In a paper published in Infectious Disease Modelling Research Progress, a team of mathematicians from Carleton University and the University of Ottawa have created a series of mathematical models to explore the effects of a zombie outbreak and determine the best course for human survival. For the purpose of the paper, the team limited their models to the George Romero slow-moving zombies, and created separate models for zombie infections that cause the infected to resurrect immediately after contact with a zombie and for zombie infections with a 24-hour incubation period.

The paper examines three possible methods of dealing with a zombie outbreak: quarantine of the zombies, treatment of zombies so that they once again become human, and impulsive eradication of the zombies whenever possible. The models found that quarantine could work, but the end result would be either the eradication of all zombies or the eradication of all humans; if a cure for being a zombie were found, humans would coexist with zombies, but only in low numbers; but eradication, if properly coordinated, could wipe out the entire zombie population in a mere ten days.

Science has proved it: aim for the head, and kill without mercy.

When Zombies Attack!: Mathematical Modelling of an Outbreak of Zombie Infection [University of Ottawa]

Researchers at Radboud University in Nijmegen, the Netherlands, staged a small proof-of-principle experiment, aimed at determining whether exposure to parasites, via insect bites, could vaccinate humans against malaria.

Knowing that humans can develop an immunity to malaria after repeated exposures and that the drug chloroquine kills malaria parasites in the late stages of infection, the researchers divided 15 subjects into two groups. They exposed the first group, periodically, to parasite-bearing mosquitoes and treated them with chloroquine. The second group, the researchers also treated with chloroquine, but didn't expose to the mosquitoes. All the volunteers stopped taking chloroquine and were later exposed to parasite-carrying mosquitoes. No members of the group previously exposed to malaria developed the disease; each member of the comparison group did.

Although it's a far cry from delivering an actual vaccine via insect — and seems more a call for widerspread distribution of antimalarial drugs — it does present the possibility that insects could someday be used to immunize populations against disease. With respect to pandemics like malaria, such a mechanism could be a lifesaver, but it also presents a profound ethical dilemma. The subjects in this test gave their consent to be infected, persons living among vaccine-carrying critters wouldn't have the same luxury.

Mosquitoes deliver malaria 'vaccine' through bites [AP via Slashdot]

Avian influenza viruses do not spread extensively in cells at 32 degrees Celsius, the temperature inside the human nose. The researchers say this is probably because the viruses usually infect the guts of birds, which are warmer, at 40 degrees Celsius.

Professor Wendy Barclay, one of the authors of the study, added:

Bird viruses are out there all the time but they can only cause pandemics when they undergo certain changes. Our study gives vital clues about what kinds of changes would be needed in order for them to mutate and infect humans, potentially helping us to identify which viruses could lead to a pandemic.

So we're not exactly off the hook, given the rate at which viruses are known to mutate. But we also know exactly what kind of mutation they'd need: Something that would allow them to feel comfy in our noses.

via Eurekalert

Led by Hong Kong medical researcher Jospeh Wu, the team used mathematical modeling to look at how a closed city like Hong Kong might respond to the outbreak of an epidemic with drug treatments. In particular, they were interested in what happens if the city responds by treating everybody with one drug, usually Tamiflu, vs. if they treat everybody with two drugs, Tamiflu and Relenza. Because flu viruses evolve resistance to drugs so quickly, their question was how best to knock the virus out quickly without it having a chance to evolve a resistance.

What they learned was that the best possible way to stop a pandemic from spreading was for every country to have stockpiles of two different antiviral drugs to treat flu: A primary stockpile and a secondary one. The first wave of cases should be treated with the secondary drug until it runs out, then the next wave should be treated with the primary drug. This knocks out the first wave of virus, and then just as it begins to evolve resistance hits it with a new drug. Apparently in scenarios where public health officials respond like this, using what's called "sequential drug multitherapy" or SMC, the spread of the virus is reduced significantly. "Monotherapy," or the treatment with just one drug, created a lot of drug-resistant flu strains and did not significantly impair the spread of the epidemic.

According to New Scientist:

The two strategies that used more than one drug decreased the number of people who finally became infected from 68 to 58 per cent. It also reduced the chance of resistance emerging from 38 to just two per cent, which would translate into a significant number of lives saved, says Wu.

Right now, swine flu is not resistant to either Tamiflu or Relenza, so their scenario is perfect for our current epidemic. Unfortunately, most nations only have a stockpile of one drug, generally Tamiflu. Let's take a look at all four scenarios.

According to the study Wu and colleagues published today in PLoS Medicine:

[Here are scenarios for] sequential multidrug chemotherapy in a global network of 105 cities. Hong Kong (HK) is the source of infection in the network with 30 wild-type seeds on day 0. Twenty-eight cities implement large-scale antiviral intervention: Hong Kong, London, New York, Geneva, and 24 other cities (randomly chosen for each stochastic realization). Cities that implemented SMC had a drug B stockpile coverage of 1%.Four scenarios are shown.

Here's what to look for in these maps. All of them show the virus starting in Hong Kong, and the blue spreading dots are attack rates from the flu (AR). As the blue slowly changes color through the rainbow, what you're seeing is a drug-resistant virus evolving. Red dots are 100% drug-resistant attack rates (RAR). Colors between show the attacks slowly developing higher percentages of drug-resistant strains.

(A) HK and all 27 cities implemented monotherapy.

(B) HK and all 27 cities implemented sequential multidrug chemotherapy (SMC).

(C) HK, New York. Geneva and 11 other randomly chosen cities implemented SMC; London and 13 other randomly chosen cities implemented monotherapy.

(D) Same as (C) except that HK did not implement SMC.

Bottom line: Based on these mathematical models, SMC is the best way to prevent the spread of flu, especially drug-resistant flu. As long as the country that is the source of the flu uses SMC, the treatment is effective even if many other countries still use monotherapy. Monotherapy will stop the spread of flu initially but then as drug-resistant strains evolve it will again explode into epidemic proportions. And the flu that spreads will be resistant to the single drug that most countries have stockpiled.

Here is the authors' full explanation, which is slightly technical but worth checking out:

If only monotherapy was used, the importation of resistance promoted the spread of the resistant strain and downstream populations had higher attack rates and drug-resistant attack rates, e.g., New York had a higher attack rate [AR] and drug-resistant attack rate [RAR] than London because the pandemic reached New York later, with a higher proportion of introduced infections being resistant. Population size also played a role. The small population of Geneva had a smaller RAR than London even though the two were hit at approximately the same time: smaller populations were less vulnerable to the local emergence of antiviral resistance because fewer cases were treated with drug A. We note that our city population sizes are only proxy measures for entire local populations which feed into major airports.

If all 28 populations that had stockpiles of antivirals implemented sequential multidrug chemotherapy (SMC) [giving first a secondary drug, then giving out a primary drug when the first runs out] rather than monotherapy, reductions in AR and RAR in these populations were similar to those in a single source population (scenario B). Therefore, the connectedness of cities had little impact on the effectiveness of SMC if all populations that implemented large-scale antiviral interventions adopted SMC. The effectiveness of SMC was attenuated (but was still significant) if only half of these 28 selected populations
adopted SMC (Scenario C). Interestingly, in this scenario, those populations that implemented only monotherapy (e.g., London) still benefited from the implementation of SMC in the other populations because fewer resistant cases were circulating within the network.

The source population was the key to the robustness of SMC as a resistance-limiting strategy at the global scale. If the source population implemented only monotherapy, then SMC had little benefit in any downstream population.

Read the complete paper [PDF] via PLoS Medicine

Image by Cynthia Goldsmith

Or at least, the cure for obesity may not be having a healthy diet and getting exercise. It may be an anti-viral. Over at Brain Blogger, Jennifer Gibson writes about new research that shows 30 percent of obese people have also been infected with the same virus.

She writes:

There are approximately 50 members of the adenovirus family, and they cause up to 5% of respiratory tract infections each year, ranging from the common cold to severe pneumonia. Some strains can also cause eye infections. Ad-36 has not been linked to any specific disease to date.

Early research found that 30% of obese people were infected with Ad-36, while only 11% of non-obese people were infected. New research finds that Ad-36 has a direct effect on human fat stem cells. The virus infects the fatty tissue and increases replication, differentiation, and accumulation of fat cells. Ultimately, this leads to larger fat cells, and more of them. The virus also increases lipid sensitivity and decreases leptin secretion of the new fat cells. However, the weight gain was not permanent in every case, lasting only long enough for the infected person to build up resistance to the virus.

That means your weight gain could be caused by exposure to somebody else who recently gained weight - due to contracting Ad-36. While a great deal more research needs to be done, several labs are tackling the question right now. What I'm curious about is whether the increase in fat cells is permanent or not. If it is permanent, it could mean people infected with Ad-36 will need to watch their weight more carefully than most people for their whole lives, because extra fat cells means might put them at greater risk for weight gain.

Check out the rest of Gibson's fascinating article here.

HealthMap could be extra helpful in places where access to public health information is hard to come by. For instance China, whose official line for a while back in 2002 and 2003 was "SARS? I don't know what you're talking about. There' no one dying of a mysterious disease here."

And according to the Wired article, plans could be in the works to bring Healthmap down to the street level:

Back in 2006, Google.org head Larry Brilliant told Wired.com about his vision for a service that looks a lot like HealthMap.

"I envision a kid (in Africa) getting online and finding that there is an outbreak of cholera down the street. I envision someone in Cambodia finding out that there is leprosy across the street," Brilliant said.

HealthMap doesn't have quite that level of resolution just yet — outbreaks are only mapped to the state/province level...

Knowing about outbreaks as they happen is a good thing, and potentially really empowering, but HealthMappers and Larry Brilliant seem to be wandering into a privacy minefield.

A house-by-house account of who's got what disease would sure help out public health researchers, but what would it do to a community? Should I be able to find out who on my block has Hepatitis, Dengue Fever, or HIV? And to what extent is someone suffering from that disease allowed to not tell anyone about it? That's a tough question, but one that'll need answering before HealthMap goes hyper-local.

Source: PLoS Medicine via Wired

Wild animals are the most likely bearers of the next plague — 60% of epidemics are from "zoonoses," diseases that jump from animals to humans living in close proximity. The more that human populations spread into previously-uninhabited areas, the more likely we are to rub up against some viruses that the local fauna are resistant to, while we are not.

According to the Earth Institute at Columbia University:

In the new study, researchers from four institutions analyzed 335 emerging diseases from 1940 to 2004, then converted the results into maps correlated with human population density, population changes, latitude, rainfall and wildlife biodiversity. They showed that disease emergences have roughly quadrupled over the past 50 years. Some 60% of the diseases traveled from animals to humans (such diseases are called zoonoses) and the majority of those came from wild creatures. With data corrected for lesser surveillance done in poorer countries, "hot spots" jump out in areas spanning sub-Saharan Africa, India and China; smaller spots appear in Europe, and North and South America.

"We are crowding wildlife into ever-smaller areas, and human population is increasing," said coauthor Marc Levy, a global-change expert at the Center for International Earth Science Information Network (CIESIN), an affiliate of Columbia University's Earth Institute. "The meeting of these two things is a recipe for something crossing over." The main sources are mammals. Some pathogens may be picked up by hunting or accidental contact; others, such as Malaysia's Nipah virus, go from wildlife to livestock, then to people. Humans have evolved no resistance to zoonoses, so the diseases can be extraordinarily lethal.

Scientists Make First Map of Emerging Disease Hotspots [Earth Institute]

The researchers also assumed that we'd be using the same disease-fighting methods we used in the SARS outbreak. This map doesn't mean that huge chunks of the world will soon be wiped out by a pandemic. It's actually, according to the researchers, a warning. They want national health organizations to be aware which areas of the world need better systems for handling viral outbreaks. That way, flu doesn't reach epidemic proportions and shoot all over the world. Of course, if governments handle the next epidemic it the way they did in 28 Weeks Later and Resident Evil: Extinction, this "help" might come in the form of nukes.

Predicting Outbreaks [BMC Medicine]