Phage , the virus that cures

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May 11, 2008
I posted this as well in off topic for fun, but it seems like an interesting tale to tell and post here in the virus thread.

Was reading here and there and learned something interesting. We are all infested with tiny mites 0.2-0.4mm in length. They crawl into your hair follicles and pores, feast there on dead skin cells and sebum, the oil substance in your skin. The males crawl over your skin at night to find females to mate with. The females lay eggs in hair follicles that hatch. With a normal healthy person, the amount of demodex mites per square inch or mm is very low. Lower than 3, i read. But when you have a compromised immune system or an unhealthy life style, the mites might become more common and this can result in serious skin diseases. Also because when they die and are numerous in numbers, they decompose and release bacterial substances that can trigger severe immune reactions which shows as itching, red skin and other issues. Even rosacea is linked to these eight legged little critters.

They do not defecate in your hair follicle, they just live for about 14 days, die and decompose. Usually our bacterial friends take care of the rest together with us having a regular shower and wash. Every adult has them.

Have a nice day...

Nice movie :

May 11, 2008
Arstechnica has some interesting articles that i will add to this thread the upcoming days :

First one :
As it turns out, Zika may be what some doomsday movies about the human race going extinct are all about. Fertility reduction in (mouse)males (Infection in the testes)and offspring that can have serious impairments.
Of course, in reality there will always be people who will be able to survive.
Zika is notorious for devastating parents. The virus seized worldwide attention last year by mercilessly causing birth defects, leaving thousands of babies with malformed brains. But the insidious virus may have another, subtler way of terrorizing families: wreaking havoc on the male reproductive system.
At least that’s the concern raised by a new study that finds that the virus causes severe damage to the testes of mice. In the course of a few weeks, the virus damaged reproductive tissue, spurred inflammation, hampered hormone production, shrunk testicles, and reduced sperm counts of the animals, researchers report Monday in Nature. Subsequent mating trials showed that the infected male mice had lower fertility, producing fewer pregnancies and viable offspring.
It’s unclear if the mosquito-borne Zika would cause the same injuries in men as it does in mice, the authors and other experts caution. However, the study begs for follow-up research—particularly given the fact that the virus is known to persist in men’s semen for weeks and cause pain and bleeding.
"Don't jump to the conclusion right off that this is definitely what is happening to the human," Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases told ABC News (Fauci was not involved with the study). But, he added, the finding is a "red flag” that researchers need to pursue.
It's not the only new red flag, either. As scientists dive deeper into Zika research, they're finding more and more potential health effects of the cunning virus. In addition to neurological conditions and the birth defect microcephaly (marked by babies born with malformed heads), which first drew worldwide attention to Zika, new research suggests that the virus can infect bone and cartilage and cause eye and hearing problems in developing fetuses, in addition to attacking the male reproductive system.
For the new study, scientists at Washington University used a Zika infection mouse model to track the effects of the virus in males. As in humans, the virus set up shop in the male reproductive tract. By two weeks, mice infected with Zika had shrunken testicles. Researchers also noted signs of inflammation and damage to the tissue structure along the reproductive tract. As a control, mice infected with dengue virus—a relative of Zika—saw no change in their testicle size and condition.
By two weeks, the Zika-infected mice also had lowered levels of two hormones important for the production of sperm: testosterone and inhibin B. At 42 days after infection, the mice had three times less motile sperm than at the start of the study. Unsurprisingly, when the mice were allowed to mate with healthy females, Zika-infected mice produced fewer pregnancies than healthy, uninfected mice. Of those successful pregnancies from infected fathers, there was a higher rate of non-viable fetuses than those from healthy fathers.

“The extent to which these observations in mice translate to humans remains unclear,” the authors concluded, “but longitudinal studies of sperm function and viability in [Zika virus]-infected humans seem warranted.”

Nature, 2016. DOI: 10.1038/nature20556 (About DOIs).
The next one will be about the famous cat parasite.
May 11, 2008
Toxoplasma gondii, the famous parasite that makes rodents "like" cats, may not have a special gimmick at all, it might just be elevated testosterone levels, linked to more aggressive or assertive behavior. New research disputes the idea that the parasite can make permanent changes to the brain of its host. As it turns out, the effect is not lasting after the infection is cleared. How this turns out to human hosts who might get mental diseases because of the infection is not yet clear. Maybe it could be because of inflammation of specific parts of the brain, where the inflammation causes some neural damage. Other neurons take up the task of the lost neurons and something goes haywire. I do not know.

About the reduced fear infected rodents have :

Vyas found that Toxo specifically affected fear of cat odors, but not learned fear or anxiety. But if you’re imagining infected rodents throwing themselves at cats and begging to be eaten, well, Toxo’s effects are considerably subtler. “They are not fearless, they’re just a little bit less fearful,” said Vyas. “That’s exactly what you’d expect—it’s not a magic wand so that there’s no fear at all.” When Vyas used a stronger source of cat odors, such as a cat collar, the fear became overpowering and the effects disappeared. “I’m very sure if we used a real cat, we probably will not see the effect,” he said.
The article is really long :

You don’t have to watch Tom and Jerry cartoons to know that mice run away from cats. Mice and rats are born with an innate, hardwired fear of their feline predators, and the very scent of a cat is terrifying to them. So it was quite a surprise when in 2000, parasitologist Joanne Webster found rats that had not only lost their fear of cat urine, they were attracted to it. The key feature of these rats? They were infected by the parasite Toxoplasma gondii.
This phenomenon, which Webster dubbed “fatal feline attraction,” is particularly fascinating given the peculiarities of the parasite. Toxoplasma, or Toxo for short, is seemingly able to infect just about any warm-blooded animal anywhere in the world—dogs, cows, kangaroos, koalas, chickens, pigeons, sea otters, dolphins, et al.
Yet despite its ubiquity, Toxoplasma reproduces sexually only in cats. One idea is that if Toxo-infected mice and rats become easier prey, the parasite can get into cats and complete its lifecycle. It’s a compelling story, and one made even more so by the fact that Toxo also hangs out in the brain cells of its hosts—a great location for a mind-manipulating parasite.
The more researchers have investigated how this peculiar parasitic puppetmaster can influence behavior, the more complicated the story becomes. But it’s an enigma worth figuring out, because Toxo infection has been associated with a lot of neurological problems in another species it infects—us. Toxo’s been associated with all kinds of behaviors and disorders, including schizophrenia, suicide attempts, traffic accidents, and even personality and cultural differences. (As for any theories about Toxo being the reason we like cats, or being responsible for crazy cat ladies, feel free to take those with a huge grain of salt.)
It’s still unclear how convincing some of these associations are, and figuring out how the parasite operates has taken a long and winding path with multiple dead ends. These days, researchers may finally have some promising leads about the mechanism behind Toxo’s behavioral effects. “There was a period of confusion, and kind of a wild goose chase,” said Ajai Vyas, a neurobiologist at Nanyang Technological University in Singapore. “I think that period is now gone.”

Toxo in the brain

Vyas first read about Toxoplasma’s behavioral effects in a New York Times article by Carl Zimmer. For a freshly minted PhD looking for his next research project, “it was love at first sight,” he told Ars. He decided to replicate the behavioral work with lab strains of parasites and rodents. In his experiments, Vyas typically released rats into a circular arena where opposite ends had been laced with rabbit urine or bobcat urine.
(Believe it or not, bobcat urine is commercially available and easier to get than an alternative: “With house cats, it’s very difficult to collect urine from them,” Vyas said.)
Uninfected rats avoided the bobcat urine, whereas Toxo-infected ones didn't.
Vyas found that Toxo specifically affected fear of cat odors, but not learned fear or anxiety. But if you’re imagining infected rodents throwing themselves at cats and begging to be eaten, well, Toxo’s effects are considerably subtler. “They are not fearless, they’re just a little bit less fearful,” said Vyas. “That’s exactly what you’d expect—it’s not a magic wand so that there’s no fear at all.” When Vyas used a stronger source of cat odors, such as a cat collar, the fear became overpowering and the effects disappeared. “I’m very sure if we used a real cat, we probably will not see the effect,” he said.
When trying to explain how Toxo produces this effect, Vyas initially focused on the obvious: the parasite’s presence in the brain. When Toxo infects, it barricades itself in thick-walled cysts to evade the immune system, and these cysts can remain for decades in a few sites, including the brain. If Toxo forms cysts in specific parts of the brain, it could do something there to affect behavior. But so far, different studies have found cysts in many different locations with no obvious pattern to their distribution, so it’s unclear if cyst location can influence behavior.
Another hypothesis is that Toxo affects behavior by influencing the levels of dopamine, a major neurotransmitter involved in attraction and reward behaviors. Studies suggested that Toxo infection increases dopamine levels in the brain, and it may do so by producing enzymes that are related to those involved in dopamine synthesis. This idea is particularly exciting given that increased dopamine is associated with many of the same psychological conditions—such as schizophrenia—associated with Toxo infection.
But a recent study has questioned whether Toxo infection actually increases dopamine levels, and some researchers suggest that these enzymes may not get involved in dopamine synthesis at all. Instead, some believe the enzymes provide some other function relevant to Toxo, such as building its cyst wall. So the jury’s still out on the dopamine hypothesis.
To make things even more confusing, other experiments have even questioned whether Toxo needs to form cysts in the brain in order to influence behavior.
Video of Wendy Ingram's experiments

What a difference a strain makes
Wendy Ingram was initially quite skeptical of Toxo’s ability to manipulate behavior. As a graduate student at UC Berkeley, “I actually set out to prove this whole thing wrong,” she told Ars. “Much to my surprise, it’s amazing, it’s really shocking how consistent it is that uninfected mice have an incredible aversion to cat urine, and when you infect them with Toxoplasma, there’s a loss of aversion,” said Ingram, who’s now a post-doctoral fellow at Geisinger Health System in Danville, California.
But the real breakthrough came when Ingram decided to test the effects of different strains of Toxoplasma. Toxo parasites in Europe and the US belong primarily to three distinct strains, cleverly called Type I, II and III. Most previous experiments were conducted with the Type II strain—the Type I strain was too lethal to use for behavioral experiments in mice. “You can’t study them; dead mice tell no tales,” Ingram joked.
But just in time for Ingram’s experiments, other researchers created a mutant Type I strain that, despite missing just one set of genes, displayed radically different behavior. It was now completely unable to kill mice and, unlike the Type II and Type III strains, the mutated Type I strain didn’t form cysts and hang out in the brain for the long term. Accordingly, Ingram expected it to have no effect on behavior.
To her surprise, infection with any of the three Toxo strains caused mice to lose their fear of bobcat urine. In fact, the behavior persisted even a month after infection with the type I strain, when there were no signs of Toxo cysts in their brains. The parasite appeared to have made some long-term change to behavior during its initial infection phase, which lasted just a few days. “That was kind of the most striking and most exciting thing that led us to totally rethink what everyone’s saying is true about what the mechanism could be,” said Ingram. “In the context of my results with the Type I parasite not forming cysts in the brain and getting completely cleared from the brain, from what we can tell, it has nothing to do with cysts.”
How might Toxo influence behavior without being camped out in the brain? Some intriguing new work suggests that the parasite injects its proteins into many neurons without ever forming cysts there. It’s possible that these proteins might be making some permanent changes to the neurons that influence behavior, but that’s still pretty speculative.
Nanyang Technological University’s Vyas has an alternative idea based on a completely different behavior: Toxo makes male rodents more sexually attractive.

Confusion between fear and sex
In addition to making rats less scared of cat urine, Vyas found that Toxo infection changed the way that rats interacted with each other. It made male rats more attractive to females. That’s actually quite unusual—females of many species typically avoid parasite-infected males. He also found a potential reason for Toxo to have evolved this behavioral effect: the parasite was sexually transmittable in rats. “I think it will be very difficult to come up with two separate mechanisms for these two behavioral changes, so we’re taking the view that these are both two sides of the same coin,” Vyas said.
Vyas’s current hypothesis is that the behavioral effects aren’t due to the parasite going to brain, but rather to its presence in another site where it forms cysts: the testes. Toxoplasma infection increases testosterone synthesis in male rats, and Vyas suggests that this increased testosterone mediates the production of pheromones that make males more attractive to females, as well as making changes in their brains that make them less scared of cats. “The beautiful thing about this system is that it explains both behavioral changes,” Vyas said.
Vyas’s results suggest that the Toxo-induced increase in testosterone causes epigenetic changes in a specific part of the brain that processes odor and pheromone information, which shifts the rat from wanting to hide or escape to wanting to breed. Artificially inducing similar epigenetic changes made rats less afraid of cats, even without a Toxo infection. Conversely, blocking such epigenetic changes in rats or castrating them so they couldn’t produce testosterone also blocked Toxo’s effects on the rats’ fearful response to cat urine.
Vyas also looked at neurons in this brain region (the medial amygdala) that were normally recruited by things that would make the rats want to breed, such as the presence of female rats. When male rats were infected with Toxo, these neurons were now being recruited by cat odors, a stimulus that should make them scared rather than horny. “In other words, there is a mix-up between defensive and reproductive behavior,” said Vyas. “The parasite then is just tapping into a pre-existing circuit.”
It’s an intriguing hypothesis, but it’s still preliminary and the studies need replication. Plus, there are still some loose ends to tie up—for instance, how would this mechanism work in females? Female rats show similar responses to cat urine as males when infected with Toxo, but they produce much less testosterone and have fewer of the neurons that are recruited by cat odors. Vyas is still trying to figure out whether the same testosterone-based mechanism that he posits in males would also work in females, or whether they have their own parallel circuit. Regardless, the findings do suggest a way that Toxo could cause its behavioral effects without needing to be in the brain.
Researchers are also considering the possibility that Toxo does need to be in the brain to have its effects, but the effects are indirect. “What we do know with Toxo is that it does elicit a very strong inflammatory immune response, it does get into the brain, and so the inflammatory response occurs in the brain itself, which is not a site that most microbes can get to,” said Vern Carruthers, a parasitologist at the University of Michigan. There’s an established link between immune response and behavior in the literature, an effect that’s been seen in rodents.
The idea that Toxo’s behavioral effects involve the immune system isn’t new. But Ingram’s work showed that all three Toxo strains, even the mutated one that didn’t form brain cysts, elicited a brief inflammatory response in the brain. It’s possible that this immune response makes some lasting changes to the brain, leading to a change in behavior, though a lot more work need to be done here.
If Toxo’s effects are due to the host’s immune response to it, then the parasite doesn’t have to do anything special to change the way its victims act. That raises a more basic question: does Toxo actively manipulate its host?

The parasite or the host?

We know Toxo infection causes behavioral effects. But is the parasite a devious puppetmaster, manipulating its host’s behavior to increase its transmission into cats? The behavioral manipulation hypothesis assumes that by making rodents lose their fear of cats, Toxo increases its transmission to its feline host. It’s a perfectly reasonable suggestion, but it turns out this idea is quite hard to demonstrate.
“There is no hard data either for or against the idea that behavioral changes increase transmission to cats,” said Amanda Kristancic, a zoologist at Murdoch University in Australia. Another parasite related to Toxo, Eimeria vermiformis , appears to similarly make mice less scared of cats. But unlike Toxo, this parasite doesn’t rely on cats for transmission—in fact, if cats kill the Eimeria -infected mice, the parasite would die, too. As a result, Eimeria researchers have no reason to think that the parasite causes this behavior or benefits from it, Kristancic said.
Both Nanyang Technological University’s Vyas and Geisinger Health System’s Ingram agreed that it would be important to confirm if the loss of fear caused by Toxo infection actually results in increased rodent predation. But again, that’s a hard experiment to do. “The perfect experiment would be release half mice that are infected, half mice that aren’t, in a barn that’s enclosed, and then let a couple of cats out, and catch all the mice at the end and figure out how many got eaten and which ones,” said Ingram. “But no one’s going to let you do that, it’s horrible.”
Researchers could also study Toxoplasma transmission by conducting more predation studies in the wild and in other animals. A recent study found that wild chimpanzees infected by Toxoplasma had a similar loss of aversion to the smell of leopard urine. There were only nine infected chimpanzees, and the study was correlative, so one can’t read too much into it. But it does at least open up the possibility that the loss of fear of feline predators occurs in species beyond mice and rats. Follow-up studies looking at Toxo’s effects in birds might be particularly interesting, as they’re also a prey species of cats.
What of Toxo’s effects in humans, such as its association with schizophrenia or suicide attempts? They may not require active manipulation by the parasite either. One idea is that, as in rodents, they may be the result of our body’s immune response to Toxo. For reasons that have nothing to do with this parasite, some researchers have suggested that immune and infectious causes might be responsible for a range of human behavioral effects and neurological disorders, including Alzheimer’s disease, schizophrenia, and autism. For now, it’s a hotly-debated topic. “It’s been known for a while that there are changes in the inflammatory status of the brain in people with schizophrenia,” said Carruthers. “What’s unknown is whether it’s playing a causal role or it’s just a consequence.” Similar things could be said about the other disorders.
So when it comes to humans, it turns out it can be quite hard to pin down exactly what Toxo does, let alone how it does it.

A hard thing to study
Toxoplasma infects a lot of us—almost a quarter of Americans, a third of all humans worldwide, and more than 90 percent of the population in some countries. We get it mostly from undercooked meat, or from handling cat litter or contaminated soil. Thankfully, as long as you’re healthy, it just feels just like a mild flu, although it can have more severe consequences if you’re pregnant or have a weakened immune system.
Toxo infection has also long been associated with a number of behavioral and neurological effects in humans. “ Evidence is strongest for schizophrenia, but also quite strong for affective disorders in general, and especially suicide attempts,” said Fuller Torrey, a psychiatrist at the Stanley Medical Research Institute. How does a loss of fear of cats translate to all these different effects in humans? “Very few of us are likely to be eaten by large cats, so Toxoplasma gondii doesn’t accomplish anything by getting in us, but it doesn’t know it’s in a dead-end host, it just kind of does its thing,” said Torrey. “It’s smart, but it’s not that smart.”
In interpreting the human studies, it doesn’t help that there’s still a distinct lack of scientific consensus about what effects Toxo actually has. “I still take lot of human studies with quite a bit of salt,” Nanyang Technological University’s Vyas said. “I’m not saying that the experiments are not good, but that the interpretation is fraught with a lot of complications.” Many researchers Ars spoke to pointed out that Toxo infection rates vary dramatically around the world, from a few percent of the population to more than 90 percent in some countries, whereas rates of schizophrenia are fairly constant around the world at 0.5-1 percent.
The reality is that human behavior and mental illness are complex, and many of the Toxo studies are not standardized and have yet to be replicated. Toxo certainly doesn’t make it easy to do this work—there’s no good way to detect Toxo cysts in a living person, and the studies rely on correlations with Toxo antibody levels. But antibodies are a crude measure that don’t tell you about a number of things that could affect behavior, such as when the infection occurred or which strain of the parasite you’re infected with.
To get at causation, larger studies that track people from a young age could help figure out if their behavioral symptoms show up before or after Toxo infection. Another approach would be to get rid of the parasite from an infected person who has a mental illness, and see if their clinical symptoms improve. But Toxo doesn’t let us do that yet—we currently don’t have a good way to get rid of Toxoplasma cysts once a person is infected.
The bottom-line? Toxo remains intriguing but complicated. “If there was some huge major behavioral differences, then we would have seen it by now,” said Zi Teng Wang, a parasitologist at Washington University in St. Louis. “It could be having some effect, but I wouldn’t worry about brain parasites making me crazy anytime soon.”
May 11, 2008
This sure is interesting.

Whole story about Henrietta Lack :


In early 1951, a woman named Henrietta Lacks visited the “colored ward” at Johns Hopkins hospital for a painful lump she found on her cervix. She was seen by Dr. Howard W. Jones, who indeed found a tumor growing on the surface of her cervix. He took a tissue sample, which confirmed Henrietta’s worst fears: She had cancer.

The treatment at the time was to irradiate the tumor with radium tubes placed in and around the cervix. The hope was that this would kill the cancerous cells while preserving the healthy tissue. Unbeknownst to Henrietta, a biopsy was taken during her radium procedure. Slivers of her tumor and of healthy cervix cells were cut away. The cancer cells were used as part of a research project. Then something amazing happened: the cancerous cells grew and continued to grow outside of her body.

As Henrietta herself lay dying, the HeLa immortal cell line was born. This cell line has been used in nearly every aspect of medical research since the polio vaccine. Millions owe their lives to it. Yet, Henrietta and her family never gave consent for any of this. Her family was not informed or compensated. In fact, until recently, they didn’t fully grasp exactly how Henrietta’s cells were being used.
Sep 7, 2001
This sure is interesting.

Whole story about Henrietta Lack :

Excerpt: "Unbeknownst to Henrietta, a biopsy was taken during her radium procedure."
Nobody knows for sure (to be able to make such a strong assertion) whether Lacks gave consent, was aware a biopsy would be taken. Nobody preserves consent forms for longer than several years. I seriously doubt any record of the medical consent forms I have signed 10 years ago are still preserved anywhere.

It is far MORE likely than not that she was informed a biopsy would be taken and would be used to research the properties of her cancer cells. Who wouldn't have gathered this for themselves? No good reason at all to believe otherwise. And she received compensation for her participation in research - she received cancer diagnosis and treatment at low cost medical clinic run by one of the finest research and teaching hospitals anywhere; heavily subsidized and possibly at no charge.


Platinum Member
Apr 22, 2011
It is far MORE likely than not that she was informed a biopsy would be taken and would be used to research the properties of her cancer cells. Who wouldn't have gathered this for themselves? No good reason at all to believe otherwise.
I started to ask if you could possibly be serious, and then realized that would be pointless... This was 1951. How old are you? Do you have even the slightest idea of the history of the concept of "informed consent" in the medical field, even for people of "preferred" social classes and middle-class-equivalent or higher incomes? I think you really must not. This sort of thing has seen truly revolutionizary changes over the past 50 years.

On the other hand, I'm also not suggesting that anything wrong was done in this case even within the spirit, if not literal practice, of modern "informed consent". As far as we're told, the biopsy was taken for reasonable and standard medical purposes in the ordinary course of her treatment and didn't inflict even "necessary" (i.e., unavoidable) harm on her of any kind, much less injuring her in any way not directly related to treating her, properly, in the context of then-current medical practice. And unless someone else makes more than an incidental financial profit from the research by, for example, "patenting" a unique aspect of someone's genetic makeup or biochemistry (to the extent that's possible), I fail to understand how the notion of financial "compensation" even enters this discussion.
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May 11, 2008
Nobody knows for sure (to be able to make such a strong assertion) whether Lacks gave consent, was aware a biopsy would be taken. Nobody preserves consent forms for longer than several years. I seriously doubt any record of the medical consent forms I have signed 10 years ago are still preserved anywhere.

It is far MORE likely than not that she was informed a biopsy would be taken and would be used to research the properties of her cancer cells. Who wouldn't have gathered this for themselves? No good reason at all to believe otherwise. And she received compensation for her participation in research - she received cancer diagnosis and treatment at low cost medical clinic run by one of the finest research and teaching hospitals anywhere; heavily subsidized and possibly at no charge.
I am sure she was fine with it. But what was interesting for me is the immortality of her HELA cell line.
Which makes me wonder, has it stable dna or is it just mutating forever with the exception of not shorting the telomeres ?
That is what makes me curious.
May 11, 2008
This is so fascinating. :sunglasses:
And more information about how viruses can cause cancer.

The Secret to HeLa’s Immortality
Henrietta’s cancer cells divide faster and were more hardy than any other human cells ever studied. What made them special though? First would be the cause of the cancer itself — Henrietta had HPV-18, a particularly nasty form of the Human Papillomavirus which is now known to cause cancer. She also had syphilis. This has been attributed to David Lacks’ infidelity.

Viruses inject parts of their genetic material into that of healthy cells. In Henrietta’s case, HPV-18 DNA was inserted into multiple sites of her cells’ DNA. HeLa cells can have anywhere from 76 to 80 chromosomes. Normal human cells have 23 pairs of chromosomes for a total of 46. These changes impacted many of the hard-coded genetic “programs” that the cells use to operate. For example, tumor suppression may have been turned off while cell growth rate was increased. Most importantly, one of these changes affected the mechanics of HeLa cell division.

The key to HeLa’s immortality is in the way cells divide. At the end of each chromosome is a repeating section of DNA called telomeres. As a normal cell divides, the number of telomeres gets smaller and smaller until it reaches a pre-set limit, called the Hayflick limit. At this point, a cell will no longer divide. When HeLa cells divide, they create an enzyme called telomerase. This enzyme prevents the telomeres from being reduced and allows the cell to divide an unlimited number of times. Telomeres are not completely understood — they also play a part in the aging of the overall organism. In humans, there are around 40,000 base pairs at birth, and only 11,000 base pairs in old age.
And this is just frightening :

There were some morally reprehensible uses of HeLa cells as well. Sloan Kettering immunologist Chester Southam wanted to see if the cells could infect other humans. He started with patients who already had cancer, injecting HeLa cells in their arms. The cells grew into tumors. The tumors were removed, but in several cases, they grew back. In one case Henrietta’s cancer metastasized to the patient’s lymph nodes. The same experiment was tried with volunteers from an Ohio prison. Once again, tumors grew in the prisoner’s arms. In this case, though, the prisoner’s healthy immune systems eventually fought off and rejected the HeLa cells.

By the end of his research, Southam had injected over 600 people with HeLa. Many of these people were gynecological surgery patients at hospitals where he worked. The patients had never given consent to be injected. For this, he was eventually brought up on charges of fraud, deceit, and unprofessional conduct. In 1963, The Regents of the University of the State of New York found him guilty, and he was placed on medical probation for one year.

Cross Contamination Risks During Cell Study
While the HeLa cell line has been incredibly beneficial for research, it needs to be handled carefully. HeLa multiplies so quickly that it will quickly destroy any other cell line it comes in contact with. Cross contamination has been and still is a huge problem. HeLa cells can travel on dust particles, through poorly cleaned lab tools, and on researchers’ gloves. Many millions of dollars of research have been lost due to the fact that the researchers were working on the wrong type of cells. The cells they intended to work on had been taken over by HeLa.

The contamination issue was first discovered by Stanley Gartler in 1967. Gartler found that many of the varied cell lines he was ordering from biological suppliers were testing positive for a specific genetic marker which is typically only found in HeLa. He presented his results and was widely criticized, as it would mean years of research was worthless. Scientists weren’t ready to throw away all that work.
Imagine what would happen if a person would breath in these cells while having a weakened immune system.
May 11, 2008
Everybody has heard of the superbugs, bacteria that cause disease and are resistant to all the antibiotics known to man.
At arstechnica is an article that explains a bit how this can happen :

As it turns out, the companies (Abbott, Astra Zeneca, Baxter, Bayer, Eli Lilly, GlaxoSmithKline (GSK), Merck/MSD, Novartis, Pfizer, Sanofi-Aventis, and Wyeth.) supplying the antibiotic cocktails sell cocktails of separate antibiotics that should never be used together because it is not effective but it can cause drug resistance for disease causing bacteria.

Insane drug cocktails in India net drug makers millions and pose global threat
The drugs are made by international companies, but they’re not approved anywhere.

In August of 2016, doctors in Washoe County, Nevada, found that one of their patients couldn’t shake a bad bacterial infection. The infection had likely taken hold years before while the local woman was on an extended visit to India. There, she had undergone multiple hospitalizations and surgery for a leg injury and developed a bone infection. By the time she got back to Nevada, the infection had spread.

The US doctors isolated her in a hospital room and threw all the antibiotics they could at the infection. It resisted all of them—26 in total, tests confirmed. In early September, the woman developed septic shock and died.

Though rare, the case highlights two important points: that drug-resistant bacteria don’t stop at borders and that India is of particular concern in the fight against antibiotic-resistant infections. While cases of drug-resistant bacterial infections are rising globally, recent data shows that India has among the highest rates of such infections in the world. The country is also the largest consumer of antibiotics per capita.

Now, new data paints a clearer picture as to why the country appears to be a breeding ground for drug resistant infections that threaten to spread within and beyond the country.

Drug companies—some international and even US-based—are selling millions of dubious and unapproved cocktails of antibiotics in India, all of which could spur the development of drug-resistant bacteria and imperil patients. The finding, published Monday in the British Journal of Clinical Pharmacology by UK health experts, suggests that the country poses a risk to global health and undermines efforts to control drug resistance.

The study authors, led by Patricia McGettigan of Queen Mary University of London, recommend firm regulatory action within India to ban these unapproved drug cocktails. They also call for the multinational drug companies producing some of the antibiotic mixtures—such as Abbott, GlaxoSmithKline, Astra Zeneca, Pfizer, and Merck/MSD—to be accountable for their products.

Drug companies “should be required to justify the sale of products in India that do not have the approval of their own national regulators and, in multiple cases, not even the approval of the Indian regulator,” they conclude.

Dodgy doses
For the study, Prof. McGettigan and her colleagues pulled antibiotic sales figures from a commercial database of Indian drug distribution called PharmaTrac. They looked at sales between October 2007 and November 2012. They then compared the inventory of drugs sold in India to the list of drugs approved by India’s Central Drugs Standard Control Organization (CDSCO) as well as those approved by the US Food and Drug Administration (FDA) and the European Medical Agency (EMA).

The researchers found that drug companies sold 86 regular, so-called “single-dose antibiotics” and 118 “fixed-dose combination” antibiotics over the five-year period. The FDC drugs are formulations composed of two or more drugs at fixed ratios in a single dose. They can include two or more antibiotics or antibiotics and a different type of drug, such as an anti-protozoal drug. Such combo formulations are rare in the US and UK; drug companies sold just five of these in the US and UK during the same period.

Many of the 118 sold in India were “poorly considered,” the authors note. Some combined antibiotics that needed to be taken at different intervals to work. For instance, one FDC paired an antibiotic that needs to be taken once a day with another that needs to be taken every eight hours to work effectively. Some combinations risked amplified side effects while others combined drugs that wouldn’t be given to treat the same illness.

Of the 118 types of FDCs, 75 (64 percent) had no approval from either the CDSCO, FDA, or EMA. Nearly all of the single-dose antibiotics were approved, on the other hand. Still, FDCs overall made up 34 percent of antibiotics sold in India by 2012—roughly 872 million doses that year. And 42 percent of the FDCs sold contained antibiotics that the World Health Organization considered “highest-priority critically important” drugs, which should be used sparingly.

Twelve multinational companies were responsible for making 53 of the 118 types of FDCs. These included Abbott, Astra Zeneca, Baxter, Bayer, Eli Lilly, GlaxoSmithKline (GSK), Merck/MSD, Novartis, Pfizer, Sanofi-Aventis, and Wyeth. Of the 53 FDCs, only four were approved by the FDA and/or the EMA, and 20 were not approved by even India's CDSCO. US-based Abbott, which has been criticized for its antibiotic sales in India before, sold 18 of those 20 unapproved combination drugs. In 2014, Abbott made $367 million from FDC profits in India, Reuters reported in 2015. At the time, a company spokesperson said that its manufacturing and marketing in India is "aligned with local regulations.”

The authors noted that the Indian government has made attempts to ban the unapproved drugs. But the efforts have been held up in courts, and drug regulation is weak, generally.

“The use of unapproved, scrutinized antibiotic FDC formulations is likely to contribute to India’s rising antimicrobial resistance,” the authors conclude. “Until definitive action is taken to ban most systemic antibiotic FDCs from manufacture and sale, [antimicrobial resistance] initiatives in India are likely to be undermined and the global action plan impeded.”

British Journal of Clinical Pharmacology, 2018. DOI: 10.1111/bcp.13503 (About DOIs).
May 11, 2008
More progress to tumor supression research from Arstechnica

I wonder if reviving and boosting the thymus with gene therapy would help reducing some old age infectious diseases and tumors because then the T cell count would increase again.

As a side note, that makes me wonder what HIV does with the thymus as lower T cell amounts is a serious effect of an HIV infection.

The dominant idea about how cancer gets started is called the "two-hit hypothesis." First proposed by Alfred Knudson in 1971, it holds that a cancer starts when one cell gets a mutation in both of its copies of a gene that normally blocks cancer formation (two hits). These two mutations disable the tumor-suppressing function in that cell, which then becomes cancerous. Eventually, the idea was expanded to include two hits not necessarily in the same gene but, rather, in genes controlling the same tumor-suppressing pathway.

But a new idea is challenging the two-hit hypothesis, shifting the focus to the role of the immune system in suppressing cancers. It's an idea that could have big implications for treatments.

Taking a hit
Getting two hits in one cell was considered to be a random and unlucky event. Since mutations occur each time a cell divides, the more times each cell divides, the greater the chances that it would happen. This was why, it was thought, cancer incidence increases with age; the longer a cell has been around, and the more times it has divided, the more opportunities it has had to accrue the two requisite mutations in the same tumor-suppressor pathway.

Evidence for the two-hit hypothesis came primarily from children with retinoblastoma, who have a germline mutation in the RB1 gene (named for the disease it causes) and are therefore born with one hit in every cell already. These kids usually end up with tumors in their eyes by the time they turn five.

Personalized medicine has been focused on the two-hit model. The idea is to identify the key mutations in a given cancer, then target and nullify them. It has been touted as the wave of the future for a while, but its successes have been mixed. Not every cancer has an obvious target gene, and many tumors can evolve resistance to targeted drugs.

Immunotherapy, by contrast, has achieved some striking successes. Much of it relies on engineered T cells designed and synthesized to kill specific tumor cells. But it also involves awakening the body's existing T cells, which would go on to help fight the tumor. Tumors generally have proteins on their surface that can activate T cells, but they also have mechanisms to suppress the immune system. Cancer immunotherapy relieves this suppression, freeing the T cells to fight the tumor.

A new analysis suggests that the relationship between the immune system and tumor cells provides not only the basis for this new therapeutic approach but also the explanation for increased cancer incidence as we age.

T cells arise in the thymus (that’s why they’re called T cells), but the thymus starts to atrophy around the time we turn one and the number of viable T cells it churns out drops continually over time. Mathematical modeling suggests that cancers do not primarily arise because getting two hits in one cell becomes more likely as we age. Instead, cancer-causing mutations seem to occur at roughly the same rate over the course of our lives, but our T cells wipe out these proto-cancer cells before they become clinically problematic.

It is only as our reservoir of T cells declines as we age that one of these continuously produced cancer cells can overcome immune surveillance and blossom into disease. The same immune system decline would explain the rising incidence of infectious diseases with age.

The authors cite a couple of observations supporting their model. One is that women get fewer cancers than men, since they have more circulating T cells and their T cell levels drop at lower rates. Another is that sharks, which have notoriously low cancer rates, do not experience this thymic atrophy as they age.

They also make a few practical recommendations. Nine out of ten of the cancers that best fit this new model have rates that spike in the late fifties, so they suggest that this might be a good age for more stringent cancer screening. And especially given the success that immunotherapies have already had in fighting some types of cancers, they suggest that more therapies that shore up T cell production or alleviate T cell exhaustion might be a better bet than trying to counteract or even prevent specific cancer-causing mutations.

It's important to emphasize that the two models aren't completely exclusive—mutations are still important for a cancer's development and progression, and they can still be targeted with treatments. The new proposal just drives home that, even if a cell picks up damaging mutations, it won't go on to form a cancer if the immune system kills it.
PNAS, 2018. DOI: 10.1073.pnas.1714478115 (About DOIs).
May 11, 2008
Since this is a thread about bacteria and viruses, i thought it would be nice to add the links about Pseudomonas syringae (The ice forming bacteria) here as well. I looked a bit further for more information how this bacteria is able to move watermolecules around and starts the ice crystal formation.

Pseudomonas syringae
Several Pseudomonas syringae bacteria slip through a stoma, or opening, to infect a leaf.

James Kremer and Sheng Yang He via Howard Hughes Medical Institute
The conditions under which microorganisms can thrive are truly amazing, at some of the most extreme conditions on the planet, and sometimes beyond. But did you know some bacteria love the cold so much that they actually cause ice to form?
A species called Pseudomonas syringae, a plant pathogen, is responsible for frost damage to crops, and is so good at nucleating ice crystals around itself that it’s used to generate artificial snow for ski resorts. Scientists have long known that P. syringae plays an important role in biology and atmospheric science, because it can form ice at temperatures above freezing. But until now, researchers have never taken a close look at what goes on right at the border between a bacterium and water, as it gets turned into ice. Using detailed imaging tools, researchers have looked at the specific proteins in the cell membrane to understand how it creates a lattice on which ice can form. They published a study with their findings today in the journal Science Advances.
The researchers used a technique called sum frequency generation spectroscopy, which uses a complex array of lasers pointed at a sample to detect the interface between a sample and a solution. Analyses with that tool revealed that P. syringae uses proteins in its cell membrane to slightly change the position of nearby water molecules so that they would fit more neatly into a lattice, as they are in ice. The bacterium can then use vibrational energy to remove heat from the area around it, coalescing the water molecules into solid ice. It does all this very efficiently, the researchers write—P. syringae is perfectly evolved to cause ice to form. Antifreeze proteins in the cell membrane protect the bacteria from damage while this is happening.
These discoveries on the tiniest scale could have big implications for the planet's hydrologic cycle and climate. P. syringae possesses such unique molecular features, the researchers write, that it might play a larger role in these global processes than was previously thought. That’s important because P. syringae has mostly been studied as a plant pathogen, not as a key player in global precipitation.

(—A combined team of researchers from Germany and the U.S. has taken a closer look at a type of bacteria that is able to cause ice to form, sometimes even under conditions above the normal freezing point.
In their paper published in the journal Science Advances, the team describes the technique they used that allowed them to watch very closely what occurs as the bacteria promote ice formation and their discovery of the means by which the bacteria cause it to come about.
Scientists have known for some time that some bacteria can promote the growth of ice crystals (they have been used to help create snow for ski resorts, as one example), but until now, the exact mechanism has not been closely studied. In this new effort, the researchers used a device called a sum frequency generation spectrometer to get a better look—it allows for a very close up view of a process as it takes place. In this instance, they watched as samples of Pseudomonas syringae went to work on both airborne water droplets and those that were on a surface. In so doing, they discovered that the bacteria use two different techniques to promote ice formation.
The first technique involved a layer of proteins that surrounded the body of the bacteria—some were hydrophobic and others were hydrophilic—the opposing forces allowed the bacteria to shuttle water molecules around like a tiny tugboat, coaxing them into formations that were conductive to crystal growth.
The second technique involved using vibrational energy to actually remove heat from the area surrounding the molecules that they had lined up, leaving them colder, which resulted in ice crystal formation at temperatures that were above freezing.
The researchers note that the bacteria also have antifreeze proteins in their bodies to keep themselves from freezing. They add that their findings may have implications for Earth scientists, as ice causing bacteria play a major role in the creation of ice crystals in the atmosphere, and in frost formation on plants. More research into the process could also lead to the development of icing, or even de-icing products.
Read more at:
If you want all the details :
Two conditions will promote interfacial ice nucleation: (i) the alignment of water into a regular structure and (ii) effective removal of latent heat due to the phase transition. The first condition of water ordering is met by the IN bacteria, as can be seen in the significant increase of the SFG signal. To test the correlation of SFG intensity increase with water ordering and to identify which water species are involved in the ordering process in the P. syringae sample, we performed MD simulations of an inaZ ice nucleation site in contact with water at 26.85° and 1.85°C and calculated the O–D stretch SFG intensity (see Fig. 3 and the Supplementary Materials for details). Water SFG spectrum calculations at interfaces have been successfully used at various surfaces such as lipid layers (33) and the air-water interface (34).


It is known that the water structure at a water-hydrophobic interface is similar to the water structure at a water-vapor interface (37). The inaZ protein uniquely features a hydrophilic-hydrophobic-hydrophilic pattern (regions 1 to 6), imposing corresponding structural changes in the adjacent water alternating between liquid- and vapor-like water interfaces. Previous theoretical and experimental studies demonstrated that ice nucleation can be enhanced at the triple line, that is, when the IN substrate is in the vicinity of the water-vapor interface (3844). Scale analysis of the triple-line tensions (ice-liquid-substrate, ice-air-substrate, and liquid-air-substrate) suggests that this effect is important for surface features on the nanometer scale (39). The inaZ protein may provide such a favorable environment for ice nucleation, even when immersed in liquid water, thereby extending this symmetric configuration over significant length. The unique feature of providing three phase contact points may result in generally observed enhanced freezing. Thus, clathrate water matching alone may not explain the exceptional IN ability of inaZ, but its alternating water structuring by the repeated hydrophilic-hydrophobic pattern may contribute significantly. This may also explain why flat hydrophilic surfaces act as good IN substrates, potentially via chemical bonds, lattice match, or active sites (45, 46), but do not exhibit the exceptional IN capability of inaZ. In addition to these very unique features, the observed promotion of water order near the hydrophilic sites also has a direct impact on the second requirement for effective ice formation—removal of latent heat.

Molecular alignment within the H-bonding network of water can promote long-range energetic coupling and therefore, by effectively funneling heat away from the interface, promote the formation of critical ice embryos necessary for nucleation. When water molecules are coaligned, their mutual dipole-dipole interaction is strongly increased, so that vibrational energy transfer can more readily occur between water molecules. The strength of the intermolecular interaction between water molecules at the P. syringae–water interface can be estimated through the vibrational energy transfer dynamics of interacting O–D groups. At surfaces, time-resolved IR pump/SFG probe spectroscopy (47, 48) enables the efficiency of energy transfer to be measured. Here, an IR excitation (pump) pulse excites O–D groups at a specific vibrational frequency. The effect of the excitation is followed in time with the SFG probe pulses (see the Supplementary Materials for more details). The excitation of O–D groups leads to a depleted SFG intensity at the excitation frequency; when vibrational energy transfer occurs, the vibrational frequency can change because of the slightly different H-bonding environments of the donor and the acceptor. The rate at which the vibrational quantum moves from one spectral band to another is a direct measure for the rate of energy transfer.

Figure 4A shows a time-resolved difference–SFG spectrum for P. syringae at 5°C after excitation with a 2470-cm−1 pump pulse (the excitation frequency is marked with a dashed black line). It can be seen that, for the P. syringae film, the bleach is strongest not at the excitation energy but at 2370 cm−1, demonstrating very efficient energy transfer within the water network to lower energies. Figure 4B displays the time-resolved bleach integrated over two spectral regions: the strongly H-bonded part near 2330 to 2430 cm−1 and the weakly H-bonded part near 2480 to 2580 cm−1. The offset visible at long delay times is due to thermal effects. The energy transfer from the weakly H-bonded to the strongly H-bonded molecules is significantly more efficient compared with that of the ice-inactive lysozyme-water interface and the bare air-water interface, which is directly visible in the reduced intensity in the signal at low frequency after excitation around 2500 cm−1 (see fig. S11). To estimate the efficiency, the data have been fitted using a coupled differential equation model (see the Supplementary Materials). This model splits the water ensemble with a continuous broad distribution of hydrogen bond strength into two spectral regions of water molecules (strongly and weakly H-bonded molecules) that can exchange population and decay to the ground state. The coupling time extracted from this model is a measure of how efficiently energy transfer occurs between more strongly and more weakly H-bonded water molecules. Modeling the time-resolved data in this way gives a coupling time between the more strongly and the more weakly H-bonded water molecules of only 80 ± 50 fs for the P. syringae and 190 ± 80 and 670 ± 250 fs for the lysozyme-water interface and the bare air-water interface, respectively. This shows that P. syringae has more efficient energy transfer than the control samples.

Figure 4C shows the time-resolved populations of the two spectral regions (more strongly and more weakly H-bonded water) extracted from the coupled differential equation model. The states become populated from the excitation pulse, over the 300-fs pump pulse duration, from energy transfer, and depopulate by decay to the ground states. The initially excited state (blue, weakly H-bonded water) has the greatest population at zero pump-probe delay time. Some of this population is transferred to the strongly H-bonded state (green). For the water–P. syringae interface, the strongly H-bonded state’s population is very high, even higher than that of the initially excited weakly H-bonded feature. This is not the case for other water interfaces (lysozyme-water and water-air; see fig. S11) and shows that P. syringae can drive the energy transfer process particularly efficiently.

We demonstrate that P. syringae bacteria can effectively order water molecules in their vicinity, which supports the hypothesis that they carry IN active sites, which can promote the nucleation of ice. In addition, vibrational energy is very rapidly exchanged through the surrounding water near the bacterial surface. Ordering and thermal energy removal through effective energetic coupling within the water network are advantageous for ice nucleation by inaZ sites at the bacterial surface. The water order is significantly enhanced with decreasing temperatures, which indicates that the molecular mechanisms involved in biogenic ice nucleation have been evolutionarily optimized for temperatures close to the freezing point of water. Heterogeneous ice nucleation initiated by substrates is little understood and contributes to large uncertainties in the prediction of climate change (49). Close analysis of the interaction of inaZ proteins with water exemplifies the fact that surface sites matching ice templates and the presence of hydrophilic sites (by matching bonds) commonly assumed to promote ice nucleation (50) are not sufficient to explain the IN properties of P. syringae but that on a nanometer scale, a symmetric hydrophobic-hydrophilic pattern can play an important role in water structuring and thus ice nucleation, an effect testable in future experimental studies. The model discussed here is valid for bacteria similar to P. syringae. Other species involved in biogenic ice nucleation, for example fungi and pollen (9), may use variations or entirely different mechanisms.

Lipids, proteins, and surfactants did not show any detectable increase of water ordering at lower temperatures. AFPs are another substance found to be capable of ordering water more effectively at low temperatures (23); AFPs can protect organisms from ice crystal formation at extremely low temperatures and can very effectively track down and bind to ice crystallites and block their growth using specific ice-binding sites. On the basis of the time-resolved SFG spectra (see the Supplementary Materials), we found that the energy transfer within the interfacial water layer was also very efficient—again similar to P. syringae. However, the underlying molecular processes are still under discussion (23, 51). Despite the structural adaptation to low temperatures in both AFPs and IN bacteria, ice-active bacteria, acting as superb ice nucleators, have additional molecular features that drastically alter their role in the environment compared to AFPs, including their participation in precipitation processes and thus in the global hydrological cycle and climate.
May 11, 2008
Yahooo. My thread is still here. :)

I was afraid that the highly technical section was erased.
May 11, 2008
Yikes, this is very scary.
Imagine walking through a field and then have hundreds or thousands of ticks crawling up your legs and they all start sucking blood.
The worst part is that these ticks (The tick, the Asian longhorned tick (or Haemaphysalis longicornis)) also carry several bacteria an parasites that causes diseases.
Now one tick bite, can already be a serious issue for the immune system.
Imagine having hundred ticks trying to suck you dry.
Of course, us humans do not get drained that easily because we have a few liters of blood but small animals can be sucked dry and will die either way.

These ticks are particulary scary because the females reproduce asexually. Each female can produce 2000 eggs and all these eggs are clones.
Imagine having a thousands ticks, within a few days there are millions. And they all want blood.

From Arstechnica :
A vicious species of tick originating from Eastern Asia has invaded the US and is rapidly sweeping the Eastern Seaboard, state and federal officials warn.
The tick, the Asian longhorned tick (or Haemaphysalis longicornis), has the potential to transmit an assortment of nasty diseases to humans, including an emerging virus that kills up to 30 percent of victims. So far, the tick hasn’t been found carrying any diseases in the US. It currently poses the largest threat to livestock, pets, and wild animals; the ticks can attack en masse and drain young animals of blood so quickly that they die—an execution method called exsanguination.
Key to the tick’s explosive spread and bloody blitzes is that its invasive populations tend to reproduce asexually, that is, without mating. Females drop up to 2,000 eggs over the course of two or three weeks, quickly giving rise to a ravenous army of clones. In one US population studied so far, experts encountered a massive swarm of the ticks in a single paddock, totaling well into the thousands. They speculated that the population might have a ratio of about one male to 400 females.
Yesterday, August 7, Maryland became the eighth state to report the presence of the tick. It followed a similar announcement last Friday, August 3, from Pennsylvania. Other affected states include New York, Arkansas, North Carolina, Virginia, and West Virginia.

Plagued paddock
It all started last August in New Jersey, the first state to identify the bloodsuckers. In a case report recently published in the Journal of Medical Entomology, infectious disease and tick experts reported the sad state of a 12-year-old Icelandic sheep housed alone in a paddock amid manicured lawns and large houses in the state’s wealthy Hunterdon County. No other animals were located on the property, and the sheep had never traveled outside of the country. Yet the beast was besieged, covered by hundreds of feasting ticks of all life-stages.
Just stepping foot in the paddock, the owner and health investigators were inundated with thirsty ticks that instantly began clawing up their pant legs. DNA analysis ultimately determined that the ticks were H. longicornis. Investigators found only one male out of 1,058 ticks collected.
To fight back the swarms, the owner doused the sheep in a wash of the insecticide permethrin. By November, it was cleared of ticks, and population levels in the vegetation around the paddock seemed to be dying down, although that was likely due to several nights of below-freezing temperatures.
In April, New Jersey’s Department of Agriculture confirmed that the population had successfully overwintered in the state, suggesting that it has now become established there.

Spreading scourge
So far, it’s unclear how, when, or where H. longicornis first arrived in the country. According to a regional consortium of vector-borne disease experts, archived tick samples suggest the species arrived several years prior to 2017. In the past, researchers have occasionally intercepted the ticks in US quarantine stations, including finding a tick on a quarantined horse at a station in New Jersey in 1969.
H. longicornis is native to parts of East Asia, namely China, Japan, the former USSR, and Korea, living in meadows and grassy areas near forests. They’re also an established invasive pest of cattle in New Zealand, parts of Australia, and several Pacific islands. They’ve been known to feed on livestock like sheep, goats, cattle, and horses as well humans, dogs, cats, birds, and a range of wild animals, including bears, foxes, raccoons, rabbits, deer, and opossum.
In Asia, the longhorned tick is known to carry a variety of pathogens, including Rickettsia japonica, the bacteria behind Oriental spotted fever, and Theileria orientalis, a parasite that causes cattle theileriosis. It has also been found harboring relatives to pathogens present in the US, including bacteria that cause anaplasmosis and ehrlichiosis, the parasite that causes babesiosis, and the Powassan virus.
Additionally, H. longicornis may harbor a newly emerging virus that causes SFTS, which is short for severe fever with thrombocytopenia syndrome. SFTS was first identified in China in 2009 and is marked by fever, vomiting, hemorrhaging, and organ failure. Reported fatality rates fall between 6 percent and 30 percent. Several studies have pointed to the longhorned tick as being a reservoir and source for the virus.

Journal of Medical Entomology, 2018. DOI: 10.1093/jme/tjy006 (About DOIs).
May 11, 2008
This is kind of disturbingly amazing. Besides people who have been misinformed and deny vaccinations there are also people who drink raw milk. Milk that has not been pasteurized.
Of course what happens, is that strange diseases start to pop up and there seems to be no clear indication why...
What people do not understand that issues like molecular mimicry is of a major concern.
Also, when a pathogen stays resident in your body, it will cause havoc when you get older and your immune system weakens.
A resident pathogen will cause havoc when you are under major stress causing seemingly totally unrelated symptoms.
Why ? Because when you have a lot of stress, your immune system is actively supressed.
And since a lot of people favor Occam's razor, the culprit is usually never found.

Centuries ago, people understood to do not do certain things. They did not understand the science behind it and because of that it was seen as magic.
I will just leave this interesting article from Arstechnica here...

If the explosion of measles cases hasn’t made you question what year it is, this health alert from the Centers for Disease Control and Prevention may inspire a double-take at the calendar: Unpasteurized milk may have sickened people in 19 states.

Anti-vaxxers plan to subvert changes to vaccination laws
Yes, as the country grapples with five—count’em, five—outbreaks of a vaccine-preventable disease, the CDC is warning that another infectious disease of yore poses a risk to widespread dairy drinkers—at least the ones who soured on the standard, decades-old process to remove deadly pathogens from their milk.

The infectious disease is Brucellosis. It’s a hard-to-define febrile illness caused by Gram-negative Brucella bacterial species that infect a variety of animals and the occasional unlucky human. There are four species that pose particular risks to humans: Brucella suis, found in pigs; Brucella melitensis, found in sheep and goats; Brucella canis, from dogs; and—the one at the center of this current health alert—Brucella abortus, which is carried by cattle. Usually, the disease pops up in developing countries. But in the US, meatpackers, hunters, veterinarians, farmers, and careless microbiologists are at risk—as well as those who consume unpasteurized dairy.

The CDC reports that a Brucella abortus strain called RB51 was found in unpasteurized milk distributed from Miller’s Biodiversity Farm in Quarryville, Pennsylvania. RB51 is a weakened strain that veterinarians use to vaccinate cows against more dangerous varieties, which cause abortions in the livestock (as the name suggests). The vaccination doesn’t cause any symptoms in non-pregnant cows, but on rare occasions, RB51 can quietly slip into milk and cause serious illnesses in humans who eschew pasteurization. It’s also resistant to a first-line antibiotic used to treat Brucellosis.

Health officials identified a cow shedding RB51 on the Pennsylvania farm and removed it from the milking herd. But that wasn't before the farm’s milk made it to an unknown number of consumers in 19 states. Those states are: Alabama, California, Connecticut, Florida, Georgia, Iowa, Maryland, Massachusetts, Michigan, Minnesota, Mississippi, New Jersey, New York, North Carolina, Ohio, Pennsylvania, Rhode Island, South Carolina, and Virginia.

So far, one case has been confirmed in New York. But Brucellosis is maddeningly tricky to diagnose, particularly if you don’t know you’ve been exposed to it.
Insidious infection

After an exposure, symptoms can arise in as little as a week or as long as several months. It starts off much like the flu, with fever, chills, body aches, headache, and sometimes diarrhea. As it progresses, it can cause fever spikes from 104 degrees Fahrenheit to 105 degrees Fahrenheit. But otherwise, it causes a scattershot of symptoms—acute or chronic, localized or systemic.

Raw milk is trending for some reason—so are nasty, drug-resistant infections
About half of Brucellosis cases are acute infections, with clear symptoms occurring quickly. The other half of affected people experience a slower unfolding of symptoms, which can roll into a chronic infection with fevers that come and go over years. The infection can affect multiple systems in the body or be localized to certain tissues or organs. It has been associated with skin problems, such as rashes and abscesses. It’s also linked to bone and joint issues, particularly inflammation and pain in the lower back (vertebral osteomyelitis) and arthritis. It can lead to inflammation of the kidney, prostate, testes, liver, and/or gastrointestinal tract. In rare cases, it can affect the heart and the central nervous system, causing inflammation of the brain and spinal cord, all of which can be fatal.

The most definitive way to diagnose Brucellosis is to try to grow the bacteria from blood, bone marrow, cerebrospinal fluids, or wounds. But it can take up to four weeks to show up in lab cultures. Treatment typically involves weeks of antibiotic treatments.

Patrons of Miller’s Biodiversity Farm may have been exposed at any time since January 2016. The CDC warns that anyone who drank milk from the farm within the last six months is at risk of coming down with the infection. People who drank the milk longer than six months ago and have symptoms but haven’t been tested should get to their doctor pronto, the agency warns.

Molecular mimicry is defined as the theoretical possibility that sequence similarities between foreign and self-peptides are sufficient to result in the cross-activation of autoreactive T or B cells by pathogen-derived peptides. Despite the prevalence of several peptide sequences which can be both foreign and self in nature, a single antibody or TCR (T cell receptor) can be activated by just a few crucial residues which stresses the importance of structural homology in the theory of molecular mimicry. Upon the activation of B or T cells, it is believed that these "peptide mimic" specific T or B cells can cross-react with self-epitopes, thus leading to tissue pathology (autoimmunity).[1] Molecular mimicry is a phenomenon that has been just recently discovered as one of several ways in which autoimmunity can be evoked. A molecular mimicking event is, however, more than an epiphmenon despite its low statistical probability of occurring and these events have serious implications in the onset of many human autoimmune disorders.'s_razor
Occam's razor (or Ockham's razor) is a principle from philosophy. Suppose there exist two explanations for an occurrence. In this case the one that requires the least speculation is usually better. Another way of saying it is that the more assumptions you have to make, the more unlikely an explanation.
May 11, 2008
I thought about my comment "Centuries ago" and wondered how far back the knowledge goes and it is interesting :

Pasteurization or pasteurisation is a process in which certain packaged and non-packaged foods (such as milk and fruit juice) are treated with mild heat, usually less than 100 °C (212 °F), to eliminate pathogens and extend shelf life. The process is intended to sterilize foods by destroying or inactivating organisms that contribute to spoilage, including vegetative bacteria but not bacterial spores.[1][2]

The process was named after the French scientist Louis Pasteur, whose research in the 1880s demonstrated that thermal processing would inactivate unwanted microorganisms in wine.[2][3] Spoilage enzymes are also inactivated during pasteurization. Today, pasteurization is used widely in the dairy industry and other food processing industries to achieve food preservation and food safety.[3]
The process of heating wine for preservation purposes has been known in China since AD 1117,[5] and was documented in Japan in the diary Tamonin-nikki, written by a series of monks between 1478 and 1618.

Much later, in 1768, Italian priest and scientist Lazzaro Spallanzani's research proved a product could be made "sterile" after thermal processing. Spallanzani boiled meat broth for one hour, sealed the container immediately after boiling, and noticed that the broth did not spoil and was free from microorganisms.[2][6] In 1795, a Parisian chef and confectioner named Nicolas Appert began experimenting with ways to preserve foodstuffs, succeeding with soups, vegetables, juices, dairy products, jellies, jams, and syrups. He placed the food in glass jars, sealed them with cork and sealing wax and placed them in boiling water.[7] In that same year, the French military offered a cash prize of 12,000 francs for a new method to preserve food. After some 14 or 15 years of experimenting, Appert submitted his invention and won the prize in January 1810.[8] Later that year, Appert published L'Art de conserver les substances animales et végétales (or The Art of Preserving Animal and Vegetable Substances). This was the first cookbook of its kind on modern food preservation methods.[9][10]

La Maison Appert (English: The House of Appert), in the town of Massy, near Paris, became the first food-bottling factory in the world,[7] preserving a variety of foods in sealed bottles. Appert's method was to fill thick, large-mouthed glass bottles with produce of every description, ranging from beef and fowl to eggs, milk and prepared dishes. He left air space at the top of the bottle, and the cork would then be sealed firmly in the jar by using a vise. The bottle was then wrapped in canvas to protect it while it was dunked into boiling water and then boiled for as much time as Appert deemed appropriate for cooking the contents thoroughly. Appert patented his method, sometimes called appertisation in his honor.[11]

Appert's method was so simple and workable that it quickly became widespread. In 1810, British inventor and merchant Peter Durand, also of French origin, patented his own method, but this time in a tin can, so creating the modern-day process of canning foods. In 1812, Englishmen Bryan Donkin and John Hall purchased both patents and began producing preserves. Just a decade later, Appert's method of canning had made its way to America.[12] Tin can production was not common until the beginning of the 20th century, partly because a hammer and chisel were needed to open cans until the invention of a can opener by Robert Yeates in 1855.[7]

A less aggressive method was developed by French chemist Louis Pasteur during an 1864[13] summer holiday in Arbois. To remedy the frequent acidity of the local aged wines, he found out experimentally that it is sufficient to heat a young wine to only about 50–60 °C (122–140 °F) for a short time to kill the microbes, and that the wine could subsequently be aged without sacrificing the final quality.[13] In honour of Pasteur, this process became known as "pasteurization".[2][14] Pasteurization was originally used as a way of preventing wine and beer from souring,[15] and it would be many years before milk was pasteurized. In the United States in the 1870s, it was common for milk to contain substances intended to mask spoilage before milk was regulated.[16]

Further information: Raw milk

180 kilograms (400 lb) of milk in a cheese vat

Milk is an excellent medium for microbial growth,[17] and when it is stored at ambient temperature bacteria and other pathogens soon proliferate.[18] The US Centers for Disease Control (CDC) says improperly handled raw milk is responsible for nearly three times more hospitalizations than any other food-borne disease source, making it one of the world's most dangerous food products.[19][20] Diseases prevented by pasteurization can include tuberculosis, brucellosis, diphtheria, scarlet fever, and Q-fever; it also kills the harmful bacteria Salmonella, Listeria, Yersinia, Campylobacter, Staphylococcus aureus, and Escherichia coli O157:H7,[21][22] among others.

Prior to industrialization, dairy cows were kept in urban areas to limit the time between milk production and consumption, hence the risk of disease transmission via raw milk was reduced.[23] As urban densities increased and supply chains lengthened to the distance from country to city, raw milk (often days old) became recognized as a source of disease. For example, between 1912 and 1937, some 65,000 people died of tuberculosis contracted from consuming milk in England and Wales alone.[24] Because tuberculosis has a long incubation period in humans, it was difficult to link unpasteurized milk consumption with the disease.[25] In 1892, chemist Earnest Lederle experimentally inoculated milk from tuberculosis-diseased cows into guinea pigs, which caused them to develop the disease.[26] In 1910, Lederle, then in the role of Commissioner of Health, introduced mandatory pasteurization of milk in New York City.[26]

Developed countries adopted milk pasteurization to prevent such disease and loss of life, and as a result milk is now considered a safer food.[27] A traditional form of pasteurization by scalding and straining of cream to increase the keeping qualities of butter was practiced in Great Britain in the 18th century and was introduced to Boston in the British Colonies by 1773,[28] although it was not widely practiced in the United States for the next 20 years. Pasteurization of milk was suggested by Franz von Soxhlet in 1886.[29] In the early 20th century, Milton Joseph Rosenau established the standards – i.e. low-temperature, slow heating at 60 °C (140 °F) for 20 minutes – for the pasteurization of milk[30][31] while at the United States Marine Hospital Service, notably in his publication of The Milk Question (1912).[32] States in the U.S. soon began enacting mandatory dairy pasteurization laws, with the first in 1947, and in 1973 the U.S. federal government required pasteurization of milk used in any interstate commerce.[33]

The shelf life of refrigerated pasteurized milk is greater than that of raw milk. For example, high-temperature, short-time (HTST) pasteurized milk typically has a refrigerated shelf life of two to three weeks, whereas ultra-pasteurized milk can last much longer, sometimes two to three months. When ultra-heat treatment (UHT) is combined with sterile handling and container technology (such as aseptic packaging), it can even be stored non-refrigerated for up to 9 months.[34]

According to the Centers for Disease Control, between 1998 and 2011, 79% of dairy-related disease outbreaks were due to raw milk or cheese products.[35] They report 148 outbreaks and 2,384 illnesses (with 284 requiring hospitalization), as well as two deaths due to raw milk or cheese products during the same time period.[35]

And here we are in the western world... Where some dumbass claims raw milk is good for you and other dumbasses believe it without investigating if the claim is correct....
May 11, 2008
Interesting story about gene manipulation and the possible consequences.
Although, i do have to say, deleting parts of the genome that are supposed to be there for a reason is not a good solution.
This story would have been more amazing if the scientists figured out a way to add a gene for specific HIV recognition.
Because HIV can evade the immune system. I do not know all the details anymore, but if the body could be tought to recognise infected cells faster and get the infected engulfed by macrophages before the cell explodes with virus particles, well maybe that would help.
Any ideas ?

A missing chunk of DNA, 32 base pairs long and smack in the middle of the CCR5 gene, might be the most studied mutation in human history. The spontaneous deletion, which arose thousands of years ago, has a striking relationship with one of the worst human diseases: HIV/AIDS. People who inherit this mutation from both of their parents are naturally immune. The only two people to have ever been cured both received bone marrow transplants from people who carry the Δ32 mutation.

The pharmaceutical industry has invested heavily in trying to recreate the benefits of this naturally evolved anomaly using drugs and genetic engineering. And last year, a Chinese scientist named He Jiankui used Crispr to try to endow two human embryos with the Δ32 mutation and immunity to HIV. He’s experiments were widely condemned for smashing through ethical boundaries and breaking Chinese law. They also culminated in the birth of twin baby girls. But that was not the end of it.

Last week, it emerged that fertility clinics around the world have been seeking He’s advice on offering a CCR5 Crispr edit as a service to prospective parents. Now, new research is suggesting that such a procedure might actually be an early death sentence.

Megan Molteni covers DNA technologies, medicine, and genetic privacy for WIRED.
That’s because the Δ32 mutation doesn’t just make people resistant to HIV—it also shaves years off of people’s lives. In a study published today in Nature Medicine, scientists at the University of California, Berkeley, combed through more than 400,000 genomes and health records housed in the UK Biobank, a massive database of Brits that was recently released to researchers. They discovered that people with two copies of the Δ32 mutation died at rates 21 percent higher than those with one or no copies.

“There might be a public perception that one mutation does one thing, but biology doesn’t work like that,” says Rasmus Nielsen, an evolutionary biologist who coauthored the paper with one of his postdocs, Xinzhu Wei. Their results illustrate how a single mutation can affect many different traits simultaneously in ways that are very hard to predict, he says. “I hope this raises awareness that before we think about modifying the human genome with Crispr, we carefully consider all the possible effects of the mutations that we create.”

Nielsen and Wei had been interested in using the UK Biobank data to investigate how patterns of gene frequencies were being shaped by the pressures of modern life. They had a number of genes they wanted to look at, but after He’s Crispr Babygate scandal broke in November 2018, they decided to zero in on CCR5.

In the UK Biobank data they found two lines of evidence to suggest that these days, CCR5 actually is a net negative. In the first analysis they tracked how long people survived after enrolling in the Biobank study. They found that between the ages of 41 and 78, people with two copies of the Δ32 mutation had significantly higher death rates. They also observed that far fewer people with two copies enrolled in the study than expected, which they interpreted to mean that these individuals were less likely to survive into middle age than the general population. “Something has removed people with two copies of the mutation, and the likely explanation is increased mortality,” says Nielsen.

The UK Biobank data did not illuminate what specifically might be killing off these individuals, but earlier research in mice has shown that lacking a functional CCR5 gene increases susceptibility to other deadly infections, including influenza and West Nile virus.

To understand how the evolutionary winds might have shifted, it’s helpful to know something about the mutation’s origin story. A few thousand years ago, somewhere in the plague- and smallpox-ravaged lands of Northern Europe, a child was born missing a large chunk of DNA in its CCR5 gene. This gene coded for a receptor on the surface of immune cells useful for coordinating responses to invading pathogens. And this spontaneous deletion torpedoed CCR5 production—one copy shrunk the number of receptors on cells, two copies erased the receptor altogether.

In another time and place, such a mutation might have been a problem, but at that moment it proved an evolutionary windfall. That person’s family and their descendants outlived and out-reproduced their peers at an astonishing rate. Today, the Δ32 mutation occurs in about 10 percent of the population of Europe, in a decreasing gradient from north to south. Natural selection pushed it through the population about 100 times faster than if it were a neutral change to the genome. But with the invention of vaccines and the eradication of diseases like smallpox over the past century, the mutation has become less useful. According to Nielsen and Wei’s analysis, it’s now downright detrimental.


The WIRED Guide to Crispr
At least in populations that look like the UK Biobank. That data can’t reasonably be extrapolated to places like China where the pathogen environment and genetic backgrounds of the people living there look very different from the Brits. But it lends urgency to efforts to monitor the Crispr’d twins throughout the entirety of their lives. According to reports from the Chinese state-sanctioned news service, the girls will remain under government supervision in Guangdong Province, near where He conducted his rogue experiments.

For bioethicists like Stanford’s Hank Greeley, these latest revelations only further skew the risks of such a procedure to far outweigh the potential benefits. “I already thought He’s experiment was somewhere around 50 times higher than the ethical limit,” he says. “This just makes it even more outrageously risky.” Much of that calculus comes from the fact that neither girl was infected with HIV—they could have avoided the disease using safer, more proven methods, such as condoms and prophylactic drugs.

But for people who’ve already been infected, says Nielsen, it’s still much more beneficial to carry the mutation. That’s why he stresses that his research shouldn’t be interpreted as a warning against HIV/AIDS cell and drug therapies that target the CCR5 gene. And ironically, if they’re successful, the usefulness of the natural Δ32 mutation will decline even further. Given a few thousand more years, it might even disappear.