Stories about: infectious disease

“Teenage” red blood cells could hold the key to a malaria vaccine

A T cell (right) launches an attack on an immature red blood cell called a reticulocyte. This immune response could help design a malaria vaccine.
A T cell (right) launches an attack on an immature red blood cell (left) infected with a malaria parasite called P. vivax. At the arrow, the T cell breaches the infected cell’s membrane to deliver death-inducing enzymes. Credit: Lieberman lab/Boston Children’s Hospital

Malaria parasite infection, which affects our red blood cells, can be fatal. Currently, there are about 200 million malaria infections in the world each year and more than 400,000 people, mostly children, die of malaria each year.

Now, studying blood samples from patients treated for malaria at a clinical field station in Brazil’s Amazon jungle, a team of Brazilian and American researchers has made a surprising discovery that could open the door to a new vaccine.

“I noticed that white blood cells called killer T cells were activated in response to malaria parasite infection of immature red blood cells,” says Caroline Junqueira, PhD, a visiting scientist at Boston Children’s Hospital and Harvard Medical School (HMS).

For red blood cells, this activity is unusual.

“Infected red blood cells aren’t recognized by our immune system’s T cells in the same way that most other infected cells of the human body are,” says Judy Lieberman, MD, PhD, chair in the Program in Cellular and Molecular Medicine at Boston Children’s Hospital.

Digging deeper, Junqueira, Lieberman and collaborators have found a completely unexpected immune response to malaria parasites that infect immature blood cells called reticulocytes. The revelation could help to design a new vaccine that might be capable of preventing malaria.

Their findings, published today in Nature Medicineuncover special cellular mechanisms and properties specific to “teenaged” reticulocytes and a strain of malaria called Plasmodium vivax that enable our T cells to recognize and destroy both the infected reticulocytes and the parasites inside them.

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Viral discussion: Epidemics experts sound off on the future of infection control

Image of flu virus, which experts think will eventually lead to future epidemics
Is the next flu pandemic around the corner?

During the 1918 influenza pandemic, the average life expectancy in the U.S. dropped below 40 years old. Today, public health and medical professionals need to be actively preparing for the next great pandemic, according to leaders of the Massachusetts Medical Society, The New England Journal of Medicine and Microsoft founder Bill Gates, who delivered the keynote address at a Boston-based meeting on April 27 called Epidemics Going Viral: Innovation vs. Nature. Here’s recap of what we heard from various panelists.

The five key drivers of epidemics are population growth/urbanization, travel, animals, environmental/climate changes and conflicts/natural disasters, according to Harvey Fineberg, MD, PhD, President of the Gordon and Betty Moore Foundation and former president of the Institute of Medicine. When it comes to predicting and preventing the next epidemic, Fineberg believes that data from a social media platform like Twitter isn’t going to help identify the next big outbreak.

But John Brownstein, PhD, an epidemiologist and Chief Innovation Officer at Boston Children’s Hospital, disagreed with that idea.

“I believe it’s possible for Twitter to find the next microbe,” Brownstein said. “This information comes in real time and at global scale.” Attendees who were live tweeting with the hashtag #epidemicsgoviral were quick to highlight this difference of opinion.

Uber flu shot, “a cool millennial thing to do”

Anne Schuchat, MD, deputy director of the Centers of Disease Control, busted the myth that non-vaccination rates are rising. She explained that media stories about anti-vaccination supporters can make it seem as though vaccination rates are falling when they actually aren’t.

“Less than one percent of kids aren’t vaccinated in the U.S.,” Schuchat said.

But some vaccinations, like the annual flu shot, still have big gaps to close. Brownstein described how a partnership with Uber — dispatching flu vaccines and nurses to people’s homes — was able to influence people to get their first-ever flu shot.

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News Note: Norovirus outbreak threatens the Olympics

The HealthMap team at Boston Children's is currently tracking norovirus at the Olympics
The Computational Epidemiology Team at Boston Children’s Hospital tracks online, informal sources for disease outbreak monitoring and real-time surveillance of emerging public health threats through a platform called HealthMap. This is an image of what their surveillance dashboard is currently tracking (Feb. 15, 2018) in South Korea. Visit http://www.healthmap.org/en/ for more.

The 2018 Winter Olympics have brought nearly 3,000 delegates from 206 countries together in PyeongChang, South Korea. But just a week after kicking off on February 8, the games and its attendees are already being interrupted by a fast-spreading norovirus outbreak.

Norovirus is an extremely infectious disease transmitted through food, water or by touching a contaminated surface. Infection causes inflammation of the stomach and intestines, which can lead to symptoms including stomach pains, nausea, vomiting and diarrhea.

In PyeongChang, there have already been 199 confirmed cases of norovirus — many of those sickened have been security guards hired for the games. Due to severe gastrointestinal symptoms, 41 guards have been hospitalized and more than 1,200 were placed in quarantine. 

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Food for thought: How your microbiome celebrates Thanksgiving

Image of microbiome superimposed over a Thanksgiving turkeySeth Rakoff-Nahoum, MD, PhD, a Boston Children’s Hospital physician-scientist who does infectious disease research and is taking an evolutionary approach to understanding the human microbiome and its effect on health, offers us some insight into what’s happening to the bugs in our gut as a result of the Thanksgiving meal. 

Q: Does the traditional American Thanksgiving meal affect the human microbiome?

A: Anything you put in your body has the potential to affect your microbiome, and Thanksgiving dinner is no different.

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Another microbiome perspective: The host holds the leash

Abstract depiction of the microbiome

Most scientists and clinicians accept that the human microbiome impacts a person’s nutrition, immune system function, physical health and perhaps even mental illness, but exactly how or why is not well understood. Now, taking an evolutionary approach, a Boston Children’s Hospital infectious disease researcher suggests the host may play a more active role in controlling the microbiome than previously appreciated.

“I think we need to re-evaluate the way in which we think about the microbiome,” says Seth Rakoff-Nahoum, MD, PhD, a physician-scientist at Boston Children’s in the Divisions of Infectious Diseases and Gastroenterology, whose perspective was published today in Nature.

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Of bugs, genes, development and intestinal biology

genes intestinal developmentThe collection of bacteria and other microorganisms living in our intestines—our microbiota—is now understood to play an important role in our physiology. Recent research indicates that it helps regulate our metabolism, immune system and other biological processes, and that imbalances in the microbiota are associated with everything from inflammatory bowel disease to diabetes.

Seth Rakoff-Nahoum, MD, PhD, wants to take this understanding to a new level. An infectious disease clinical fellow at Boston Children’s Hospital, he has systematically probed how genetics interact with environment—including the microbiota—to shape intestinal biology during different stages of development.

His investigations provide interesting clues to disorders that have their origins early in life, ranging from necrotizing enterocolitis in newborns to Hirschsprung’s disease (marked by poor intestinal motility) to food allergies.

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Infecting bacteria show surprising genetic diversity; we may need to adapt too

New research may change the way we culture and treat infections. (Burkholderia cepacia complex, CDC/Wikimedia Commons)
New research may change the way we culture and treat infections. (Burkholderia cepacia complex, CDC/Wikimedia Commons)

Ed. note: A longer version of this story appeared on Harvard Medical School’s website.

A boy with cystic fibrosis develops a potentially deadly Burkholderia dolosa infection in his lungs. Various genetic mutations allow some bacterial strains to survive assaults from his immune system and antibiotics, while others perish. Eventually, the strongest mutant dominates the B. dolosa colony.

Right? Maybe not, say the authors of a new study. Examining sputum samples from infected patients, they found that dozens of different kinds of B. dolosa may coexist in that boy’s lungs—each adapting and surviving in different ways. The findings, published last month in Nature Genetics, warn of possible shortfalls in the way infections are currently cultured and treated.

“We found that when a pathogen like B. dolosa infects us, it diversifies. Many cells discover ways to survive, and these successful mutants coexist,” says senior author Roy Kishony, PhD, professor of systems biology at Harvard Medical School.

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Bacteria use pain as a weapon

It’s bad enough that invasive infections are painful. New work suggests that pain is only a means to an end for virulent bacteria: It’s how they suppress our immune system.

Staph found near fibers from pain neurons
Invasive methicillin-resistant Staphylococcus aureus (labeled by green fluorescent protein) are found close to pain nerve fibers (labeled by red fluorescent protein) in dermal skin tissue following infection

Previously, the pain from invasive infections like meningitis, necrotizing fasciitis, urinary tract infections, dental caries and intestinal infections was thought to be due to the body’s immune response, causing the infected tissue to become inflamed and swollen.

Not so, says Boston Children’s Hospital neuro-immunologist Isaac Chiu, PhD. Studying invasive skin infections caused by methicillin-resistant Staphylococcus aureus (MRSA) in live mice, his team’s research demonstrates that the pain is induced by the bacteria themselves, and kicks in well before tissue swelling peaks.

Adding outrage to insult, once the pain-sensing neurons are activated, they suppress the immune system, potentially allowing the bacteria to proliferate, finds the study, published last week in Nature.

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A Lego-like approach to vaccine design

A syringe made of Legos.
A robust, reproducible vaccine with low risk of side effects is hard to come by. A new design strategy could balance the benefits and risks of different vaccine approaches while making them as easy to build as Legos. (seanmichaelragan/Flickr)

A good vaccine should confer robust, long-lasting immunity against a given pathogen without causing side effects. Striking this balance has fueled a long-standing debate over whole-cell and acellular vaccines.

Whole-cell vaccines rely on killed or weakened pathogens. Acellular or subunit vaccines contain only defined sets of antigens known to stimulate an effective immune response against the pathogen in question.

Both approaches have their strengths and weaknesses. Whole-cell vaccines carry a bacterium’s full complement of antigens and can activate many arms of the immune system at once. And they are inexpensive to manufacture. But these vaccines can be hard to reproduce and run the risk of causing frequent or serious side effects.

Acellular vaccines are very reproducible and run a much lower risk of side effects. But the immune responses they trigger aren’t as robust or durable, as evidenced by the recent failures of the acellular pertussis vaccines.

What if you could bring together the effectiveness of a whole-cell vaccine and the safety and reproducibility of an acellular one? That’s what Boston Children’s Hospital’s Fan Zhang, PhD, Yingjie Lu, PhD, and Richard Malley, MD, want to do with the Multiple Antigen Presenting System, or MAPS.

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A vaccine that works in newborns?

If we could immunize infants at birth, far more could be protected from infections.(DFID-UK Dept for International Development)

Right now, immunizations against most infections begin at 2 months of age. But that leaves newborns at risk for infections like rotavirus, whooping cough and pneumococcus during a highly vulnerable time.

In resource-poor countries, this is a serious problem: Many children see a health care provider only at birth, so may miss their chance to be protected. Worldwide, each year, more than 2 million infants under 6 months old die from infections, especially pneumonia. If we could immunize infants at birth, it would be a huge win for global health.

Unfortunately, though, newborns don’t respond to most vaccines. Their immune systems are too immature—which is why few vaccines for newborns exist.

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