West Nile virus

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West Nile is primarily a bird virus, but people occasionally get infected because some bird-biting mosquitoes dine on human blood as well.

West Nile virus In 2018

After the West Nile virus appeared on the U.S. East Coast in 1999, it spread across the entire country in just a few years, sickening thousands of people and striking down whole flocks of robins, crows, and other birds. Now, a new study suggests the mosquito-borne virus may have had an unexpected helper: light pollution. Birds infected with West Nile can spread the virus twice as long when they are exposed to night light, according to a study presented here over the weekend at the annual meeting of the Society for Integrative and Comparative Biology.

The work “shows that light pollution is not only bad for our [daily rhythms], but also can affect disease prevalence and transmission,” says Jenny Ouyang, an integrative physiologist at the University of Nevada in Reno. “Perhaps infection in humans and other animals is also affected by light,” adds Yale University epidemiologist Durland Fish. (Neither Ouyang nor Fish were involved in the study.)

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9,west nile meningitis icd 9 code,west nile virus encephalitis icd 9,icd 9 west nile virus,icd 9 west nile encephalitisWest Nile is primarily a bird virus, but people occasionally get infected because some bird-biting mosquitoes dine on human blood as well. Human infections can cause fevers, body aches, rashes, diarrhea, long-term fatigue, and, in some cases, inflammation of the brain and its membranes. In the United States, almost 2000 people have died from West Nile since its arrival.

Because birds play such a key role in West Nile’s epidemiology, bird health is an important topic, says Meredith Kernbach, an ecoimmunologist at the University of South Florida in Tampa. Extra light at night is known to increase birds’ levels of corticosteroids and other stress hormones, which in turn can affect the animals’ health. So Kernbach decided to see whether city life makes birds more susceptible to disease.

She and her colleagues infected about 50 house sparrows with the West Nile virus; they left a dim light on at night in half the birds’ cages, whereas the other half spent the night in complete darkness. The team watched both groups for disease symptoms and monitored their body weight and blood levels of virus and stress hormones.

In both groups, most birds got sick and became infectious within 2 days, and almost half died. Those exposed to light didn’t get sicker, or stay sick longer. But they did remain infectious for a longer period of time, the team reported at the meeting.

Previous research had shown that after an average of 2 days, a bird’s immune system beats back a West Nile virus infection to levels low enough that biting mosquitoes no longer get infected with the virus. That’s what happened with the “dark night” group in this study. But in the birds exposed to light, viral concentrations remained high for 2 more days, Kernbach reported. “This doubles the infectious period, which may double the number of infected mosquitoes,” she says. As a result, adds Fish, “we expect to have greater [disease] transmission in urban areas.” More transmission could translate into more cases of West Nile disease both in humans and in birds.

Kernbach and her colleagues had thought that the light would stress out the birds and that this might lower their resistance to West Nile. But the blood tests indicated that the birds were not more stressed; their stress response systems remained intact. Kernbach suspects that instead, the light may have altered levels of another hormone, melatonin, which may also have an influence on immune responses.

Light pollution occurs in the country as well, Kernbach warns, so it’s not just city dwellers who may be at increased risk of West Nile. Humans “may be influencing infectious disease dynamics to a level far greater than we thought.”

Clinton Francis, an ecologist at the California Polytechnic State University in San Luis Obispo, agrees. “The ways that we influence sensory environments”—whether it’s with sound or light”—can have all sorts of unintended consequences,” he says.

Memory loss from West Nile virus may be preventable

More than 10,000 people in the United States are living with memory loss and other persistent neurological problems that occur after West Nile virus infects the brain.

Now, a new study in mice suggests that such ongoing neurological deficits may be due to unresolved inflammation that hinders the brain’s ability to repair damaged neurons and grow new ones. When the inflammation was reduced by treatment with an arthritis drug, the animals’ ability to learn and remember remained sharp after West Nile disease.

“These memory disturbances make it hard for people to hold down a job, to drive, to take care of all the duties of everyday life,” said senior author Robyn Klein, MD, PhD, a professor of medicine at Washington University School of Medicine in St. Louis. “We found that targeting the inflammation with the arthritis drug could prevent some of these problems with memory.”

The findings are available online in Nature Immunology.

Spread by the bite of a mosquito, West Nile virus can cause fever and sometimes life-threatening brain infections known as West Nile encephalitis. About half the people who survive the encephalitis are left with permanent neurological problems such as disabling fatigue, weakness, difficulty walking and memory loss. These problems not only persist but often worsen with time.

Klein and colleagues previously had shown that during West Nile encephalitis, the patient’s own immune system destroys parts of neurons, leading to memory problems.

“We started wondering why the damage isn’t repaired after the virus is cleared from the brain,” said Klein, vice provost and associate dean for graduate education for the Division of Biology & Biomedical Sciences. “We know that neurons are produced in the part of the brain involved in learning and memory, so why weren’t new neurons being made after West Nile infection?”

To find out, Klein; co-first authors Michael Vasek, PhD, a postdoc researcher, and graduate research assistant Charise Garber; and colleagues injected mice with West Nile virus or saltwater. During the acute infection, the mice received several doses of a chemical compound that tags neural cells as they are formed. Forty-five days after infection, the researchers isolated the tagged cells from the mice’s brains and assessed how many and what kinds of cells had been formed during the first week of infection.

Mice ill with West Nile disease produced fewer neurons and more astrocytes – a star-shaped neural cell – than uninfected mice. Astrocytes normally provide nutrition for neurons, but the ones formed during West Nile infection behaved like immune cells, churning out an inflammatory protein known as IL-1.

IL-1 is an indispensable part of the body’s immune system. It is produced by immune cells that swarm into the brain to fight invading viruses. Once the battle is won, the immune cells depart and IL-1 levels in the brain fall.

But in mice recovering from West Nile infection, astrocytes continue to produce IL-1 even after the virus is gone. Since IL-1 guides precursor cells down the path toward becoming astrocytes and away from developing into neurons, a vicious cycle emerges: Astrocytes produce IL-1, which leads to more astrocytes while also preventing new neurons from arising.

Hampered by an inability to grow new neurons, the brain fails to repair the neurological damage sustained during infection, the researchers said.

“It’s almost like the brain gets caught in a loop that keeps IL-1 levels high and prevents it from repairing itself,” said Klein, who is also a professor of neuroscience and of pathology and immunology.

To see whether the cycle could be broken, Klein and colleagues infected mice with either West Nile virus or saltwater as a mock infection. Ten days later, they treated both groups of mice with a placebo or with anakinra, an FDA-approved arthritis drug that interferes with IL-1.

After giving the mice a month to recover, they tested the animals’ ability to learn and remember by placing them inside a maze. Mice that had been infected with West Nile virus and treated with a placebo took longer to learn the maze than mock-infected mice. Mice that were infected and treated with the IL-1 blocker learned just as quickly as mock-infected mice, indicating that blocking IL-1 protected the mice from memory problems.

“When we treated the mice during the acute phase with a drug that blocks IL-1 signaling, we prevented the memory disturbance,” Klein said. “The cycle gets reversed back: They stop making astrocytes, they start making new neurons, and they repair the damaged connections between neurons.”

But, Klein cautions, IL-1 itself may not be a good drug target for people because of the important role it plays in fighting viruses. Suppressing IL-1 while the virus is still in the brain could exacerbate encephalitis, already a potentially lethal condition.

“This is a proof of concept that a drug can prevent cognitive impairments caused by viral encephalitis,” Klein said. “This study sheds light on not just post-viral memory disturbances but other types of memory disorders as well. It may turn out that IL-1 is not a feasible target during viral infections, but these findings could lead to new therapeutic targets that are less problematic for clearing virus or to therapies for neurologic diseases of memory impairment that are not caused by viruses.”

The ongoing neurological deficits caused by West Nile virus infecting the brain may be due to unresolved inflammation that hinders the brain’s ability to repair damaged neurons and grow new ones, a new study with mice suggests.

When researchers used an arthritis drug to reduce the inflammation, the animals’ ability to learn and remember remained sharp.

“…targeting the inflammation with the arthritis drug could prevent some of these problems with memory.”

More than 10,000 people in the United States are living with memory loss and other persistent neurological problems that occur after West Nile infection.

“These memory disturbances make it hard for people to hold down a job, to drive, to take care of all the duties of everyday life,” says senior author Robyn Klein, a professor of medicine at Washington University School of Medicine in St. Louis.

“We found that targeting the inflammation with the arthritis drug could prevent some of these problems with memory,” Klein says.
West Nile’s impact

Spread by the bite of a mosquito, West Nile virus can cause fever and sometimes life-threatening brain infections known as West Nile encephalitis.

About half the people who survive the encephalitis are left with permanent neurological problems such as disabling fatigue, weakness, difficulty walking, and memory loss. Further, problems not only persist but often worsen with time.

Klein and colleagues had previously shown that during West Nile encephalitis, the patient’s own immune system destroys parts of neurons, leading to memory problems.

“We started wondering why the damage isn’t repaired after the virus is cleared from the brain,” says Klein. “We know that neurons are produced in the part of the brain involved in learning and memory, so why weren’t new neurons being made after West Nile infection?”

To find out, the researchers injected mice with West Nile virus or saltwater. During the acute infection, mice received several doses of a chemical compound that tags neural cells as they are formed.

Forty-five days after infection, researchers isolated the tagged cells from the mice’s brains and assessed how many and what kinds of cells had been formed during the first week of infection.

Mice with West Nile disease produced fewer neurons and more astrocytes—a star-shaped neural cell—than uninfected mice. Astrocytes normally provide nutrition for neurons, but the ones formed during West Nile infection behaved like immune cells, churning out an inflammatory protein known as IL-1.

“It’s almost like the brain gets caught in a loop that keeps IL-1 levels high and prevents it from repairing itself.”

IL-1 is an indispensable part of the body’s immune system. It is produced by immune cells that swarm into the brain to fight invading viruses. Once the battle is won, the immune cells depart and IL-1 levels in the brain fall.

But in mice recovering from West Nile infection, astrocytes continue to produce IL-1 even after the virus is gone. Since IL-1 guides precursor cells down the path toward becoming astrocytes and away from developing into neurons, a vicious cycle emerges: Astrocytes produce IL-1, which leads to more astrocytes while also preventing new neurons from arising.

Hampered by an inability to grow new neurons, the brain fails to repair the neurological damage sustained during infection, the researchers say.

“It’s almost like the brain gets caught in a loop that keeps IL-1 levels high and prevents it from repairing itself,” says Klein, who is also a professor of neuroscience and of pathology and immunology.
Breaking the cycle

To see whether they could break the cycle, Klein and colleagues infected mice with either West Nile virus or saltwater as a mock infection. Ten days later, they treated both groups of mice with a placebo or with anakinra, an FDA-approved arthritis drug that interferes with IL-1.
Insulin resistance may boost risk of memory loss

After giving the mice a month to recover, they tested the animals’ ability to learn and remember by placing them inside a maze.

Mice that had been infected with West Nile virus and treated with a placebo took longer to learn the maze than mock-infected mice. Mice that were infected and treated with the IL-1 blocker learned just as quickly as mock-infected mice, indicating that blocking IL-1 protected the mice from memory problems.

“When we treated the mice during the acute phase with a drug that blocks IL-1 signaling, we prevented the memory disturbance,” Klein says. “The cycle gets reversed back: They stop making astrocytes, they start making new neurons, and they repair the damaged connections between neurons.”

But, Klein cautions, IL-1 itself may not be a good drug target for people because of the important role it plays in fighting viruses. Suppressing IL-1 while the virus is still in the brain could exacerbate encephalitis, already a potentially lethal condition.

“This is a proof of concept that a drug can prevent cognitive impairments caused by viral encephalitis,” Klein says.

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9,west nile meningitis icd 9 code,west nile virus encephalitis icd 9,icd 9 west nile virus,icd nile encephalitis“This study sheds light on not just post-viral memory disturbances but other types of memory disorders as well. It may turn out that IL-1 is not a feasible target during viral infections,” Klein explains, “but these findings could lead to new therapeutic targets that are less problematic for clearing virus or to therapies for neurologic diseases of memory impairment that are not caused by viruses.”

Why you should care about rare tropical diseases

They’re rare, they’re tropical, and they affect mostly the poor—so why should Americans be concerned about neglected tropical diseases?

For chemistry professor Mike Pollastri, a man who has dedicated his life to finding cures for these diseases, the answer is simple: We have a moral imperative to improve the lives of all of humanity.

But if Pollastri’s altruistic answer doesn’t convince you, he has another.

“Some of these diseases are going to become our problem soon,” he says. “It’s just a matter of time. With increased travel and continued climate change, they’re going to move north from the tropics. Dengue fever has already reached Miami and so has the West Nile virus.”

Chagas disease, a major cause of congestive heart failure, currently affects about 300,000 people in the U.S. It isn’t spreading at the moment because the Triatoma protracta, which transmits the parasite, is still confined to tropical regions. But this will change.

“It’s only a matter of time before the insects moving north meet the reservoir of people who have Chagas in the U.S.,” says Pollastri.

When they do meet, it will take years to develop the drugs needed to combat the disease.

Pollastri says the Ebola virus offers an instructive preview of what could happen if we fail to start work now.

“When we had the Ebola outbreak in the U.S. people asked, ‘Why don’t we have a vaccine for this?’ The answer is that we ignored this disease for 15 years. In the pharmaceutical industry, people work where the money is. You can’t fund your lab on altruism.”

But in universities like Northeastern, you can.
Major progress

Three years ago, Pollastri launched a $25,000 crowdfunding campaign. His initial goal was to create a broad data-sharing network among tropical disease researchers throughout the world, so the few labs that are doing this kind of work could build off each other.

The impact of that rather modest sum has been dramatic. Five collaborating labs in the U.S. and Europe have produced 29 published papers and five new chemical classes that are now in animal testing. In addition, this seed money has produced $9.2 million in federal funding—a 370-fold return on the donor investment.

That seed money was essential, says Pollastri, because of the chicken-and-egg nature of government research funding: You can’t get funding without proof that your research is promising, and you can’t prove your research is promising without money to conduct that research.

So Pollastri used $10,000 of the donor money to conduct preliminary research that produced the data needed to convince agencies like the National Institutes of Health to fund his projects.

He also convinced a few pharmaceutical giants to contribute research for free. For example, GlaxoSmithKline funded three projects in its Madrid labs, and AstraZeneca performed a series of experiments that would have cost Pollastri’s group about $300,000 a year.

The results have been impressive. Pollastri’s group has synthesized more than a thousand new compounds that have led to work on five new drugs currently in the preclinical stage of development.

Pollastri considers himself a man on a mission—one who has been fortunate enough to have found a home that supports that mission.

“I was driven by the moral requirement,” he says. Pollastri left a lucrative job in the pharmaceutical industry when he realized that private drug companies had no financial incentive to invest in research that affected the poorest parts of the world.

“I came to Northeastern because universities exist to generate knowledge to better humankind,” he says. “The drugs we develop will be used to treat the poorest of the poor—the bottom billion.”

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9,west nile meningitis icd 9 code,west nile virus encephalitis icd 9,icd 9 west nile virus,icd 9 west nile encephalitisChagas disease, a major cause of congestive heart failure, currently affects about 300,000 people in the U.S. It isn’t spreading at the moment because the Triatoma protracta, which transmits the parasite, is still confined to tropical regions. But this will change.

“It’s only a matter of time before the insects moving north meet the reservoir of people who have Chagas in the U.S.,” says Pollastri.

When they do meet, it will take years to develop the drugs needed to combat the disease.

Pollastri says the Ebola virus offers an instructive preview of what could happen if we fail to start work now.

“When we had the Ebola outbreak in the U.S. people asked, ‘Why don’t we have a vaccine for this?’ The answer is that we ignored this disease for 15 years. In the pharmaceutical industry, people work where the money is. You can’t fund your lab on altruism.”

But in universities like Northeastern, you can.
Major progress

Three years ago, Pollastri launched a $25,000 crowdfunding campaign. His initial goal was to create a broad data-sharing network among tropical disease researchers throughout the world, so the few labs that are doing this kind of work could build off each other.

The impact of that rather modest sum has been dramatic. Five collaborating labs in the U.S. and Europe have produced 29 published papers and five new chemical classes that are now in animal testing. In addition, this seed money has produced $9.2 million in federal funding—a 370-fold return on the donor investment.

That seed money was essential, says Pollastri, because of the chicken-and-egg nature of government research funding: You can’t get funding without proof that your research is promising, and you can’t prove your research is promising without money to conduct that research.

So Pollastri used $10,000 of the donor money to conduct preliminary research that produced the data needed to convince agencies like the National Institutes of Health to fund his projects.

He also convinced a few pharmaceutical giants to contribute research for free. For example, GlaxoSmithKline funded three projects in its Madrid labs, and AstraZeneca performed a series of experiments that would have cost Pollastri’s group about $300,000 a year.

The results have been impressive. Pollastri’s group has synthesized more than a thousand new compounds that have led to work on five new drugs currently in the preclinical stage of development.

Pollastri considers himself a man on a mission—one who has been fortunate enough to have found a home that supports that mission.

“I was driven by the moral requirement,” he says. Pollastri left a lucrative job in the pharmaceutical industry when he realized that private drug companies had no financial incentive to invest in research that affected the poorest parts of the world.

“I came to Northeastern because universities exist to generate knowledge to better humankind,” he says. “The drugs we develop will be used to treat the poorest of the poor—the bottom billion.”

Since West Nile virus made its debut in New York City over a decade ago, outbreaks of mosquito-borne diseases, especially West Nile virus, have become increasingly commonplace. As temperatures reach new highs as a result of global climate change, mosquitoes that once called the tropics home find the United States just as habitable. A recent report from the Centers for Disease Control and Prevention found that Aedes aegypti—which is capable of transmitting the Zika, dengue, and chikungunya viruses—could find suitable breeding habitats in 75 percent of the contiguous United States.

Efforts to deal with the unwelcome vectors, however, are already running into trouble. In a poorly executed plan to suppress mosquitoes in South Carolina last year, officials in Dorchester County misted an insecticide called Naled—deadly to both honeybees and mosquitoes—through the air over Summerville without warning local beekeepers. The subsequent deaths of millions of bees served as a wake-up call that weapons beyond pesticides are needed to fight the spread of mosquito-borne diseases.

According to Jose Luis Ramirez, an entomologist with the USDA’s Agricultural Research Service in Peoria, Illinois, many pesticides can not only cause adverse reactions in animals and humans, but they also become ineffective over time. “It’s an arms race,” he says. “At the same time we’re trying to kill them, mosquitoes are evolving to evade death and developing resistance to pesticides.”

In order to prevent mosquitoes from developing resistance, Ramirez and his team of scientists are developing bio-pesticides made from fungi that kill mosquitoes but do not impact other insects or humans. The fungi are entomopathogenic—that is, they act like parasites—and are particularly effective at killing mosquitoes.

The magic of the fungi is in their ability to morph. When fungal spores land on a mosquito, they awaken from a resting phase and burrow into the insect. Once inside, the fungus changes into a blastopore, a simpler structure that lacks molecules that could alert the insect’s immune system. This allows them to multiply in great numbers, eventually killing the mosquito. Soon after the insect is dead, the fungal blastopores continue to grow and re-emerge from the corpse as threadlike filaments called hyphae.

“We’re trying to pinpoint the best fungal candidates and the compounds found in the fungi that allow the fungi to kill or evade the mosquito’s immune system,” Ramirez says. If his team can pinpoint such compounds, they could be extracted from the spores and made into targeted bio-pesticides designed to kill mosquitoes without harming anything else.

ARS entomologist Ephantus Juma Muturi is working on another possible approach—identifying a chemical in blackberry leaves that both attracts and kills mosquito larvae. Muturi says that mosquitoes of the genus Culex, which also transmit West Nile, like to lay their eggs in water laden with bacteria that the larvae can consume. But when blackberry leaves are put into water, mosquitoes will lay their eggs there even when the environment isn’t good for offspring survival. Field tests are still in the future, he says. “First, we need to isolate and identify the chemical(s) that attract egg-laying mosquitoes to blackberry infusions and those that are toxic to mosquito larvae. We’re not sure whether it’s a toxic chemical that blackberry leaves produce that kills the larvae or whether a blackberry infusion lacks enough bacteria for the larvae to survive.”

Scientists from the biotech company Oxitec are working on a more controversial approach. They have genetically modified mosquitoes to produce a protein that kills them in the absence of the antibiotic tetracycline, which they are given in the lab to survive. Once released, however, the mosquitoes die, but not before passing this trait on to their offspring. Field trials in other countries such as Brazil have reported an 86-to-90 percent decrease in the number of mosquitoes after the introduction of this modified variety. U.S. field tests were to have taken place in Key Haven, Florida, but residents fought hard to oppose it, concerned about unforeseen repercussions from the genetically modified insects.

The issue is complex, and scientists need to carefully weigh the risk of disease with that of GMO mosquitoes, according to Stephen Mahoney, conservation chair of the Sierra Club Miami Chapter. “The Sierra Club recognizes that action is needed now using the best available techniques that are reasonably safe for the environment, which, at the moment, appear to include the use of genetically modified sterile mosquitoes in Zika-infected areas of Florida,” Mahoney said in a statement.

Last year, the EPA also approved the use of mosquitoes that are not genetically modified but are infected with the Wolbachia pipientis bacterium in the lab. The males are then separated from the females and released into the wild. The males then mate with wild female Aedes albopictus mosquitoes, which can transmit a number of tropical diseases. The resulting fertilized eggs fail to hatch.

Whatever the method, the race is on to blunt this potentially deadly aspect of climate change. “We need as many tools as possible to be successful at stopping the spread of mosquito-borne disease,” Ramirez says.