A virus to be used as an effective immunotherapy in patients with brain cancer


Fecal Transplants Transmit Viruses, Too

Fecal matter transplants may transfer nonpathogenic viruses along with beneficial bacteria, scientists show.

Fecal matter transplantation can help to boost populations of “good” gut bacteria in patients undergoing treatment for persistent infections by pathogenic bacteria such as Clostridium difficile, and is being trialed as a therapy for other gastrointestinal problems like irritable bowel syndrome and ulcerative colitis. But bacteria are not the only microbes being transplanted, according to a study led by researchers at the University of Pennsylvania’s Perelman School of Medicine. The findings, published today (March 29) in mBio, show that nonpathogenic viruses also make the trip.

“Donors are screened very extensively for gastrointestinal diseases and other infectious diseases,” study coauthor Frederic Bushman of Penn said in a statement. “However you worry about the unknown unknowns, infectious agents that might be bad, but [are] not screened for.”

To investigate what else might be transplanted by the technique, the researchers analyzed fecal matter administered to three children with chronic ulcerative colitis from a single healthy donor. Each child received up to 30 of these transplants over two to four months.

“We could see bacterial viruses moving between humans and we were able to learn some things about transmission,” said Bushman in the statement. However, he added, “we did not see any viruses that grow on animal cells that may be of concern for infecting and harming patients. We saw mostly temperate bacteriophages.”

These phages are of relatively little concern as a health risk, although they could conceivably carry toxins or contribute to antibiotic resistance in a recipient. In their paper, the authors concluded that further characterization of the microbes being transferred during fecal transplantation could help to “guide development of safest practices.”

Viruses Win Approval as Anti-Cancer Treatment | Big Think

Earlier this week, the FDA approved the first-ever virus as a medical treatment for melanoma. The strain has the mouthful of a name — talimogene laherparepvec (T-VEC) — but the virus’s debut into the realm of medical science has been long awaited. According to Nature, as far back as the 19th century, scientists noticed that viruses mysteriously shrunk certain tumors and currently in China there is a booming medical tourism industry for the treatment of head and neck cancer with oncolytic adenovirus H101.


So how exactly does virus therapy work? When we get sick from a virus, it invades our bodies and changes the DNA of certain cells, essentially making them zombie cells that do the virus’ bidding. With virus therapy, the same mechanism is at work, except the virus switches off the DNA that is expressing cancer.

While using viruses to treat cancer may sound like science fiction, virology is definitely pushing the boundaries of pathogen study into the realm of fascinating paradox.

What’s fascinating about using virus therapy to cure cancer is the propensity for viruses to cause cancer. In fact, 15 percent of all cancer deaths are caused by a virus, with the most common being human papillomavirus (HPV). What’s even more fascinating is that most of cancer research is done with HeLa cells, or immortal cancer cells that were taken from a woman in the 1950s who contracted the HPV virus.

The strange loops between viruses and DNA point to the growing opportunities in medical research, but also the more nebulous line between virulence and vitality. Already, it is well-known in scientific communities that the genetic disorder sickle cell anemia can prevent mortality in young children who are exposed to the malaria virus. Even stranger is the co-dependence of archaebacteria and viruses deep within the ocean crust, which has even been purported as evidence of life on other planets.

While using viruses to treat cancer may sound like science fiction, virology is definitely pushing the boundaries of pathogen study into the realm of fascinating paradox.

Could deadly viruses’ rapid evolution be turned against them? And could we ever control the pace of our own evolution?


Camel tests positive for Mers virus.

A camel has tested positive for the Sars-like virus that emerged in the Middle East last year and has killed 64 people worldwide.

The animal had been owned by a person diagnosed with Mers (Middle East respiratory syndrome) coronavirus, the Saudi health ministry said.

Dromedary camel

It remains unclear, however, if camels are responsible for passing the disease to humans.

Coronaviruses cause respiratory infections in humans and animals.

It is possible the virus is spread in droplets when an infected person coughs or sneezes.

Experts believe the virus is not very contagious – if it were, we would have seen more cases.

Globally, since September 2012, there have been 153 laboratory-confirmed cases of infection with Mers coronavirus.

The Saudi government statement said “preliminary” laboratory checks had proved positive.

The health ministry said it was working with the ministry of agriculture and laboratories to “isolate the virus and compare its genetic structure with that of the patient’s”.

If the virus carried by the camel and that of the patient “prove to be identical, this would be a first scientific discovery worldwide, and a door to identify the source of the virus”, it added.

The World Health Organization, which has been monitoring the global situation, says there is currently no reason to impose any travel restrictions because of the virus.

Food Additive TBHQ May Protect from Avian Influenza Virus H7N9.

Tert-butyl hydroquinone (TBHQ) – a common food additive – may protect people from the avian influenza A strain H7N9, according to a new study published in the journal PLoS ONE.

This image shows H7N9 virions. Image credit: Cynthia S. Goldsmith / Thomas Rowe.

This image shows H7N9 virions. Image credit: Cynthia S. Goldsmith / Thomas Rowe.

“The recent H7N9 outbreak in China this past March had a mortality rate of more than 20 percent. That strain, which is new, is already showing resistance to the majority of existing drugs used to treat it. The need to develop new antiviral therapeutics now is crucial,” said senior author Dr Michael Caffrey from the University of Illinois.

Flu viruses enter host cells using a special protein called hemagglutinin, which acts as a key that opens receptors on the cell surface. If hemagglutinin is disabled, the virus is locked out and can’t infect cells.

Dr Caffrey’s team found that the FDA-approved TBHQ sticks to a specific region on the hemagglutinin molecule.

TBHQ is an effective antioxidant. It is used as a preservative for vegetable oils and edible animal fats. its E number is E319.

“The additive attaches to the Achilles’ heel of the virus – a loop-shaped portion of hemagglutinin necessary for binding to cells, making cell infection impossible. The loop on the hemagglutinin molecule represents a new therapeutic target, since existing drugs don’t go after it.”

“Any drugs that focus on the hemagglutinin loop would be totally novel to flu viruses, and so resistance, if developed, would still be a long way off.”

The team was looking at a different class of viruses when the first outbreak of the H7N9 virus was reported in China last spring.

“TBHQ was known to have virus-blocking effects for H3 viruses. So when the H7N9 outbreak occurred, we thought we’d see if it had any effect on H7 viruses,” Dr Caffrey said.

The team fused the hemagglutinin of the H7N9 virus to a less dangerous virus in order to study it safely. They found that TBHQ was able to prevent the virus from infecting human lung cells in the lab.

The researchers are now looking for ways to enhance TBHQ’s ability to prevent infection.


Source: Antanasijevic A et al. 2013. Inhibition of Influenza H7 Hemagglutinin-Mediated Entry. PLoS ONE 8 (10): e76363; doi: 10.1371/journal.pone.0076363

Pandoravirus: missing link discovered between viruses and cells

Researchers at IGS, the genomic and structural information laboratory (CNRS/Aix-Marseille University), working in association with the large-scale biology laboratory (CEA/Inserm/Grenoble Alpes University) have just discovered two giant viruses which, in terms of number of genes, are comparable to certain eukaryotes, microorganisms with nucleated cells. The two viruses – called “Pandoravirus” to reflect their amphora shape and mysterious genetic content – are unlike any virus discovered before.

With the discovery of Mimivirus ten years ago and, more recently, Megavirus chilensis , researchers thought they had reached the farthest corners of the viral world in terms of size and genetic complexity. With a diameter in the region of a micrometer and a genome incorporating more than 1,100 genes, these giant viruses, which infect amoebas of the Acanthamoeba genus, had already largely encroached on areas previously thought to be the exclusive domain of bacteria.

For the sake of comparison, common viruses such as the influenza or AIDS viruses, only contain around ten genes each.In the article published in Science, the researchers announced they had discovered two new giant viruses: •Pandoravirus salinus, on the coast of Chile;•Pandoravirus dulcis, in a freshwater pond in Melbourne, Australia.Detailed analysis has shown that these first two Pandoraviruses have virtually nothing in common with previously characterized giant viruses. What’s more, only a very small percentage (6%) of proteins encoded by Pandoravirus salinus are similar to those already identified in other viruses or cellular organisms. With a genome of this size, Pandoravirus salinus has just demonstrated that viruses can be more complex than some eukaryotic cells . Another unusual feature of Pandoraviruses is that they have no gene allowing them to build a protein like the capsid protein, which is the basic building block of traditional viruses.Despite all these novel properties, Pandoraviruses display the essential characteristics of other viruses in that they contain no ribosome, produce no energy and do not divide.This groundbreaking research included an analysis of the Pandoravirus salinus proteome, which proved that the proteins making it up are consistent with those predicted by the virus’ genome sequence. Pandoraviruses thus use the universal genetic code shared by all living organisms on the planet.

This shows just how much more there is to learn regarding microscopic biodiversity as soon as new environments are considered. The simultaneous discovery of two specimens of this new virus family in sediments located 15,000 km apart indicates that Pandoraviruses, which were completely unknown until now, are very likely not rare. It definitively bridges the gap between viruses and cells – a gap that was proclaimed as dogma at the very outset of modern virology back in the 1950s. It also suggests that cell life could have emerged with a far greater variety of pre-cellular forms than those conventionally considered, as the new giant virus has almost no equivalent among the three recognized domains of cellular life, namely eukaryota (or eukaryotes), eubacteria, and archaea.

Source: http://www.cea.fr

What Most Doctors Won’t Tell You About Colds and Flus.


The next time you experience a cold or the flu, remember this: rather than take conventional drugs to suppress uncomfortable symptoms, it’s better for your health to allow the cold or flu to run its course while you get plenty of physical and emotional rest.

Conventional medicine and the pharmaceutical industry would have you believe that there is no “cure” for the common cold, that you should protect yourself against the flu with a vaccine that is laden with toxic chemicals, and that during the midst of a cold or flu, it is favorable to ease your discomfort with a variety of medications that can suppress your symptoms.

Unfortunately, all three of these positions indicate a lack of understanding of what colds and flus really are, and what they do for your body.

Colds and flus are caused by viruses. So to understand what colds and flus do at a cellular level, you have to understand what viruses do at a cellular level.

Do you remember learning about cellular division in grade seven science class? Each of your cells are called parent cells, and through processes of genetic duplication (mitosis) and cellular division (cytokinesis), each of your parent cells divides into two daughter cells. Each daughter cell is then considered a parent cell that will divide into two more daughter cells, and so on.

Viruses are different from your cells in that they cannot duplicate themselves through mitosis and cytokinesis. Viruses are nothing but microscopic particles of genetic material, each coated by a thin layer of protein.

Due to their design, viruses are not able to reproduce on their own. The only way that viruses can flourish in your body is by using the machinery and metabolism of your cells to produce multiple copies of themselves.

Once a virus has gained access into one of your cells, depending on the type of virus involved, one of two things can happen:
The virus uses your cell’s resources to replicate itself many times over and then breaks open (lyses) the cell so that the newly replicated viruses can leave in search of new cells to infect. Lysis effectively kills your cell.

The virus incorporates itself into the DNA of your cell, which allows the virus to be passed on to each daughter cell that stems from this cell. Later on, the virus in each daughter cell can begin replicating itself as described above. Once multiple copies of the virus have been produced, the cell is lysed.

Both possibilities lead to the same result: eventually, the infected cell can die due to lysis.

Here is the key to understanding why colds and flus, when allowed to run their course while you rest, can be good for you:

By and large, the viruses that cause the common cold and the flu infect mainly your weakest cells; cells that are already burdened with excessive waste products and toxins are most likely to allow viruses to infect them. These are cells that you want to get rid of anyway, to be replaced by new, healthy cells.

So in the big scheme of things, a cold or flu is a natural event that can allow your body to purge itself of old and damaged cells that, in the absence of viral infection, would normally take much longer to identify, destroy, and eliminate.

Have you ever been amazed by how much “stuff” you could blow out of your nose while you had a cold or the flu? Embedded within all of that mucous are countless dead cells that your body is saying good bye to, largely due to the lytic effect of viruses.

So you see, there never needs to be a cure for the common cold, since the common cold is nature’s way of keeping you healthy over the long term. And so long as you get plenty of rest and strive to stay hydrated and properly nourished during a cold or flu, there is no need to get vaccinated or to take medications that suppress congested sinuses, a fever, or coughing. All of these uncomfortable symptoms are actually ways in which your body works to eliminate waste products and/or help your body get through a cold or flu. It’s fine to use over-the-counter pain medication like acetaminophen if your discomfort becomes intolerable or if such meds can help you get a good night’s rest. But it’s best to avoid medications that aim to suppress helpful processes such as fever, coughing, and a runny nose.

It’s important to note that just because colds and flus can be helpful to your body doesn’t mean that you need to experience them to be at your best. If you take good care of your health and immune system by getting plenty of rest and consistently making health-promoting dietary and lifestyle choices, your cells may stay strong enough to avoid getting infected by viruses that come knocking on their membranes. In this scenario, you won’t have enough weak and extraneous cells to require a cold or the flu to work its way through your body to identify and lyse them.

Curious about how to differentiate the common cold and the flu? Here is an excellent summary of the differences from cbc.ca:
A cold usually comes on gradually — over the course of a day or two. Generally, it leaves you feeling tired, sneezing, coughing and plagued by a running nose. You often don’t have a fever, but when you do, it’s only slightly higher than normal. Colds usually last three to four days, but can hang around for 10 days to two weeks.

Flu, on the other hand, comes on suddenly and hits hard. You will feel weak and tired and you could run a fever as high as 40 C. Your muscles and joints will probably ache, you will feel chilled and could have a severe headache and sore throat. Getting off the couch or out of bed will be a chore. The fever may last three to five days, but you could feel weak and tired for two to three weeks.

One final note on this topic: because the common cold and the flu are both caused by viruses, antibiotics are not necessary. People who take antibiotics while suffering with a cold or flu often feel slightly better because antibiotics have a mild anti-inflammatory effect. But this benefit is far outweighed by the negative impact that antibiotics have on friendly bacteria that live throughout your digestive tract. In this light, if you really need help with pain management during a cold or flu, it is usually better to take a small dose of acetaminophen than it is to take antibiotics.

Sources: drbenkim.com & realfarmacy.com







Universal flu jab ‘edges closer’.

A way of creating more effective vaccines which could protect against a broad range of flu viruses has been reported by US researchers.

A different seasonal flu jab is produced every year as the virus is a constantly shifting target.

This animal study, published in the journal Nature, showed a single jab could protect against multiple strains.

Flu scientists said it was an important advance, but a vaccine which could defeat all flu was a long way off.

While there are different strains of flu circulating each year, there are bits of the flu virus which do not change.

Many groups of researchers believe that targeting these weak spots could lead to a single, universal flu vaccine.

Synthetic biology

The normal seasonal flu jab is made by growing the virus in chicken eggs. It is then inactivated and injected into people to train the immune system to fight off that virus.

A group at the pharmaceutical company Sanofi used a different approach to design a new protein which was half virus.

Spikes which stick out from the surface of the virus, which hardly vary between strains, were fused with a ‘transporter protein’ which is naturally found in blood.

Groups of these hybrid proteins then spontaneously formed tiny spheres, which were tested in ferrets.

Flu researchers use ferrets as they are can be infected with human viruses, which results in similar symptoms.

The vaccine gave the animals immunity against multiple batches of flu ranging from viruses circulating in 1934 through to 2007.

Dr Gary Nabel, the chief scientific officer at Sanofi, told the BBC: “We think this is a step down the path towards a universal vaccine. It’s not a universal vaccine yet.

“There’s lots of research in the early phases and this looks as good as anything out there.”

Not everything

The spike used in the vaccine was haemagglutinin, but there are many different types of haemagglutinin. It is how viruses are classified – swine flu in 2009 was H1N1, with the H standing for haemagglutinin.

This vaccine was designed to protect against H1 flu viruses. It would not protect against others such as the current bird flu in China, H7N9.

Prof Sarah Gilbert, who works on universal vaccines at Oxford University, told BBC News: “It is an improvement on the current vaccine. It’s not a ‘universal vaccine’ but it’s definitely a step in the right direction.”

She said it might be able to get over the problems of “mis-match” when there are differences between the seasonal vaccine and the flu being targeted.

However, the vaccine has not yet been tested in people. Clinical grade vaccine has not yet been developed so even safety trials are thought to be a year away.

There is a risk that the flu virus could find ways to evade the vaccine.

Prof Wendy Barclay, from Imperial College London, said: “I think the important question to explore in the field now is…will the virus be able to escape by ‘drift’ like it does each year to our natural antibody response, or can it be ‘pinned in’ by the immune response induced by this new era of vaccines?”

Dr Nabel agreed that viruses could be difficult to pin down: “It is like squeezing a balloon. You squish one place and another pops out. The viruses are very clever and under pressure they find a new way to escape.”

Source: BBC

groundr�t’8(� �� yle=’font-size:13.0pt; font-family:”Arial”,”sans-serif”;color:#333333′>In contrast, previous research on the link between intelligence and reaction times, colour discrimination and sensitivity to pitch found only a 20-40% correlation.


But the ability to ignore background movements is not the only indicator of intelligence.

“Because intelligence is such a broad construct, you can’t really track it back to one part of the brain,” says Duje Tadin, who also worked on the study.

“But since this task is so simple and so closely linked to IQ, it may give us clues about what makes a brain more efficient, and, consequently, more intelligent.

“We know from prior research which parts of the brain are involved in visual suppression of background motion.

“This new link to intelligence provides a good target for looking at what is different about the neural processing, what’s different about the neurochemistry, what’s different about the neurotransmitters of people with different IQs.”

Source: BBC

Viruses: Nature’s Self-Packing, Nanoscale Suitcases.

This the season, from Thanksgiving to New Year, when tens of millions of us will travel to see family and friends. As these trips draw near everyone will face the same dilemma — what to pack? After laundry, ironing and folding, the next problem is which suitcase to choose; too small, too big, just right. What none of us think about during this time is the myriad of invisible virus particles that will be making the trip with us.

These nanoscale objects (a nanometer is one millionth of a millimeter, or 10,000 times smaller than the width of your hair) cling to our bodies looking for ways to get inside our cells and make new copies of themselves. During our trip, they will readily be exchanged with viruses taking trips with other people, either by transferring on surfaces or as aerosols in the air, especially if someone forgets to cover their face when they sneeze. Despite their apparently insidious size, and their potential for causing everything from the common cold to AIDS, viruses are not actively malign. They are in fact non-living collections of proteins and nucleic acids that simply fulfill Darwinian predictions about evolution. In their case they have evolved the property of infecting cells and replicating by using the host’s molecular machinery to produce new virus particles that escape the cell looking for a new victim. Making their hosts ill, or even killing them, is just an unfortunate side effect of this process. It is, however, a side effect that results in devastating losses in crops, as well as being the cause of many serious illnesses and deaths in animals and people every year. Understanding these events in detail is a major goal of researchers who hope to find ways to deter these pesky hitchhikers.

Working with one group of viruses that contain RNA genomes, similar to those that cause the common cold or polio, Alex Borodavka, Roma Tuma and I have just made an interesting discovery about the ways that viruses pack for their trips. In the viral world the content of the suitcase is the nucleic acid that carries the instructions for making new viruses. The suitcase is made from viral coat protein molecules that clump together to form a protective shield for that nucleic acid. Just as we do when we get to our destinations, when viruses enter cells they unpack their nucleic acids from the protein shell and the process of making new virus particles can begin. The first stages of this process are making new copies of the nucleic acid instruction book and more coat proteins to make the newly required suitcases to pack them in. The RNA in our test viruses emerges from these events rather like our clothes do after a few days at our destination, crumpled in a heap and no longer neatly folded. At the end of our trips we may discover that our suitcase is a little too small after all because we have to work hard at getting everything to fit back in. Similarly new viral suitcases are pretty cramped, and something has to happen to fold their nucleic acid molecules neatly so that they will fit inside.

Using a spectroscopic technique that allows us to see viral particles one at time, we noticed the equivalent of a Harry Potter moment for virus assembly. When viral RNAs and viral proteins are mixed together the proteins leap onto the RNA and fold it up neatly. It is as if the suitcase and the contents pack themselves. Previously people assumed that the process was much more gradual than this. Interestingly, when viral coat proteins are given non-viral RNAs they leap onto those molecules too but are not able to fold them up. That means that the viral suitcases they try to build do not close properly and so their contents cannot survive the trip to a new host. These observations pose an interesting question.

Can we mess up a viral nucleic acid’s travel plans by getting their coat proteins to treat them like non-viral equivalents? If we could we would have a powerful way to treat viral infections. Something to think about the next time you are stuck waiting for your plane, train or bus.

Happy Holidays!!

Source: http://www.huffingtonpost.com


2011–12 Outbreak of Variant Swine Flu Represents ‘Significant Increase’ .

A novel swine-origin influenza A virus — H3N2 variant — has sickened 29 people since July 2011, including 16 in the past few weeks, the CDC confirmed in a press briefing on Friday. CDC epidemiologist Joseph Bresee called the 29 cases “a significant increase in the number of detections for these types of virus we’ve seen in recent years.”

All 16 recent cases had known contact with swine; however, 3 cases occurring in November 2011 suggested human-to-human transmission. None of the 16 recent cases required hospitalization; the 3 from November 2011 did. In all 29 patients, the H3N2 variant contained a gene from the 2009 pandemic virus that “may confirm increased transmissibility to and among humans compared with other variant influenza viruses,” Bresee said.

Since most swine contact occurred during agricultural fairs, Bresee stressed the importance of taking precautions in such settings (e.g., wash your hands before and after exposure to animals; don’t put anything in your mouth while in animal areas).

Source: CDC