when you die. Cancer is a nice example of such alterations.

It's also common knowledge that certain viruses can cause cancer (increase chance you get a certain type of cancer). Can't tell you if it's known why.
 

Gibsons

Lifer
Aug 14, 2001
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As I said in a previous post (#4), there are sequences in the human genome that originated from retroviruses, quite a few in fact.

There are at least three ways viruses can cause cancer. The simplest to explain is that viruses often express genes that cause the infected cells to grow (all viruses don't just simply reproduce and lyse the host cell). The E6 and E7 genes from HPV are pretty well described in lots of places.

The cancers caused from the viral gene therapy experiments are from a different mechanism.
 
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As I said in a previous post (#4), there are sequences in the human genome that originated from retroviruses, quite a few in fact.

There are at least three ways viruses can cause cancer. The simplest to explain is that viruses often express genes that cause the infected cells to grow (all viruses don't just simply reproduce and lyse the host cell). The E6 and E7 genes from HPV are pretty well described in lots of places.

The cancers caused from the viral gene therapy experiments are from a different mechanism.

You are right indeed. When i posted i was getting weary and my memory was letting me down. usually, a swift look at the posts is enough to revive memories.
 
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Time to add a post over parasite using behaviour control over there prey making them do what the parasite wants them to do, even if the prey will die from it :

Rabies the virus that makes it's prey afraid of water and makes it's prey bite you and in the course you get infected as well...
http://en.wikipedia.org/wiki/Rabies

Rabies (pronounced /ˈreɪbiːz/. From Latin: rabies) is a viral disease that causes acute encephalitis (inflammation of the brain) in warm-blooded animals.[1] It is zoonotic (i.e., transmitted by animals), most commonly by a bite from an infected animal but occasionally by other forms of contact. Rabies is almost invariably fatal if post-exposure prophylaxis is not administered prior to the onset of severe symptoms.

The rabies virus travels to the brain by following the peripheral nerves. The incubation period of the disease is usually a few months in humans, depending on the distance the virus must travel to reach the central nervous system.[2] Once the rabies virus reaches the central nervous system and symptoms begin to show, the infection is effectively untreatable and usually fatal within days.

Early-stage symptoms of rabies are malaise, headache and fever, progressing to acute pain, violent movements, uncontrolled excitement, depression, and hydrophobia.[1] Finally, the patient may experience periods of mania and lethargy, eventually leading to coma. The primary cause of death is usually respiratory insufficiency.[2] Worldwide, the vast majority of human rabies cases (approximately 97%) come from dog bites.[3] In the United States, however, animal control and vaccination programs have effectively eliminated domestic dogs as reservoirs of rabies.[4] In several countries, including the United Kingdom, Australia and Japan, rabies carried by ground dwelling animals has been eradicated entirely, they have not in fact been eradicated in airborne mammals such as bats.[citation needed]

The economic impact is also substantial, as rabies is a significant cause of death of livestock in some countries.


The parasite that makes rodents think cats are harmless :
http://arstechnica.com/science/news/2007/04/how-a-parasite-can-help-a-cat-catch-its-mouse.ars

Here's the interesting bit: Toxoplasma fixes the odds. A new study from Ajai Vyas and colleagues at Stanford University, published in PNAS this week, has discovered the mechanism by which the parasitic protozoa does this. Previous studies had shown that infected rodents lacked the instinctive aversion to cat urine; instead they had a vague preference for it. The work in this paper confirms those findings, and also shows how it happens.

By using genetically modified Toxoplasma that produced firefly luciferase (the enzyme fireflies use to glow), Dr. Vyas' team were able to track the sites of infection in animals. After a few days, the infection cleared up throughout the rodents with the exception of cysts localized to the amygdala. Although the infected animals no longer exhibited a fearful response to cat urine, they did still respond normally to learned fear, anxiety-like behavior, and other behavioral tests.

This data proves that the behavioral modification of rodents by Toxoplasma is incredibly specific for advancing the needs of the parasite without affecting many other brain processes, and makes a powerful case for the behavior manipulation hypothesis.


The fungus that makes ants do anything the fungus wants wants even kill itself :
http://www.scientificamerican.com/article.cfm?id=fungus-makes-zombie-ants

After the ant death, the fungus began growing hyphae inside the insect’s body; in a few days, the hyphae would emerge from the exoskeleton—"always … from a specific point at the back of the head," write the authors of the study, which was led by Sandra Andersen of the Center for Social Evolution at the University of Copenhagen in Denmark. Within a week, the fungus had grown to about twice the length of the host ant’s body and had started sexual reproduction. Meanwhile, "the ant cuticle is … remodeled into a protective case by reinforcing the weaker parts," and the parts of the fungus inside the ant’s body appear to differentiate into separate functions, write the researchers.


How about a parasite turns you into a nice juicy red berry. At least that's what your predator thinks. Because the parasite wants to be eaten by your predator :.
http://www.innovations-report.com/html/reports/life_sciences/report-101536.html

"It's phenomenal that these nematodes actually turn the ants bright red, and that they look so much like the fruits in the forest canopy," said co-author Stephen P. Yanoviak, an insect ecologist and assistant professor of biology at the University of Arkansas at Little Rock, who noted that numerous tropical plants produce small red, orange and pink berries. "When you see them in the sunlight, it's remarkable."

Or a parasitic hair worm that lets a grashopper jump into his death and as such the hairworm can travel on :
http://www.nytimes.com/2005/09/06/science/06hopp.html?_r=1

The hairworm seems to have perfected an equally intimate manipulation of its host by inducing a fantastical desire to swim, of which the grasshopper is scarcely more capable than the worm is of flying.

This is not the parasite's only trick. No one knows how, from its aquatic home, the hairworm manages to infect a terrestrial species. Dr. Thomas said he suspects that the larvae, minuscule on hatching, first infect aquatic insects like mosquito larvae and hide as cysts in their tissues.

When the adult mosquito flies away and when it dies, its body may be eaten by a grasshopper or cricket. The hairworm "will then develop, eating absolutely everything not essential to keep its host alive," Dr. Thomas said. The zombified grasshopper is reduced to just its head, legs and outer skeleton by the time it goes for its final swim.

There are some 300 species of hairworm found around the world. Their billions of larvae "will infect everything - frogs, fish, snails," Dr. Thomas said. But it is only in grasshoppers, crickets and katydids that these uninvited guests are able to usurp both the body and mind of their hosts.

How about a wasp that takes control of the movement of it's prey, a cock roach :
http://news.nationalgeographic.com/news/2007/12/071206-roach-zombie.html

The parasitic jewel wasp uses a venom injected directly into a cockroach's brain to inhibit its victim's free will, scientists have discovered.
The venom blocks a chemical substance called octopamine in the cockroach's brain that controls its motivation to walk, the study found.
Unable to fight back, the "zombie" cockroach can be pulled into the wasp's underground lair, where an egg is laid in its abdomen. The larva later hatches and eats the still living but incapacitated cockroach from the inside out.
"The whole thing takes about seven to eight days, during which the meat has to be fresh," said study co-author and neurobiologist Frederic Libersat of Ben-Gurion University of the Negev in Be'ér Sheva, Israel.
"If you kill a cockroach, it rots within a day."

A wasp that controls the web building ability of a spider :
http://www.simpletoremember.com/articles/a/wasp-manipulation/

The larva makes small holes in the spider’s abdomen to imbibe haemolymph1. As the spider continues to build the cocoon web even when the larva is removed shortly before construction would normally start, the changes in the spider’s behaviour must be induced chemically rather than by direct physical interference. The effects are both rapid (removal earlier in the evening did not result in the formation of typical cocoon webs) and long-lasting (spiders from which larvae were removed built similar webs the following night, although some slowly reverted to more normal orbs on subsequent nights).

A parasite that castrates you so all that energy of reproduction is instead used to make you grow larger and thus you will get eaten by the next prey of the parasite :
http://en.wikipedia.org/wiki/Microphallus

Several species are notable for manipulating or influencing their hosts. Microphallus piriformes causes its host, the rough periwinkle, to move upwards, making it more vulnerable to predation by herring gulls. Microphallus pseudopygmaeus chemically castrates (parasitic castration) its host, the snail Onoba aculeus, and causes it to grow larger than normal (it is not clear if this gigantism benefits the host or parasite or if it is a non-adaptive side-effect).[4] Microphallus papillorobustus causes its host, the lagoon sand shrimp (Gammarus insensibilis) to swim upwards, making it more vulnerable to predation.[5] Some species of this genus "hitch-hike" on the manipulations of other species; for example, Microphallus hoffmanni parasitizes the same sand shrimps as Microphallus papillorobustus but does not manipulate the shrimps itself, instead benefiting from the latter's manipulation of the host.
 
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I was curious if they discovered something new on the phoenix virus ...
Nothing so far it seems.

Human Endogenous Retroviruses are expected to be the remnants of ancestral infections of primates by active retroviruses that have thereafter been transmitted in a Mendelian fashion. Here, we derived in silico the sequence of the putative ancestral “progenitor” element of one of the most recently amplified family—the HERV-K family—and constructed it. This element, Phoenix, produces viral particles that disclose all of the structural and functional properties of a bona-fide retrovirus, can infect mammalian, including human, cells, and integrate with the exact signature of the presently found endogenous HERV-K progeny. We also show that this element amplifies via an extracellular pathway involving reinfection, at variance with the non-LTR-retrotransposons (LINEs SINEs) or LTR-retrotransposons, thus recapitulating ex vivo the molecular events responsible for its dissemination in the host genomes. We also show that in vitro recombinations among present-day human HERV-K loci can similarly generate functional HERV-K elements, indicating that human cells still have
the potential to produce infectious retroviruses.

Here is the link :

http://genome.cshlp.org/content/early/2006/10/31/gr.5565706.abstract

http://www.nytimes.com/2006/11/07/s...rss&adxnnlx=1163032655-5nRqAOkgWGeKvh/qQcSYCg
 
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That is interesting indeed.

In a study of monkeys, scientists at Oregon Health Sciences University found that the common cytomegalovirus (CMV), which has infected up to 80 percent of the adult population, can overcome the body's ability to clean out infected cells unlike most viruses.

"In essence, CMV is able to cutoff an infected cell's call for elimination. This allows CMV to overcome this critical immune barrier during re-infection," explained Klaus Frueh, a senior scientist at the university.

The cmv virus is also suspected of being the cause or at least an agent in cancer.

http://www.newsweek.com/id/178660
Two excerpts...
In 2002, UCSF neurosurgeon Charles Cobbs published a novel finding in a prominent cancer journal: nearly all of the two-dozen brain tumors he had analyzed were teeming with a common herpes virus called cytomegalovirus, or CMV. Normally, CMV is harmless—it lies dormant in roughly 80 percent of the population—but in Cobbs's tumor samples, the virus appeared to be actively replicating, even as it remained dormant in nearby healthy tissue. "When I first saw the data, I couldn't sleep for a week," says Cobbs. "I kept asking myself, 'can this be?'" If his findings were correct, they might shed light on the causes of brain cancer, or better yet, provide a new target for battling—maybe even preventing—the disease.



The findings have opened a new avenue of inquiry for one of the most intractable cancers—Glioblastoma Multiforme, an aggressive brain tumor, diagnosed in 10,000 new patients every year and fatal in virtually all cases. (Sen. Ted Kennedy was stricken with the disease last year). The alleged link between CMV and brain cancer may also represent the latest reversal of a decades-old consensus that generally speaking, viruses don't cause cancer. While some scientists are urging caution in interpreting this growing body of evidence, others say that a bias against "cancer-virus" research highlights a major flaw in the way science works. Ideas that challenge the conventional wisdom are often shunned in favor of "safer" hypotheses that stand a better chance of gaining acceptance and securing research dollars. "The powers that be are really opposed to funding this kind of research," says Cobbs who is now at California Pacific Medical Center. "They would rather put their money on more discreet projects where the outcomes are clear."


This would explain a lot.
A hypothetical situation :
Cell turns cancerous for some reason. CMV virus disable attention call for immune cells to come by and destroy the cancerous cell.
Cell keeps growing and dividing. A tumor arises...
That would add a piece to the puzzle. It could be then that the CMV virus does not make you sick, but does makes you more susceptible for cancer. How about that, if that is true... Nice evolutionary 1-2 punch. And another possible example of how 2 or more different and not connected variables match up for a most undesirable outcome.

And another link about the cmv virus possibly linked to some respect with colon cancer.
http://www.rense.com/general31/linked.htm

BIRMINGHAM, Ala. (UPI) -- A common human virus might have some role in the development of colon cancer, according to a new, small study released Thursday.

Preliminary findings from researched conducted at the University of Alabama in Birmingham suggest the cytomegalovirus, or CMV, a widespread organism particularly dangerous to people with weakened immune systems, could be associated with the cellular breakdown that leads to colon cancer.

"This virus is strongly associated with malignant brain tumors," lead researcher Dr. Charles S. Cobbs, also a neurosurgeon with the Birmingham VA Medical Center, told United Press International. "The more I learned about virus, the more I realized it had many properties important for cancer in general."

As described in the Nov. 16 issue of the British journal, The Lancet, Cobbs and his team took colorectal polyps, tumors and surrounding healthy cells from 29 patients. They found proteins from the cytomegalovirus in approximately 80 percent of the polyps and in about 85 percent of the colon cancer samples.

"I'm not trying to say this virus is causal in colon cancer," Cobbs said. "I've just made a preliminary observation ... whether or not it's influencing the cancer remains to be determined."

The virus might be inducing unwanted cell behavior that could lead later to uncontrollable cell growth or cancer, Cobbs explained, but more study is needed to confirm these findings.

Cytomegalovirus resides in about 50 to 80 percent of the U.S. population, Cobbs said, and age and socioeconomic status are risk factors. The virus also can cause ulcers, he explained. It is a relative of the herpes virus and, like herpes or chicken pox, when an individual contracts it, the virus cannot be eradicated. It can lie dormant in a person for years or even decades and not cause any harm.
 
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An interesting article over how 1 bacteria harmless to humans tricks the human inmmune system to attack another bacteria which is also harmless to humans. At least so it seems.

http://www.physorg.com/news195996047.html


"For many microbes, living in harmony with their host is the best option, so why do some suddenly turn nasty?" asks Dr Sam Brown, a Wellcome Trust Research Career Development Fellow at the University of Oxford. "Sometimes the answer is obvious - for example, the cold virus makes its host sneeze, helping it spread wider. But for other bacteria and viruses, which do not normally cause disease, the reason isn't at all clear."

In a study published today in Current Biology, scientists have modelled in mice how a commonly-found bacterium known as Streptococcus pneumoniae interacts with other bacteria, showing that competition for space between rival bacteria can cause deadlier forms of bacteria to evolve. S. pneumoniae usually exists in the nasal passage, where it sits quietly: as many as two in five people in some countries will carry the bug without being aware of it.

When S. pneumoniae is forced to share space with Haemophilus influenzae, another common and ordinarily asymptomatic bacterium, the two begin a tussle for space. But H. influenzae has an extra trick up its sleeve, calling on our immune system to help get rid of its competitor by recruiting white blood cells called neutrophils, which surround and attack the S. pneumoniae bacteria.

"Many bacteria are not a problem to our immune system, so can be left alone," explains Dr. Lysenko. "But the H. influenzae bacteria stir up trouble, saying to the body, 'S. pneumoniae are bad guys - beat them up'. The neutrophils respond, attacking the innocent bacteria and thus helping H.
influenzae to survive."

Many strains of S. pneumoniae exist, each coated with a thick sugar capsule. In some strains, the capsule is particularly protective, and appears to act as armour against the host's immune response. This allows the bacterium to enter the blood stream where it can go on to replicate and cause serious diseases such as pneumonia, bacteraemia (blood infection), septicaemia and meningitis.
 
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Post above this one is the new one.

I just thought this text was something that should be in this thread as well.

http://www.wired.com/wired/archive/11.04/quorum.html

The Bacteria Whisperer

Bonnie Bassler discovered a secret about microbes that the science world has missed for centuries. The bugs are talking to each other. And plotting against us.

By Steve Silberman

Trim and hyperkinetic at 40, Bonnie Bassler is often mistaken for a graduate student at conferences. Five mornings a week at dawn, she walks a mile to the local YMCA to lead a popular aerobics class. When a representative from the MacArthur Foundation phoned last fall, the caller played coy at first, asking Bassler if she knew anyone who might be worthy of one of the foundation's fellowships, popularly known as genius grants. "I'm sorry," Bassler apologized, "I don't hang out with that caliber of people."

The point of the call, of course, was that Bassler - an associate professor of molecular biology at Princeton - is now officially a genius herself. More than a decade ago, she began studying a phenomenon that even fellow biologists considered to be of questionable significance: bacterial communication. Now she finds herself at the forefront of a major shift in mainstream science.

The notion that microbes have anything to say to each other is surprisingly new. For more than a century, bacterial cells were regarded as single-minded opportunists, little more than efficient machines for self-replication. Flourishing in plant and animal tissue, in volcanic vents and polar ice, thriving on gasoline additives and radiation, they were supremely adaptive, but their lives seemed, well, boring. The "sole ambition" of a bacterium, wrote geneticist Fran�ois Jacob in 1973, is "to produce two bacteria."

New research suggests, however, that microbial life is much richer: highly social, intricately networked, and teeming with interactions. Bassler and other researchers have determined that bacteria communicate using molecules comparable to pheromones. By tapping into this cell-to-cell network, microbes are able to collectively track changes in their environment, conspire with their own species, build mutually beneficial alliances with other types of bacteria, gain advantages over competitors, and communicate with their hosts - the sort of collective strategizing typically ascribed to bees, ants, and people, not to bacteria.

Last year, Bassler and her colleagues unlocked the structure of a molecular language shared by many of nature's most fearsome particles of mass destruction, including those responsible for cholera, tuberculosis, pneumonia, septicemia, ulcers, Lyme disease, stomach cancer, and bubonic plague. Now even Big Pharma, faced with a soaring number of microbes resistant to existing drugs, is taking notice of her work.

What Bassler and other pioneers in her field have given us, however, is more than a set of potential drug targets. Their discoveries suggest that the ability to create intricate social networks for mutual benefit was not one of the crowning flourishes in the invention of life. It was the first.

The bobtail squid lives in the knee-deep coastal shallows in Hawaii, burying itself in the sand during the day and emerging to hunt after dark. On moonlit nights, the squid's shadow on the sand should make it visible to predators, but it possesses a "light organ" that shines with a blue glow, perfectly matching the amount of light shining down through the water.

The secret of the squid's ability to simulate moonlight is a densely packed community of luminescent bacteria called Vibrio fischeri. Minutes after birth, a squid begins circulating seawater through a hollow chamber in its body. The water contains millions of species of microbes, but cilia in the squid's light organ expel all but the V. fischeri cells. Fed with oxygen and amino acids, they multiply and begin to emit light. Sensors on the squid's upper surface detect the amount of illumination in the night sky, and the squid adjusts an irislike opening in its body until its shadow on the sand disappears. Each morning, the squid flushes out most of its cache of glowing vibrios, leaving enough cells to start the cycle anew.

In the early '60s, Woody Hastings, a microbiologist at the University of Illinois, noticed a curious thing about the V. fischeri grown in his lab. The bacterial population would double every 20 minutes, but the amount of the cells' light-producing enzyme, called luciferase, would stay the same for four or five hours, dispersed among more and more cells. Only when the bacterial population had vastly increased would the flask begin to glow brightly.

From the perspective of a single V. fischeri cell, delaying light production makes sense. The emission of photons is metabolically expensive, as biologists say, and the puny glow of a lone organism is apt to be overlooked in the vastness of the ocean. So how do the cells know when they have reached critical mass? One of Hastings' students, Ken Nealson, theorized that they were secreting a chemical that accumulates in their environment until the group reaches some threshold density. He christened this unknown molecule an "autoinducer." Nealson's hunch turned out to be correct, and the chemical process by which V. fischeri keep track of their own numbers - determining, like a group of senators, that enough members are present to take a vote - was eventually dubbed "quorum sensing."

More recently, scientists have begun to understand that the importance of cell-to-cell communication goes far beyond mere head counting. Many things that bacteria do, it turns out, are orchestrated by cascades of molecular signals. One such behavior is the formation of spores that make bacteria more resistant to antibiotics. Another is the unleashing of virulence. For disease-causing pathogens like Staphylococcus aureus, waiting for a quorum to assemble before getting down to business has distinct benefits. A few microbes dribbling out toxins in a 200-pound host will succeed only in calling down the furies of the immune system. En masse, they can do serious damage. The first "sleeper cells" were bacterial cells.

Hastings, who is now at Harvard, admits that he underestimated the significance of what he saw in his lab. He assumed that quorum sensing was limited to the marine microbes he was studying. "I accepted the view that these bacteria were in a very specific situation," he says, with a burr of regret. "It doesn't take much reflection to think this must occur elsewhere."

The conclusion that only highly evolved organisms have the ability to act collectively proved to be a stubborn prejudice, however. On several occasions, Nealson tried to publish a diagram in microbiology journals illustrating cell-to-cell signaling in V. fischeri, but peer reviewers rejected it. Bacteria just don't do this, the critics told him.

Bassler proved that they did, by discovering that V. fischeri were not the only chatty microbes in the sea.

As an undergraduate at UC Davis, Bassler decided that she wanted to become a veterinarian. But there was a problem: Dissections in biology class made her faint. She also loathed the rote memorization of lists of muscles and bones. Then she volunteered to work in a biochemistry lab. "I was planning to cure cancer," she recalls, smiling, "then I discovered that bacteria were these totally fantastic creatures."

In 1990, she joined geneticist Mike Silverman for postdoctoral work at the Agouron Institute in La Jolla, California. Microbial light was in the water; the institute was located on a cliff above the Pacific Ocean, where luminescent organisms sparkled on balmy nights. It was Silverman and a graduate student, Joanne Engebrecht, who had mapped the quorum-sensing circuit in Vibrio fischeri by cloning the genes that made luciferase.

At Agouron, Bassler turned her attention to another marine organism, Vibrio harveyi. Unlike V. fischeri, these cells live in the open ocean or in the gut tracts of fish, in bacterial consortia composed of many different species. While the pampered existences of symbiotic V. fischeri are dully predictable, the lives of cosmopolitan V. harveyi are more like ours - having to make sense, minute to minute, of swarms of changing conditions.

Like V. fischeri cells, V. harveyi light up when their own population reaches quorum density. But if a "soup" made of extracts of other species of bacteria is introduced into a V. harveyi culture, they glow as well.

Bassler determined that what looked like one signaling system was actually two: The first sensed the presence of other V. harveyi cells, and the second received signals from many other kinds of bacteria. She and her colleagues created mutant "reporter strains" of V. harveyi - capable of responding to only one signal or the other - to tease the two circuits apart.

The work required an intensity perfectly suited to Bassler, who obsesses about everything - her weight, her guilt that she hasn't put in enough hours at the lab, and especially her bacteria, which she speaks of with unabashed awe. "Did you know that 'vibrio' means vibrate? Unlike E. coli, which are fat and sleepy, these guys zip around under the microscope," she gushes. "Each bacterium in a species is perfect for the niche in which it resides, and if one survives, the whole species survives. They're better than us. They're the ultimate, stripped-down version of life."

Silverman, who is now retired, recalls that while Bassler was "starry-eyed and deferential" to him when she first arrived at his lab, she was soon advancing the research further than he had hoped. "Once she got some traction, she really started pulling," he says.

But in part because Bassler's cute glow-in-the dark microbes seemed to have little impact on the health or commercial success of humankind, her discoveries were considered a sideline curiosity in the world of mainstream science. Just before Bassler left Agouron, she recalls, "I was in the lab, streaking out my bacteria, and I thought, 'I love this job. But I'm gonna be selling shoes at Thom McAnn's next year, because Mike and I are the only people who care about this.'"

Bassler had more reasons to be optimistic than she knew. In 1994, she was hired as an associate professor at Princeton. Thomas Silhavy, who chaired the search committee, admired how far she had pushed the young science of quorum sensing in such a short time. "Figuring out that there were two circuits was a difficult problem, and Bonnie solved it," he says. "It was a gutsy move. Now the whole field rests on it."

That field is expanding at an astonishing rate. In the early '90s, papers were published describing cell-to-cell signaling in Agrobacterium tumefaciens, which causes gall tumors in plants, in Erwinia carotovora, the architect of soft rot in carrots, and in a particularly nasty bug called Pseudomonas aeruginosa, which accounts for 10 percent of all infections contracted in hospitals. Often deadly for cystic fibrosis patients, burn victims, and others with impaired immune systems, P. aeruginosa makes itself impervious to antibiotics by surrounding itself with a biofilm - the bacterial equivalent of a fortress. University of Iowa researcher E. Peter Greenberg, whose daughter has cystic fibrosis, determined that the manufacture of biofilms in P. aeruginosa is mobilized by molecular signals.

Some exceptionally opportunistic bugs have learned to hack the network. The staph microbes responsible for toxic shock, for instance, send out molecular signals in order to compete against nearby staph colonies, disabling their rivals' quorum-sensing circuits before they become virulent.

Quorum sensing has profound implications in the war against disease. With the Age of Antibiotics, we launched a brute force assault on pathogenic bacteria, emphasizing drugs that outright kill. This monolithic approach has brought what geneticists call maximum selective pressure to bear on pathogens. In essence, we have given a 50-year course in antibiotic resistance to an enemy that reproduces every 20 minutes. Bassler's research points to new ways of fighting disease that will aim not to kill but to scramble data in the bacterial network. One approach would be to block the receptors that receive the molecular signals so that cells never become virulent; another would target the DNA-replication mechanisms set in motion inside cells when the signals are received.

Once at Princeton, Bassler turned to identifying the elusive molecule that enabled V. harveyi to communicate with other species. In 2002, her team finally nailed it, christening it AI-2 (autoinducer 2). With the help of Princeton's chemistry department, they determined that the AI-2 molecule contains the element boron, trace amounts of which lurk everywhere in the biosphere, though few biological roles for it have ever been found. When they cloned the gene that makes AI-2, they discovered that at least 50 bacterial species possess the genetic machinery to produce the molecule.

To Bassler, AI-2 is bacterial Esperanto: a molecular language for interspecies conversation and conspiracy that has been spoken on earth for more than a million years.

Not everyone is convinced. Last year, Nottingham University's Paul Williams published a paper titled "Bacterial Cell-to-Cell Communication: Sorry, Can't Talk Now - Gone to Lunch!" Williams claims that while AI-2 plays the role of a signaling molecule in V. harveyi, in most organisms, it's garbage - a metabolic byproduct.

As recently as the late '90s, the National Institutes of Health routinely rejected Bassler's grant applications, politely suggesting that she apply again to a different committee the following year. Her most dependable sources of funding were the National Science Foundation and the Office of Naval Research, which is tracking quorum sensing carefully because biofilms degrade naval steel, foul water lines, and slow the progress of ships at sea. "The good news was that you weren't competing with anyone for money," Bassler recalls. "The bad news was that there was no money."

Papers published over the past year by researchers around the world, however, suggest that Bassler is right about AI-2. And now there's a little more money. Bassler's lab got its first NIH grant this year. She may use some of her $500,000 MacArthur windfall to bring scientists from other fields to study the implications of cell-to-cell communication at Princeton. Quorum-sensing research groups are sprouting up in the UK, Germany, Singapore, Sweden, and Brazil, as well as several dozen universities in the US.

For a growing number of researchers, the term "quorum sensing" already feels too narrowly defined. They favor the use of the broader phrase "cell-to-cell signaling" to stress that communication seems to be the rule, rather than the exception, in every domain of life. Some propose that molecular discourse may even have been one of the things that propelled us up the ladder toward becoming the complex creatures we are; the mechanisms that orchestrate the division of labor in bacterial colonies are similar to the signals that regulate the growth and specialization of animal tissues. "How does your heart know itself from your liver?" asks Bassler. "This may be how multicellular organisms evolved in the first place."

While the post-MacArthur buzz has elevated Bassler from an obscure academic into (in her own half-ironic hyperbole) "the queen of quorum sensing," she is refreshingly unpretentious about her new celebrity. She's grateful that her Advanced Genetics course is as popular as her aerobics classes at the Y, but she's still happiest in the lab, among her bioassays and pipettes, where, as she says, there's a surprise in the incubator every morning.

Through Bassler's discoveries, we're learning that those on the lowest rungs of the Darwinian ladder share one of the traits that has, until recently, been thought of as distinctly human: the propensity to create a continuous stream of commentary about the world. As Bassler puts it, for microbial communities, the advent of the cell-to-cell network made "the difference between subsistence farming and living in Manhattan. These guys know self and other, friend and foe, and have been doing biological warfare for over a million years."
 
May 11, 2008
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For the sake of gathering and storing, i added this as well.

A bit superficial (not to me, to be honest) but ...
Since many chemicals in our daily life can cause changes in our body. It is not surprising that bacteria can do the same while producing chemicals.



http://www.physorg.com/news94707017.html

http://www.physorg.com/news193928997.html

These findings, identified by researchers at the University of Bristol and colleagues at University College London, aid the understanding of why an imbalance in the immune system leaves some individuals vulnerable to mood disorders like depression.

Dr Chris Lowry, lead author on the paper from Bristol University, said: "These studies help us understand how the body communicates with the brain and why a healthy immune system is important for maintaining mental health. They also leave us wondering if we shouldn’t all be spending more time playing in the dirt."

Interest in the project arose after human cancer patients being treated with the bacteria Mycobacterium vaccae unexpectedly reported increases in their quality of life. Lowry and his colleagues reasoned that this effect could be caused by activation of neurons in the brain that contained serotonin.

When the team looked closely at the brains of mice, they found that treatment with M. vaccae activated a group of neurons that produce the brain chemical serotonin. The lack of serotonin in the brain is thought to cause depression in people, thus M. vaccae’s effects on the behavior of mice may be due to increasing the release of serotonin in parts of the brain that regulate mood.

The new research supports this hypothesis, but future studies will be designed to determine if M. vaccae, other bacteria, or pharmaceutical compounds have antidepressant properties through activation of this group of serotonin neurons.

"Mycobacterium vaccae is a natural soil bacterium which people likely ingest or breath in when they spend time in nature," says Dorothy Matthews of The Sage Colleges in Troy, New York, who conducted the research with her colleague Susan Jenks.

Previous research studies on M. vaccae showed that heat-killed bacteria injected into mice stimulated growth of some neurons in the brain that resulted in increased levels of serotonin and decreased anxiety.

"Since serotonin plays a role in learning we wondered if live M. vaccae could improve learning in mice," says Matthews.

Matthews and Jenks fed live bacteria to mice and assessed their ability to navigate a maze compared to control mice that were not fed the bacteria.

"We found that mice that were fed live M. vaccae navigated the maze twice as fast and with less demonstrated anxiety behaviors as control mice," says Matthews.

In a second experiment the bacteria were removed from the diet of the experimental mice and they were retested. While the mice ran the maze slower than they did when they were ingesting the bacteria, on average they were still faster than the controls.

A final test was given to the mice after three weeks' rest. While the experimental mice continued to navigate the maze faster than the controls, the results were no longer statistically significant, suggesting the effect is temporary.

"This research suggests that M. vaccae may play a role in anxiety and learning in mammals," says Matthews. "It is interesting to speculate that creating learning environments in schools that include time in the outdoors where M. vaccae is present may decrease anxiety and improve the ability to learn new tasks."

Provided by American Society for Microbiology
 
May 11, 2008
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Research about the link between bacteria "Enterococcus faecalis " and colon cancer.


The research, published in the October issue of the Journal of Medical Microbiology, sheds light on the way gut bacteria can cause colon cancer.

There are more bacteria in our bodies than there ever have been people on the Earth. In fact, there are more bacteria in the colon than there are human cells in our bodies. Most of the bacteria in our guts are harmless and many are beneficial to our health. However, for several decades scientists have thought that some microbes living in the gut may play a role in the formation of sporadic colorectal cancer.

Enterococcus faecalis is a normal gut bacterium. Unlike most gut bacteria, it can survive using two different types of metabolism: respiration and fermentation. When the bacteria use fermentation they release by-products. One of these is a kind of oxygen molecule called superoxide, which can damage DNA and may play a role in the formation of colon tumours.

"We wanted to investigate how colon cells respond to normal gut bacteria that can damage DNA, like E. faecalis," said Professor Mark Huycke from the Department of Veterans Affairs Medical Center in Olklahoma City, USA. "We found that superoxide from E. faecalis led to strong signalling in immune cells called macrophages. It also altered the way some cells in the gut grew and divided and even increased the productivity of genes that are associated with cancer."

The team found that 42 genes in epithelial cells in the gut are involved in the regulation of the cell cycle, cell death and signalling based on the unique metabolism of E. faecalis. This suggests that cells of the lining of the colon are rapidly affected when E. faecalis switches to fermentation. It also indicates that E. faecalis may have developed novel mechanisms to encourage colon cells to turn cancerous.

Intestinal cancers occur almost exclusively in the colon where billions of bacteria are in contact with the gut surface. For years scientists have tried to identify links between gut bacteria and people who are at risk of colon cancer. This has been made difficult by the enormous complexity of the microbial communities in the intestine.

"Our findings are among the first to explore mechanisms by which normal gut bacteria damage DNA and alter gene regulation in the colon that might lead to cancer," said Professor Huycke. "This research puts n to perspective the complexity of the effects normal gut bacteria can have on the health of an individual."


http://www.sciencedaily.com/releases/2008/09/080921201716.htm

EDIT:

Forgot to mention we have the common cytomegalovirus (CMV) virus that can suppress immune system calls( See posts above) and a bacteria that can turn cells cancerous in the colon. Seemingly not related to each other. But a most undesirable outcome is possible. I wonder if this virus and bacteria if these 2 could combined cause cancer. Reading this i would think so.

Could this be true ?
The bacteria Enterococcus faecalis would then be the cause and the virus cytomegalovirus would be the reason the immune system can not properly destroy the cancerous turned cell. Thus the cancer can grow.

The good researchers mentioned :
In essence, CMV is able to cutoff an infected cell's call for elimination. This allows CMV to overcome this critical immune barrier during re-infection," explained Klaus Frueh, a senior scientist at the university.

As described in the Nov. 16 issue of the British journal, The Lancet, Cobbs and his team took colorectal polyps, tumors and surrounding healthy cells from 29 patients. They found proteins from the cytomegalovirus in approximately 80 percent of the polyps and in about 85 percent of the colon cancer samples.

"I'm not trying to say this virus is causal in colon cancer," Cobbs said. "I've just made a preliminary observation ... whether or not it's influencing the cancer remains to be determined."
 
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I noticed the link to the CMV virus article does not work anymore.

I have acquired a more detailed version of text :


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC538736/

Here is an abstract :

Human cytomegalovirus (HCMV) has evolved multiple strategies for suppression of the antiviral response of the infected cell. DNA array technology has revealed that HCMV clearly regulates host gene expression during the course of a productive infection by enhancing, sustaining, or suppressing steady-state levels of cellular transcripts. Interleukin-6 (IL-6) is a pleiotropic cytokine that plays a central role in the immune response to infection. Here we report a detailed study of the effects of HCMV infection on IL-6 expression by human fibroblasts. UV-inactivated virus was found to induce high levels of IL-6 mRNA and protein expression, and IL-6 mRNA remained abundant in cells 16 h after inoculation even though the level of ongoing IL-6 transcription was not significantly enhanced. In lytic HCMV infections, the onset of viral gene expression resulted in two apparently antagonistic effects on IL-6 expression: (i) transcriptional activation, mediated at least in part by the IE2p86 protein, and (ii) posttranscriptional suppression mediated by destabilization of IL-6 mRNA. Transcriptional activation was outweighed by the suppressive effect, such that cells undergoing productive infection produced less IL-6 than cells challenged with inactivated virus. Suppression of IL-6 expression was independent of the viral IL-10 homologue, cmvIL-10. Destabilization of IL-6 mRNA was observed to coincide with the enhanced expression and aberrant intracellular localization of HuR, an mRNA-binding protein known to interact with IL-6 and other mRNAs containing 3′ AU-rich elements. Our data suggest a novel mechanism for gene regulation by HCMV at the posttranscriptional level.

Human cytomegalovirus (HCMV) is a ubiquitous, clinically important herpesvirus. Following primary infection, HCMV persists throughout the lifetime of the host, during which the virus must avoid elimination by host immune mechanisms. Thus, HCMV has become a paradigm for viral immune evasion (1, 35, 44). In recent years a remarkable series of HCMV immune evasion or modulation systems have been elucidated, including the following: down-regulation of surface MHC-I expression (1), evasion of natural killer (NK) cell-mediated killing (60), and altered expression of immune signaling molecules and interferon response genes (1, 6, 47). Furthermore, these studies have shown that the virus has acquired or evolved in its genome a number of homologues of immune regulators, including chemokines and chemokine receptors (35, 58). The assumption that such molecules play a direct role in persistence and pathogenesis in the host is supported by the fact that attenuated laboratory strains (AD169 and Towne) lack a set of additional genes, associated with immunomodulatory functions, that are present in virulent clinical or low-passage isolates of HCMV (10, 42). Thus, HCMV has a direct impact on normal immune signaling, to promote an infection associated with a wide range of life-threatening conditions in the immune-compromised host (41).
Interleukin-6 (IL-6) plays a central role in both innate and acquired immune responses. IL-6 is the predominant inducer of the acute-phase response, an innate immune mechanism which is triggered by infection and inflammation (45). IL-6 also plays multiple roles during subsequent development of acquired immunity against incoming pathogens, including regulation of cytokine and chemokine gene expression, stimulation of antibody production by B cells (45), regulation of macrophage and dendritic cell differentiation (12), and response of regulatory T cells to microbial infection (40). In addition to these roles in pathogen-specific inflammation and immunity, IL-6 levels are elevated in chronic inflammatory conditions, such as rheumatoid arthritis, and indeed antibodies against IL-6 and the soluble form of its receptor have been used therapeutically for this condition (30). The inflammatory effects of IL-6 have also been implicated as a factor in the failure of organ and tissue grafts; moreover, elevated levels of the cytokine have been reported to accompany HCMV replication in transplanted lungs and bone marrow during episodes of inflammation or rejection (18, 28, 48, 55, 56). Given the ability of HCMV to persist in the infected host, it might be anticipated that the virus has evolved mechanisms to modulate the expression or signaling of IL-6 as part of the viral armory of immune evasion strategies. However, the effects of productive HCMV infection on IL-6 expression are not well understood.
Transcription of the IL-6 gene can be induced by several cellular factors in response to a range of physiological stimuli; moreover, the mRNA is subject to extensive regulation at the posttranscriptional level. Some inducers, such as IL-1, induce both transcription and stabilization of IL-6 mRNA, whereas tumor necrosis factor alpha induces transcription but not stabilization of the mRNA (39). Regulation of IL-6 mRNA stability is mediated through the 3′ untranslated region (UTR), which contains a number of AU-rich elements (AREs). AREs occur in the mRNAs of many genes involved in inflammation, immune signaling, and cell growth and proliferation (4). Their presence in an mRNA generally promotes its degradation in the unstimulated cell but can confer stability in response to appropriate—typically inflammatory—stimuli such as IL-1; these effects on mRNA stability are mediated by a number of both positive (stabilizing) and negative (destabilizing) proteins in the cell, although the precise mechanism of action of ARE-binding proteins has not yet been elucidated fully.
The effects of HCMV infection on cellular gene expression are initiated with binding of the virion to the cell surface (22), with interaction between glycoprotein B and Toll-like receptor 2 playing a major role in this process (13). The binding of virions, or even glycoprotein B in isolation, leads to the induction of inflammatory cytokines and interferon-responsive genes (3, 47, 61). IL-6 mRNA expression is up-regulated by HCMV infection in the absence of de novo expression of viral genes (6, 8, 24, 62, 63), although the IL-6 promoter does not contain recognized interferon response elements. However, virion binding activates multiple intracellular signal transduction pathways, including the phosphatidylinositol kinase, mitogen-associated protein/extracellular signal-regulated kinase, and protein kinase C pathways, all of which lead to the activation of nuclear factors such as NF-κB and p38 (13, 22), which are known inducers of IL-6 gene transcription (45). Since the prolonged expression of inflammatory and antiviral genes would likely be detrimental to viral replication, HCMV has evolved mechanisms to counter the host cell's innate antiviral defenses: another virion protein, the matrix protein pp65, has recently been shown to inhibit expression of many of the interferon-responsive genes that are induced by HCMV infection (5). Nevertheless, wild-type HCMV virions still induce up-regulation of a substantial number of proinflammatory genes, showing that the presence of pp65 is not sufficient to completely overcome the innate immune response. Indeed, elevated levels of prostaglandins appear to be required to activate viral gene expression (64). Thus, the induction of many inflammatory cytokines and interferon response genes is transient (6, 27), and de novo expression of virus-encoded genes acts in concert with incoming pp65 to suppress cellular antiviral gene functions (5).
While HCMV infection is known to produce profound changes in the regulation of cellular genes, published studies provide only limited insight into the control of IL-6 gene expression in the productively infected cell. Although the 72-kilodalton HCMV immediate-early (IE) protein 1 (IE1p72) can mediate transcriptional activation of the IL-6 promoter in monocytic cells (24), expression of IE genes is limited in undifferentiated monocytes (49), and it is not known whether such activation occurs during productive infection. Moreover, most previous work has been carried out in the presence of serum, which has profound effects on the expression of cytokines and induces IL-6 expression in fibroblasts (29). In this study, we analyzed in detail the regulation of IL-6 expression in HCMV-infected primary human fibroblasts, in both the absence and the presence of serum. Fibroblasts remain the best-characterized cell system for the study of productive HCMV replication and are a potential source of IL-6 during localized episodes of viral replication in vivo. Our data reveal a hitherto-unsuspected level of complexity in the regulation of IL-6 expression in the infected cell and an apparently novel mode of gene regulation by HCMV at the posttranscriptional level.
 

Ancalagon44

Diamond Member
Feb 17, 2010
3,274
202
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Sorry for being anal - its just a very common grammar mistake and irritates the crap out of me.
 

tcsenter

Lifer
Sep 7, 2001
18,616
385
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Sorry for being anal - its just a very common grammar mistake and irritates the crap out of me.
It's = it is (contraction).

And probably more appropriate to use that rather than and to join those two phrases. e.g.

"....it's just a very common grammar mistake THAT irritates the crap out of me."
 

Gibsons

Lifer
Aug 14, 2001
12,530
35
91
Not gonna even attempt to comment on the wall of text, but point out one thing. The immune avoidance mechanisms noted for CMV aren't uncommon, EBV has a few tricks as do most herpes viruses.

Given any immune defense against viruses, there's usually a viral means of avoiding it. They don't work perfectly however, or we might all be dead.

For instance, CMV has a really neat way of avoiding NK cells, so it might seem that NK cells wouldn't be effective as part of a response to CMV. However, people with defects in NK cell function tend to have much worse outcomes from CMV infections.
 
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