Researchers have shown that they can create entirely new strains of infectious proteins known as prions in the laboratory by simply mixing infectious prions from one species with the normal prion proteins of another species. The findings are reported in the September 5th issue of the journal Cell, a Cell Press publication.

Prion diseases, also known as transmissible spongiform encephalopathies (TSEs), are infectious neurodegenerative diseases affecting the brain of several species of mammals including humans. Creutzfeldt-Jakob disease (CJD) is the most common prion disease in humans, along with scrapie in sheep, bovine spongiform encephalopathy (BSE, aka mad cow) in cattle, and chronic wasting disease (CWD) in deer and other cervids.

Unlike conventional infectious microorganisms, the infectious agent in the case of prion diseases consists exclusively of a misfolded form of the prion protein, earlier studies showed.

The researchers now find that prion strains produced by combining normal hamster proteins with infectious mouse proteins can infect hamsters and vice versa. Although they are both rodents, prions from one of the two species normally don’t readily infect the other, a common phenomenon amongst prions known as a species barrier, the researchers explained.

The novel prions they produced not only look different, but they also produce symptoms in the animals that differ from any known strain found in nature, they report.

” We are forcing the system by putting everything together, but this suggests that the variety of possible prions is really very large,” said Claudio Soto of the University of Texas Medical Branch. “We shouldn’t be surprised if new barriers are crossed and new prions arise. There is the potential for a large variety of new infectious prions—some of which may have dramatic effects.”

“The infectous agent is nothing like what we’re used to,” Soto said. “It’s just a protein with a different shape from the normal protein we all have.” Those misfolded and misshapen proteins can spread by causing normal protein to change their shape. Those aberrant forms band together, forming fibrils.

Soto’s team recently reported the generation of infectious prions by amplification of prion misfolding in the test tube. In those experiments, they used a technology called protein misfolding cyclic amplification (PMCA) that mimics some of the fundamental steps involved in the replication of infectious prions in living animals, but at an accelerated rate. The method involves placing small quantities of infectious prions with large quantities of the normal protein from the same species together, allowing the infectious form to imprint on the normal form and thereby replicate itself.

Now, they show that the same method can generate new strains when infectious prions from one species are mixed with normal prion proteins from another species. The finding provides conclusive evidence that the imprinting of disease-causing prions on normal forms can overcome species barriers, and doesn’t require any other infectious agent.

This new insight has profound implications for public health, according to the researchers.

” One of the scariest medical problems of the last decades has been the emergence of a new and fatal human prion disease–variant CJD–originated by cross-species transmission of BSE from cattle,” the researchers said. BSE has also spread to other animals, including exotic cats, other primates and domestic cats, after they ate feed derived from diseased cows.

The new method might provide insight into the risk that other prion diseases could spread from one species to another, Soto said. For instance, scientists don’t know whether chronic wasting disease, a condition now on the rise amongst deer in some parts of the U.S., can be transmitted to humans or not.

Test tube studies like this one might help answer that question, and– in the case that the deer prions can make the leap—such studies may inform scientists about what those prions might look like, he said. By studying any new prion strains created in mice with the human prion protein, scientists might also gain insight into the potential symptoms associated with those diseases.

” The data demonstrate that PMCA is a valuable tool for the investigation of the strength of the barrier between diverse species, its molecular determinants, and the expected features of the new infectious material produced,” the researchers concluded. “Finally, our findings suggest that the universe of possible prions is not restricted to those currently known but that likely many unique infectious foldings of the prion protein may be produced and that one of the sources for this is cross-species transmission.”

This research makes it extremely clear that there is an inherent risk in feeding one species to another. As prions are believed to be able to cross the blood brain barrier, if you eat an animal that has infectious prions, even if those prions are not capable in and of themselves of infecting you, there is a risk that they will interact with your own prions to create a whole new variety of infectious prion protein that CAN harm us. Perhaps this is how Creutzfeldt-Jakob disease originated.

The sensible thing to do is to take great care in ensuring our food animals are free of prion disease, all the way down their food chain. Cattle feed is often surprisingly high in animal protein. Feeding animal protein to herbivores seems to me to be an entirely unnecessary risk factor in disease transmission. Equally, just because a prion disease is not known to be transferable in the traditional sense, does not mean that we should be eating infected deer or rabbits.

The North Carolina Department of Agriculture has a handy guide for removing all the parts of a deer that are especially high in prions.

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Chickenpox usually occurs in childhood, is one of childhood diseases.
At the age of adult Varicella virus usually causes a rash localized to one or more dermatomes,
known as herpes zoster or shingles, hence the name of the Varicella-zoster virus.

Chickenpox is a classic disease of childhood, which usually is easy for children but
for teenagers and adults may have an increased risk of complications.
The disease can take about a week. Chickenpox in children is characterized by a very aggressive rash which occurs in waves, it includes
several areas of the body, starting in early stages, with head; chickenpox is a form of viral infection, caused by the Varicella-zoster, which is part of the family Herpesviridae.
Varicella infection is a very contagious
condition; sick child is the main source of infection for other children in that school communities, kinder gardens, and nursery.

Child with Varicella (chickenpox) can easily contaminate other children, especially in the first 2-3 days after onset, before actual clinical onset of disease,
when symptoms are almost unnoticeable. Contamination can be done directly, by touching contaminated areas
and liquid vesicles that appear on the skin or by respiratory secretions, which also
contain the virus.

Time after the eruption, usually must isolate sick child at home
for 14 days to heal and to avoid infection of other children. The incubation period for chickenpox is about 15 days, the child does not show many symptoms, apart from feeling bad and tiredness.

Follow pre-eruptive period, characterized by mild fever, headaches and other muscle pain, followed
closely by eruptive period, which covers up to
10 days. During this time a rash appears, nearly always accompanied by
fever and the child becomes agitated. The first elements of rash appear
on the body, and then extend the head and limbs, most finding
it on the trunk, the arm and thrust. But they also appear on the face, hairy skin of the head and hands.

Symptoms of chickenpox

- Fatigue and irritability for 1 or 2 days before rash manifestation
- Characteristic skin rash and itching on the trunk, under the arms, on the face, limbs, mouth and sometimes the trachea and bronchial tubes.

- Fever, general malaise
- Loss of appetite
- Muscle pain and / or joints
- Cough, runny nose
The chickenpox symptoms resemble those of other diseases, so you should see your doctor for diagnosis.

What are we doing in case of chickenpox in children?

In children is usually enough to take general measures to improve symptoms.
For fever is administered paracetamol or ibuprofen, always
avoiding aspirin (acetylsalicylic acid), whose use for Varicella is associated
with complications. Itching can be treated with oral
antihistamines or antipruritic lotions. Other measures that can be taken to avoid skin damage caused by scratching
are totally cut nails and a daily bath with shampoo with neutral PH.

General treatment in case of Varicella or chickenpox consists of bed rest
and light diet, lacto-flour-sugar, in fever period. Fever can be controlled with
aspirin (in adults) and paracetamol. It should be given special attention to hygiene skin and
mucous membranes to avoid vesicle infection. Child must not scratch, this
causing other bacterial infections. Nails should be cut to
reduce the effectiveness of scratch. It is indicated to
use powder the skin with mint talc.

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