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PARASITES

House dust mites evolved a new way to protect their genome

House dust mites are common pests with an unusual evolutionary history. They are tiny, free-living animals that evolved from a parasitic ancestor, which in turn evolved from free-living organisms millions of years ago.

A new genetic study suggests that, as a consequence of its tumultuous evolutionary history, the house dust mite developed a novel way to protect its genome from internal disruptions. The study was published Jan. 29 in the journal PLOS Genetics.

All animals and plants face a threat from transposable elements, pieces of non-coding DNA that can change their position in the genome, often causing mutations and disease. Organisms have evolved complex ways to watch for, target and silence transposable elements.

In most animals, this surveillance mission is carried out by small RNA fragments that find and break offending genetic sequences. The mechanism is called the piwi-associated RNA pathway — named for the protein Piwi, first discovered in fruit flies.

Recently, a team of researchers, led by University of Southern Mississippi scientists and including a University of Michigan biologist, sequenced the DNA and the RNA of the American house dust mite, Dermatophagoides farinae. Then they looked at the populations of small RNA molecules encoded there.

They found that house dust mites do not have Piwi proteins or the associated small RNAs that most animals use to control transposable elements. Instead, dust mites have replaced the Piwi pathway with a completely different small RNA mechanism that uses small-interfering RNAs. The dust mite genome also encodes a protein that can amplify small-interfering RNAs.

“We believe that the evolution of this novel mechanism to protect genomes from transposable elements is linked to the unusual evolution of the dust mite,” said Pavel Klimov, an associate research scientist in the U-M Department of Ecology and Evolutionary Biology and a co-author of the PLOS Genetics paper.

“These animals evolved from parasitic ancestors. Frequently, the transition to parasitism is associated with dramatic genetic changes, a legacy carried by the dust mite when it moved back to a free-living lifestyle.”

The PLOS Genetics paper reports the first high-quality assembly of the genome of the house dust mite, Klimov said.

House dust mites are ubiquitous inhabitants of human dwellings, thriving in the mattresses, sofas and carpets of even the cleanest homes. They are the primary cause of indoor allergies in humans, affecting up to 1.2 billion people worldwide.

Today’s free-living house dust mite evolved from a parasitic ancestor 48 to 68 million years ago, long before humans were around. Ancient dust mites lived in bird nests for millions of years before moving into human dwellings relatively recently.

The PLOS Genetics paper is titled “Rewired RNAi-mediated genome surveillance in house dust mites.” The other authors are Mosharrof Mondal and Alex Flynt of the University of Southern Mississippi.

Support for the research was provided by the National Science Foundation and the Mississippi INBRE program, which is funded by the National Institutes of General Medical Sciences.

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Materials provided by University of Michigan.


Journal Reference:

  1. Mosharrof Mondal, Pavel Klimov, Alex Sutton Flynt. Rewired RNAi-mediated genome surveillance in house dust mitesPLOS Genetics, 2018; 14 (1): e1007183 DOI: 10.1371/journal.pgen.1007183
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PARASITES

WARNING!! TAPEWORM SUSHI! Would You Eat This?

Afterwards, the fish was thrown out in its’ entirety, and the complete work area was cleaned off and sanitized properly. We used our liquid detergent to scrub down the entire area of the cutting board including the cooler top as well as the knives and utensils, and then sprayed the entire area with a mixture of 2 tablespoons of bleach to a gallon of water and let that entire area air dry. The knives, after cleaned off with detergent were also soaked in this bleach liquid and then taken out to air dry.

If you’re a sushi fan, this is why you need to visit only the places that have a good reputation; if not you’ll be faced with some dangerous eating that could get you sick for many many months. Furthermore, we know that many restaurants, upon finding parasites like what we have shown, cut out the “infected areas” and use the rest. They may also cook the infected area as well. We choose to discard the entire fish as this is what a reputable establishment should do. Profit has no place when a patron’s safety is in question.

The cameraman actually had an experience with eating fish infected with parasites. He ate raw wild salmon from a Publix in Lake City FL, a large chain supermarket and the fish was infected. A couple months later, he went to use the toilet and when he was finished, he went to wipe himself and saw a white stringy substance that looked almost like strand of mucus hanging from his anus into the toilet. When he went to wipe away, thinking it was mucus, it kept coming out from his anus and would wipe away. When he took a closer look, he saw that it was moving and was alive! Needless to say, he was in a state of panic and called his doctor who prescribed some pills to take. An hour after, the pills gave him a very bad case of diarrhea which when he looked in the toilet, were signs of the dead tapeworms. It was an experience he has vowed never to go through again…

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PARASITES

OMG! Are You Infected With Spirochete Parasites? Please Sit Down While Watching This!

So far to date. Six people and myself I have seen tested, most people tested had never been tested for spirochetes! Half of them in decent health. All tested positive for this bacterium. 100% infection rate. This literally means that healthy people could be infected at low infestation levels or loads. Bordello strain Spirochetes have a life cycle similar to egg layers! A larva stage may exist too.

Treatment must deal with Ammonia toxicity aka Herx reaction.Treatment must be sustained over more than one life cycle and may have to be interrupted of 24 /48 hrs for any toxicity reactions related to parasite die off.

I would not recommend a Western Blot Test. That raises eyebrows. Dark field microscopy is essential if you have chronic illness.

Lyme is susceptible to ultra violet, infra red, gamma radiation especially in pupil and larval stages. Sudden die off will cause sudden symptoms. If you have intense knee pain, please consider that you could be one of the 90 percent with this infection.

Spirochetes will target dead, dying, injured tissues. May be the reason for cystic response including Lipoma and Rheumatoid cysts. May hide in nerve tissue but I doubt it. Epstein Barr hides in nerve tissue.

If you have cardiac damage to progression of disease, or acute infarction, heavy steroid use, congestive failure spirochetes can infect your heart, similar to Sarcoidosis.

Spirochetes can hide but must feed in plasma. But seem to love red cells at the non oxygenated side of hemoglobin or in venous blood cells that are O2 deficient.

Spirochete will leave people susceptible to viral infections and yeast infections, black mold, tuberculosis and other infections.

Epstein Barr and Spirochetes make a dangerous combination and Spirochete load may actually determine the type and nature of your Epstein Barr / Autoimmune disease.

Longer term, untreated will present like Lyme disease but secondary infections can be more acute and require immediate attention while the baseline Parasitic virus or bacterium goes unaddressed.

Support provocative theory and stimulating discussions. Searching for TRUTH involves all of us!

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PARASITES

Parasite-schizophrenia connection: One-fifth of schizophrenia cases may involve the parasite T. gondii

Many factors, both genetic and environmental, have been blamed for increasing the risk of a diagnosis of schizophrenia. Some, such as a family history of schizophrenia, are widely accepted. Others, such as infection with Toxoplasma gondii, a parasite transmitted by soil, undercooked meat and cat feces, are still viewed with skepticism.

A new study by Gary Smith, professor of population biology and epidemiology at the University of Pennsylvania’s School of Veterinary Medicine, used epidemiological modeling methods to determine the proportion of schizophrenia cases that may be attributable to T. gondii infection. The work, published in the journal Preventive Veterinary Medicine, suggests that about one-fifth of cases may involve the parasite.

“Infection with Toxoplasma is very common, so, even if only a small percentage of people suffer adverse consequences, we could be talking about problems that affect thousands and thousands of people,” Smith said.

In the United States, just over a fifth of the population is infected with T. gondii. The vast majority aren’t aware of it. But there are some populations that need to be concerned. For example, if a woman becomes infected for the first time during pregnancy, her fetus can die or suffer serious developmental problems. People with HIV or other diseases that weaken the immune system are susceptible to a complication of T. gondii infection called toxoplasmic encephalitis, which can be deadly.

Though the medical community has long believed that most healthy people suffer no adverse effects from a T. gondii infection, recent studies have found evidence of worrisome impacts, including an association with schizophrenia because the parasite is found in in the brain as well as in muscles. Other work has shown that some antipsychotic drugs can stop the parasite from reproducing. In addition, field and laboratory studies in mice, rats and people have shown that infection with T. gondii triggers changes in behavior and personality.

To further investigate this connection, Smith sought to calculate the population attributable fraction, or PAF, a metric epidemiologists use to determine how important a risk factor might be. In this case, Smith explained that the PAF is “the proportion of schizophrenia diagnoses that would not occur in a population if T. gondii infections were not present.”

The usual method of calculating the PAF was not well suited to examining the link between schizophrenia and T. gondii, because some of the variables are constantly in flux. For example, the proportion of people infected by T. gondii increases with age. Using a standard epidemiological modeling format, but taking into account all of the age-related changes in the relevant factors, Smith found the average PAF during an average lifetime to be 21.4 percent.

“In other words, we ask, if you could stop infections with this parasite, how many cases could you prevent?” Smith said. “Over a lifetime, we found that you could prevent one-fifth of all cases. That, to me, is significant.”

Smith noted that in some countries, the prevalence of T. gondiiinfection is much higher than in the U.S., and these countries also have a higher incidence of schizophrenia.

People with schizophrenia have greatly reduced life expectancies, and many are unable to work. Family members may also leave the workforce to care for relatives with the disease. For these reasons and others, schizophrenia acts as a large drain on the economy, responsible for $50 to $60 billion in health-care expenditures in the U.S. each year.

“By finding out how important a factor T. gondii infection is, this work might inform our attitude to researching the subject,” Smith said. “Instead of ridiculing the idea of a connection between T. gondii and schizophrenia because it seems so extraordinary, we can sit down and consider the evidence. Perhaps then we might be persuaded to look for more ways to reduce the number of people infected with Toxoplasma.”

The study was supported by the University of Pennsylvania School of Veterinary Medicine.

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