Protecting biodiversity is essential to our health and longevity on this planet. But can we quantify that value? Especially the economic value?

Late last year, researchers from the US and France attempted to put dollar amounts on the importance of biodiversity by correlating it to the prevalence of tropical disease in developing countries. According to their introduction in PLoS Biology:

Along with 93% of the global burden of vector-borne and parasitic diseases (VBPDs), the tropics host 41 of the 48 “least developed countries” and only two of 34 “advanced economies.”

They contend that economic growth falters when people get sick. (Seems reasonable.) And the spread of disease among humans, many scientists argue, can increase or decrease depending on factors in the natural environment, including biodiversity.

The more diverse an ecosystem, the greater the chance that a pathogen is diluted among numerous and potentially less-than-ideal host species and, therefore, the less abundant the disease. In 2002, researchers found this to be true with Lyme disease. NPR sums it up well:

If you have a rich community of tick hosts, like squirrels, mice and other small mammals, the disease is diluted among them. But if the habitat is degraded, and ticks carrying Lyme have only white-footed mice as hosts, the disease risk to humans can rise dramatically.

The Academy’s microbiologist, Shannon Bennett, weighed in on biodiversity’s impact on human diseases. In a recent email, she wrote:

I am sure biodiversity influences the transmission of infectious diseases one way or another.  Over 75% of new, emerging or re-emerging human diseases are caused by pathogens from animals, according to the World Health Organization. That means that the ecological communities we live in, and how pathogens cycle through the different players, are key to human health. Biodiversity is one way that we measure the complexity of these communities. In what way biodiversity is important, or how these communities specifically affect infectious diseases and risk, depends on the pathogen ecology and life history, and host species relationships.

Stanford researchers brought up this same point last month—“depends on the particulars,” as Bennett put it—in a study in Ecology Letters. A summary from the Stanford Report states:

The researchers found that the links between biodiversity and disease prevalence are variable and dependent on the disease system, local ecology and probably human social context.

The role of individual host species and their interactions with other hosts, vectors and pathogens are more influential in determining local disease risk, the analysis found.

That dovetails exactly with the research Bennett and Academy entomologist Durrell Kapan are conducting. They’re currently studying mosquito vector communities and the relationships between their biodiversity, the diversity of their microbes, and the presence of pathogens.

As for putting a price tag on biodiversity, Bennett encourages the PLoS study’s authors:

I find the authors’ argument intriguing and certainly a significant angle to consider in support of the health value of biodiversity, and one that is unique—no one has teased out the financial correlations between biodiversity and human societies. That it includes human health and infectious diseases is the angle I find particularly intriguing and worth following up on with empirical studies.

And on these studies of human disease and biodiversity in general? Bennett is excited about the possibilities of further research, including her own:

Increasingly we are recognizing and appreciating that humans are members of complex communities of other species, and that the make-up of these communities, whether they live inside of us or outside, can be very important to human health, as well as the health of all life. Human health and the health of life on this planet are coupled. We need to understand those coupling mechanisms better to ensure sustainability of that life, and the best way to understand those coupling mechanisms is with a multi-disciplinary approach, bringing together human health researchers with ecologists and evolutionary biologists, to name a few!

Some organizations have sprung up to do just that. Bennett points to two examples: the One Health Initiative and the EcoHealth Association. Whatever dollar value we assign to biodiversity and other ecosystem services, let’s wish these organizations luck in improving human health and well-being.

Image: CDC

That was the subject of the first event of Brilliant!Science, a week long biosciences festival co-hosted by the Academy and the Gladstone Institutes. “Infectious Cures: Hijacking Viruses To Overcome Disease” was an “intimate conversation” with Dr. Leor Weinberger of the Gladstone Institutes held Thursday at the Commonwealth Club.

Moderated by the Academy’s microbiologist, Shannon Bennett, Weinberger started the conversation by giving us the background of the bad guy virus—in this case, HIV.

First he gave us the numbers—HIV has killed 30 million people, 34 million are currently living with AIDS (the disease caused by HIV), 3.4 million of those are children and 16.6 million children have been orphaned due to the disease.

The antiviral drugs used to treat those infected with HIV are good, Weinberger stressed, but don’t reach everyone who needs them. Plus, the extreme regimen of taking the drugs makes it difficult for many who do have access. Weinberger also introduced the idea of the “superspreaders”—these are small groups of people that engage in high-risk behaviors and are more likely to transmit the virus. In the case of HIV in Africa, many of these superspreaders are sex workers and truck drivers.

With antivirals or a potential vaccine—even if these treatments were able to reach a large percentage of a population—superspreaders would greatly diminish the efficacy of these treatments. Think of superspreaders as the bad guy’s evil sidekick.

After Weinberger gave us an idea of how wicked a bad guy HIV truly is, he then explained how the virus commits its crimes inside our bodies.

HIV is perfectly suited to attack our white blood cells. Its external keys target white blood cells, hijacking them and turning the white blood cells into HIV-making factories.

Weinberger, like many researchers, wants to stop HIV in its tracks. In his lab, his team is genetically engineering HIV—keeping its outer structure virtually the same. He copies the genetic material within the virus and “erases” much of the code, making a smaller version that can replicate faster. He calls this smaller version TIPS, for Therapeutic Interfering Particles.

Because TIPS is similar to HIV, it can enter the white blood cell just as easily. But since TIPS is smaller and faster it can outcompete HIV, turning that white blood cell into a TIPS-making factory instead of an evil HIV factory.

Even better, TIPS is transmitted just like HIV, meaning those evil sidekicks—the superspreaders—actually begin transmitting TIPS, instead of HIV, to the very people that need access to something that stops HIV.

Even better still, TIPS is able to evolve as HIV evolves. One challenge of viruses is that they evolve quickly, becoming resistant to vaccines (think of our yearly flu shots). But TIPS is able to keep up with HIV.

This all sounds too good to be true, right? Weinberger and team have TIPS working well in petri dishes in their lab. But as with many new solutions, it needs more testing, more funding. From bench to market is at least five years in any situation, Weinberger said. So keep your fingers-crossed.

And if it works on bad guys like HIV, why not other viruses? Stay-tuned.

Uncovering the human microbiome represents a new frontier in science. Thanks to new technology, we’re beginning to understand what these microscopic organisms do, how they do it, and why they exist inside of us.

Last Friday, the awesome Bay Area Science Festival presented “Gut Check: The Hidden World of Microbes.” The panel included two UC San Francisco researchers—our friend, Joe DeRisi, and Michael Fischbach—and science writer extraordinaire, Carl Zimmer. If you follow Zimmer’s Discover blog, The Loom, you know that he loves anything tiny and gross—parasites, bacteria, fungus, the like—so we knew it would be a juicy discussion.

DeRisi developed the ViroChip—a technology that allows scientists to scan samples for several different viruses—over 10,000 things at a time—and bacteria, fungi, and parasites. When Fischbach looks at us, he sees the 100 trillion microorganisms living inside us. These microorganisms make up 10% of our genes, so he uses genome-sequencing technology to study all of them at once.

The following are some of the topics discussed by the panel:

Antibiotics and other Good Bacteria

Fischbach got into human microbiome research looking for drugs. Your gut (and skin and oral) bacteria are natural antibiotics and statins (cholesterol-lowering drugs). They could also possibly control obesity and diabetes. Microbes support your immune system and metabolism, and many of the bacteria in your gut create neurotransmitters, fueling research about how our gut bacteria affect our brains.

Fischbach pointed out how current antibiotics take a “carpet bomb” approach—killing all bacteria in our bodies, good and bad. With more research, he believes that specific good bacteria could target specific bad bacteria—taking a more “scalpel” approach to antibiotics.

Tending the Garden

Among the microorganisms in our body, there are those that help us digest food and create energy and those that just feed themselves. Insoluble fiber may keep us healthy, but we’re not actually absorbing any of it—the microbes keep it all to themselves! As Zimmer said, “You’re not eating it for yourself, but rather tending the garden.” The garden of gut flora.

The Virome

Did you know we have seven trillion viruses in our body when we’re healthy? Some of these viruses attack us and some attack other viruses or bacteria. And, are you ready for this? DeRisi can’t “think of any example of a beneficial virus.” So what are they all doing there? DeRisi has no clue, and every time he sequences he finds new viruses, wondering what role they might play.  Bringing up the question, is there a virome in addition to the biome of the human body?

With trillions of viruses and new ones evolving, does DeRisi lay awake at night in a panic? No. (Phew!)

So whether riding BART or keeping your child in a germ-free environment, the message of the panel was don’t worry about these tiny organisms (at least, for now). More research is needed to find out exactly what kind of tug of war is going on inside of our bodies.

The PLoS study does read a bit like a movie. A New World titi monkey fell ill with a cough in May 2009 at the California National Primate Research Center. Its condition worsened and the monkey was put down five days later. ScienceNOW reports that

Four weeks later, another titi monkey came down with the same symptoms. Then another. And another. Within 2 months, 23 of the 65-strong population had become sick, and 19 eventually died.

The center contacted UC colleague and virus researcher Charles Chiu, MD, PhD to help identify the pathogen and prevent its spread to other animals. (We interviewed Chiu, director of the viral diagnostics center at UC San Francisco, two years ago when the swine flu outbreak began.)

Examining tissues from the affected monkeys, Chiu and his team found that the virus clearly belonged to the adenovirus family, yet was unlike any adenovirus ever reported to infect humans or monkeys, including from large-scale studies by public health agencies. The new virus, named titi monkey adenovirus (TMAdV), is so unusual, in fact, that it shares only 56 percent of its DNA to its closest viral relative.

Adenoviruses naturally infect many animals, including humans, monkeys and rodents, and are known to cause a wide range of clinical illnesses in humans, from cold-like symptoms to diarrhea and pneumonia. Unlike influenza or coronaviruses, adenoviruses had not been known to spread from one species to another.

But Chiu noticed something in the lab about the new adenovirus, Nature News writes:

“It was unusual to see it grow well in human cell lines, but not monkey” cells, he says. This suggested that the virus could infect humans as well as titi monkeys. “After we interviewed all of the staff, the only person who said they had been sick was one researcher — the one who had had the closest daily contact with the colony,” says Chiu.

That researcher experienced flu-like upper-respiratory-tract symptoms for four weeks. More crucially, a family member who had never visited the primate center also became ill — demonstrating that TMAdV can spread between humans.

Because the researcher’s illness was minor, it was not reported for several months and the virus could no longer be detected directly. So Chiu worked with the California Department of Public Health to conduct antibody testing on the monkeys, the researcher and the family member. Both the monkeys and two humans tested positive for antibodies to the TMAdV virus. No other humans at the center were infected.

“Now adenoviruses can be added to the list of pathogens that have the ability to cross species,” says Chiu. “It’s been hinted at before, but this study is the first to document these viruses crossing the species barrier in real time.”

Chiu says the lack of previous records of this virus in humans indicates that it is also unlikely to have started with the researcher. In testing other monkeys at the primate center, the team found one healthy rhesus (Old World) monkey with antibodies to TMAdV, which Chiu says could indicate that the virus originated in Old World monkeys, then spread to the New World colony that lacked antibodies against it.

The viral center is conducting further studies in both humans and monkeys in Brazil and Africa to determine whether the virus is common in wild populations of either Old World or New World monkeys, and whether it has crossed species in those settings to humans who live nearby.

It’s very important to note that the humans infected with the virus recovered fully without medical treatment. Contagion this story is not.

In fact, TMAdV may someday be beneficial to humans. From ScienceNOW:

TMAdV’s rarity in humans could make it a potentially powerful tool as a viral vehicle for delivering gene therapy, Chiu adds. Researchers already use custom adenoviruses stitched with beneficial snippets of DNA to treat diseases; for instance, the cancer-fighting virus Gendicine introduces genes that code for the tumor-suppressing protein p53. The problem is that many people have antibodies to these viruses and their immune responses can make such treatments dangerous or even deadly. That problem likely wouldn’t occur with an engineered version of TMAdV because nobody has antibodies to it. Chiu has a patent pending for using TMAdV as a gene-therapy vehicle.

Photograph courtesy of Kathy West

Domesticated honey bees have been disappearing for the last several years due to Colony Collapse Disorder, or CCD. This past fall, researchers found that CCD is potentially caused by a deadly one-two punch from a virus-fungus combination.

In a recent study, published in PLoS One, researchers found that bee pollen pellets can contain the contributing viruses.

The scientists found that even if a bee were not infected with a virus, their pollen pellets could contain viruses, indicating that pollen itself may harbor the deadly agents. When infected pollen is stored in a hive, researchers found the queen could become infected and lay infected eggs, creating an entirely new generation carrying the virus.

Sadly, virus-laden pollen affects more than just honey bees. The researchers found eleven wild species carrying infected pollen pellets, as well. The authors suggest that the pollen is potentially responsible for transmitting the disease from the domestic to wild populations. Perhaps this could be the reason that wild pollinators, such as bumble bees and wasps, have also been in recent decline.

Both natural ecosystems and agriculture depend on pollinators—natives and honey bees. Their health (or lack there of) is essential to all of us. The more we know, the better prepared we are to protect them.

Image by Eli Shany/Wikimedia

A group of scientists who study biodiversity and infectious diseases, reviewed several dozen research papers published in the last five years and found a link between biodiversity loss and an increase in transmittable disease.  Specifically, they discovered that species losses in ecosystems from forests to fields results in increased pathogens in the system.

The pattern holds true for various types of pathogens—viruses, bacteria, fungi—and for many types of hosts, whether humans, other animals, or plants. The researchers found two familiar human diseases that fit this pattern—West Nile virus and Lyme disease.

Sadly, the animals, plants, and microbes most likely to disappear as biodiversity is lost are often those that buffer infectious disease transmission. Those that remain tend to be species that magnify the transmission of infectious diseases.

In one example, three different studies found strong links between low bird diversity and increased occurrence of West Nile encephalitis in the United States. Ecosystems with low bird diversity contained bird species more susceptible to the virus; thus increasing infection rates in mosquitoes and people. In comparison, ecosystems that contained a higher diversity of birds had many species that were unfit as hosts for the virus.

The authors are hoping these results will spur action. For humans and other species to remain healthy, it will take more than a village—we need an entire planet, the scientists say, one with its diversity thriving.

Global biodiversity has declined at an unprecedented pace since the 1950s. Current extinction rates are estimated at 100 to 1,000 times higher than in past epochs, and are projected to increase at least a thousand times more in the next 50 years.

“When a clinical trial of a drug shows that it works,” says lead author Felicia Keesing of Bard College, “the trial is halted so the drug can be made available. In a similar way, the protective effect of biodiversity is clear enough that we need to implement policies to preserve it now.”

Image of West Nile virus by PhD Dre/Wikipedia