Engaging in These 8 Mindfulness Practices Daily Decreased HIV Patients’ Viral Loads

Article Image

Mindfulness meditation has been practiced in East Asia for thousands of years. In the 1960s and 70s, interest in it brought this Zen staple to the US and Europe. It was common within the counterculture movement and continued over the decades among “crunchy granola” and “New Age” types. Since, several studies have shown remarkable health benefits gained by those engaging in such meditation.

Renowned Zen master Thich Nhat Hanh calls mindfulness “present-focused awareness.” This is clearing one’s mind of all the chatter, what Buddhists call the “monkey mind,” as well as any thoughts of the past or future. In reality they don’t exist. All that is real is the omnipresent now.

Time unfolds moment to moment. So we must live fully in the now to truly be free and at one with nature and our place within it. Mindfulness is therefore recognizing everything that is before you with a sharpened focus. In a way, this is jettisoning worry and instead, embracing wonder and gratitude for the rich sensual tapestry unfolding at each moment in one’s life.

Today lawyers, tech professionals, and executives at some of the top companies in the world including: Goldman Sachs, Aetna, Google, Bank of American, and Salesforce, all practice mindfulness. Studies have shown that it increases focus, memory, and may even improve cognition.

One surprising find, it alters attitudes, even the ones we don’t consider malleable. A 2015 study out of Central Michigan University, found that regularly practicing mindfulness reduces implicit ageism and racial bias.

English Bobbie meditating.

People from all walks of life practice mindfulness medication. Getty Images.

Engaging in mindfulness reduces stress. Chronic stress elevates the hormone cortisol in the bloodstream, which in turn raises our blood pressure, increases our awareness of pain, weakens our immune system, and causes chronic inflammation—implicated in a whole host of conditions including heart disease, cancer, and diabetes.

Such meditation can also save you from wrinkles and gray hair. Practicing regularly has been proven to lengthen the telomerase or “caps” at the end of chromosomes. By doing so, cell damage is reduced and the aging process, slowed.

Common virus may be celiac disease culprit

A VIRAL TRIGGER A reovirus (illustrated here) may jump-start celiac disease by turning the immune system against gluten, a new study in mice suggests.

A common and usually harmless virus may trigger celiac disease. Infection with the suspected culprit, a reovirus, could cause the immune system to react to gluten as if it was a dangerous pathogen instead of a harmless food protein, an international team of researchers reports April 7 in Science.

In a study in mice, the researchers found that the reovirus, T1L, tricks the immune system into mounting an attack against innocent food molecules. The virus first blocks the immune system’s regulatory response that usually gives non-native substances, like food proteins, the OK, Terence Dermody, a virologist at the University of Pittsburgh, and colleagues found. Then the virus prompts a harmful inflammatory response.

“Viruses have been suspected as potential triggers of autoimmune or food allergy–related diseases for decades,” says Herbert Virgin, a viral immunologist at Washington University School of Medicine in St. Louis. This study provides new data on how a viral infection can change the immune system’s response to food, says Virgin, who wasn’t involved in the study.

Reoviruses aren’t deadly. Almost everyone has been infected with a reovirus, and almost no one gets sick, Dermody says. But if the first exposure to a food with gluten occurs during infection, the virus may…

CRISPR had a life before it became a gene-editing tool

Bacteria and archaea armed with CRISPR systems have been at war with viruses for eons. Here, hordes of viruses known as phages assault a bacterium to turn it into a virus-making factory.


It is the dazzling star of the biotech world: a powerful new tool that can deftly and precisely alter the structure of DNA. It promises cures for diseases, sturdier crops, malaria-resistant mosquitoes and more. Frenzy over the technique — known as CRISPR/Cas9 — is in full swing. Every week, new CRISPR findings are unfurled in scientific journals. In the courts, universities fight over patents. The media report on the breakthroughs as well as the ethics of this game changer almost daily.

But there is a less sequins-and-glitter side to CRISPR that’s just as alluring to anyone thirsty to understand the natural world. The biology behind CRISPR technology comes from a battle that has been raging for eons, out of sight and yet all around us (and on us, and in us).

The CRISPR editing tool has its origins in microbes — bacteria and archaea that live in obscene numbers everywhere from undersea vents to the snot in the human nose. For billions of years, these single-celled organisms have been at odds with the viruses — known as phages — that attack them, invaders so plentiful that a single drop of seawater can hold 10 million. And natural CRISPR systems (there are many) play a big part in this tussle. They act as gatekeepers, essentially cataloging viruses that get into cells. If a virus shows up again, the cell — and its offspring — can recognize and destroy it. Studying this system will teach biologists much about ecology, disease and the overall workings of life on Earth.

But moving from the simple, textbook story into real life is messy. In the few years since the defensive function of CRISPR systems was first appreciated, microbiologists have busied themselves collecting samples, conducting experiments and crunching reams of DNA data to try to understand what the systems do. From that has come much elegant physiology, a mass of complexity, surprises aplenty — and more than a little mystery.

Spoiled yogurt

The biology is complicated, and its basic nuts and bolts took some figuring out. There are two parts to CRISPR/Cas systems: the CRISPR bit and the Cas bit. The CRISPR bit — or “clustered regularly interspaced short palindromic repeats” — was stumbled on in the late 1980s and 1990s. Scientists then slowly pieced the story together by studying microbes that thrive in animals’ guts and in salt marshes, that cause the plague and that are used to make delicious yogurt and cheese.

None of the scientists knew what they were dealing with at first. They saw stretches of DNA with a characteristic pattern: short lengths of repeated sequence separated by other DNA sequences now known as spacers. Each spacer was unique. Because the roster of spacers could differ from one cell to the next in a given microbe species, an early realization was that these differences could be useful for forensic “typing” — investigators could tell whether food poisoning cases were linked, or if someone had stolen a company’s yogurt starter culture.

Bacteria use CRISPR/Cas as a form of immunity or self-defense against invaders. A bacterium builds a library of genetic material from past invaders so that, if the same invader attacks again, the bacterium and its offspring can disable it.

L. Marraffini/Nature 2015, Adapted by J. Hirshfeld

But curious findings piled up. Some of those spacers, it turned out, matched the DNA of phages. In a flurry of reports in 2005, scientists showed, to name one example, that strains of the lactic acid bacterium Streptococcus thermophilus contained spacers that matched genetic material of phages known to infect Streptococcus. And the more spacers a strain had, the more resistant it was to attack by phages.

This began to look a lot like learned or adaptive immunity, akin to our own antibody system: After exposure to a specific threat, your immune system remembers and you are thereafter resistant to that threat. In a classic experiment published in Science in 2007, researchers at the food company Danisco showed it was so. They could see new spacers added when a phage infected a culture of S. thermophilus. Afterward, the bacterium was immune to the phage. They could artificially engineer a phage spacer into the CRISPR DNA and see resistance emerge; when they took the spacer away, immunity was lost.

This was handy intel for an industry that could find whole vats of yogurt-making bacteria wiped out by phage infestations. It was an exciting time scientifically and commercially, says Rodolphe Barrangou of North Carolina State University in Raleigh, who did a lot of the Danisco work. “It was not just discovering a cool system, but also uncovering a powerful phage-resistance technology for the dairy industry,” he says.

The second part of the CRISPR/Cas system is the Cas bit: a set of genes located near the cluster of CRISPR spacers. The DNA sequences of these genes strongly suggested that they carried instructions for proteins that interact with DNA or RNA in some fashion — sticking to it, cutting it, copying it, unraveling it. When researchers inactivated one Cas gene or another, they saw immunity falter. Clearly, the two bits of the system — CRISPR and Cas — were a team.

It took many more experiments to get to today’s basic model of how CRISPR/Cas systems fight phages — and not just phages. Other types of foreign DNA can get into microbes, including circular rings called plasmids that shuttle from cell to cell and DNA pieces called transposable elements, which jump around within genomes. CRISPRs can fend off these intruders, as well as keep a microbe’s genome in tidy order.

The process works like this: A virus injects its genetic material into the cell. Sensing this danger, the cell selects a little strip of that genetic material and adds it to the spacers in the CRISPR cluster. This step, known as immunization or adaptation, creates a list of encounters a cell has had with viruses, plasmids or other foreign bits of DNA over time — neatly lined up in reverse chronological order, newest to oldest.

Older spacers eventually get shed, but a CRISPR cluster can grow to be long — the record holder to date is 587 spacers in Haliangium ochraceum, a salt-loving microbe isolated from a piece of seaweed. “It’s like looking at the last 600 shots you had in your arm,” says Barrangou. “Think about that.”

New spacer in place, the microbe is now immunized. Later comes targeting. If that same phage enters the cell again, it’s recognized. The cell has made RNA copies of the relevant spacer, which bind to the matching spot on the genome of the invading phage. That “guide RNA” leads Cas proteins to target and snip the phage DNA, defanging the intruder.

Scientists have divided the array of known CRISPR systems into five types and 16 subtypes based on DNA sequence data. The distribution of types differs in archaea and bacteria.

K.S. Makarova et al/Nat. Rev. Microbio. 2015, Adapted by J. Hirshfeld

Researchers now know there are a confetti-storm of different CRISPR systems, and the list continues to grow. Some are simple — such as the CRISPR/Cas9 system that’s been adapted for gene editing in more complex creatures (SN: 4/15/17, p. 16) — and some are elaborate, with many protein workhorses deployed to get the job done.

Those who are sleuthing the evolution of CRISPR systems are deciphering a complex story. The part of the CRISPR toolbox involved in immunity (adding spacers after phages inject their genetic material) seems to have originated from a specific type of transposable element called a casposon. But the part responsible for targeting has multiple origins — in some cases, it’s another type of transposable element. In others, it’s a mystery.

Given the power of CRISPR systems to ward off foes, one might think every respectable microbe out there in the soils, vents, lakes, guts and nostrils of this planet would have one. Not so.

Numbers are far from certain, partly because science hasn’t come close to identifying all the world’s microbes, let alone probe them all for CRISPRs. But the scads of microbial genetic data accrued so far throw up interesting trends.

Tallies suggest that CRISPR systems are far more prevalent in known archaea than in known bacteria — such systems exist in roughly 90 percent of archaea and about…

Getting dengue first may make Zika infection much worse

dengue antibody and dengue virus
FRIEND OR FOE A dengue antibody (blue, shown bound to a dengue virus protein, red, in this molecular model) can ease Zika’s entry into cells, a new study finds.

Being immune to a virus is a good thing, until it’s not. That’s the lesson from a study that sought to understand the severity of the Zika outbreak in Brazil. Experiments in cells and mice suggest that a previous exposure to dengue or West Nile can make a Zika virus infection worse.

“Antibodies you generate from the first infection … can facilitate entry of the Zika virus into susceptible cells, exacerbating the disease outcome,” says virologist Jean K. Lim. Lim and colleagues report the results online March 30 in Science.

The study is the first to demonstrate this effect in mice, as well as the first to implicate West Nile virus, notes Sharon Isern, a molecular virologist at Florida Gulf Coast University in Fort Myers.

Zika is similar to other members of its viral family, the flaviviruses. It shares about 60 percent of its genetic information with dengue virus and West Nile virus. Dengue outbreaks are common in South and Central America, and dengue as well as West Nile are endemic to the United States.

Exposure to a virus spurs the body to create antibodies, which prevent illness when a subsequent infection with the virus occurs. But a peculiar phenomenon called antibody-dependent enhancement has been described in dengue patients (SN: 6/25/16, p. 22). The dengue virus has four different versions. When a person with immunity to one dengue type becomes sick with another type, the illness is worse the second time. The antibodies from the previous dengue exposure actually help the subsequent dengue virus infect cells, rather than blocking them.

Outcomes of Zika infections for mice depended on whether certain viral antibodies were present in their systems….

Rapid Ebola test to detect early infection in the works

Ebola virus
TEAM PLAYERS Researchers are designing antibody pairs that can help detect the Ebola virus (shown) sooner.

WASHINGTON — Diagnosing Ebola earlier is becoming almost as easy as taking a home pregnancy test.

Scientists are developing antibodies for a test that can sniff out the deadly virus more quickly and efficiently than current tests, researchers reported February 6 at the American Society for Microbiology Biothreats meeting.

Detecting Ebola’s genetic material in patients’ blood samples now takes a full day and requires access to a specialized laboratory. Simpler and speedier tests are available. They use antibodies — specialized proteins that latch onto and flag virus particles — and work somewhat like a pregnancy test. Within…