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How do you find good stocks for great short-term trading opportunities? Do you hunt for value, growth or price momentum?

I look for all three, but with a twist that gives me an added 'edge'. I want to buy solid growth stocks after the market has 'temporarily' and irrationally thrown them out with the bath water. If I am right that the selling insanity is temporary, I am also getting value that is about to resume a momentum price trajectory.

The exaggerated reports of a great stock's death are often terrific 'one shot, one kill' trading opportunities. Here are my essential screening gauntlet for 'killer' swing trades with an edge:

1) Industry Dominator, Moat Optional
2) Earnings Machine with Institutional Sponsorship
3) Juicy Price Collapse that makes me say: 'This stock is on sale!'

The first criterion is pretty straight forward. I want to be looking at a well-run business with an established niche, if not industry domination. Obviously, a competitive moat is ideal. It's hard to get excited about price momentum if the company doesn't have other kinds of momentum going for it.

The second criterion is all about growth. And when steady earnings momentum is confirmed by institutional investors accumulating and holding shares over long periods, you know you are in good company for higher prices in early to mid-stage growth.

The third criterion is all about relative value. Sometimes good stocks get trashed for some of the following unwarranted reasons:

Missed EPS or revenue target
Warned about a soft patch in business or economy
Made an acquisition the Street didn't like
New competitor is knocking on their niche
Concerns about the economy that cause a correction and sink all stocks with the market tide
Management change or a legal/regulatory/environmental battle cry from some assailant

The assault could be any one of a dozen things that drive the price of a good company down 20% or more. In all cases, if you can confirm that criterion #1 and #2 are still intact, you may have just found a juicy bargain.

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Only Hours to Go for Hidden Bulls

Saturday, February 18 is your last chance to target quick bull market swings that few are seeing. Time's running out to take advantage of the irrational behavior of other investors. The door must close to Zacks' new short-term investor group because if too many members were accepted, it would be harder for everyone to profit fully.

Don't miss four powerful investment opportunities that are emerging...

See them now >>

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3 Stocks That Screamed 'Buy Me!'

1) CME Group (NasdaqGS:CME - News)

The most dominant derivatives exchange in the world saw a slow drift lower in its shares for all of 2011. Falling from above $325 to support at $240 in the fall, the stock met strong resistance at its 200-day moving average in November at $280. And then things really got scary when one of its largest clearing members filed for bankruptcy on Halloween.

The implosion of MF Global sent institutional investors running for the hills, and sent the stock to lows not seen since April of 2009. When I saw the stock trading at $225 in early January, I decided to take a closer look at the earnings picture. Estimates had definitely come down after the Corzine debacle, but the core business was intact, still dominant and still growing.

Plus, the company was poised for potentially outstanding growth as trillions in the OTC interest rate derivatives business was destined to move to the exchange 'mark-to-market' model. Sensing a fantastic opportunity, I bought March 260 calls for under $2.50. After CME's strong earnings report in February, the stock exploded from $240 to $290, handing my Tactical Trader subscribers at least a triple (200% gain) in those options, while some held on to see ten times their money!

2) Coinstar (NasdaqGS:CSTR - News)

Remember when Netflix (:NFLX) shot themselves in the foot by making their subscriber service more complicated and costly? Customers said 'who needs this?' And investors punished the stock because they saw the company headed in all the wrong directions.

Well a tiny little competitor for movie entertainment appeared to be headed down the same path after its October earnings report. Coinstar, owner of the Redbox DVD rental kiosks, raised their price by a whole 20 cents! The stock fell nearly 20% as investors thought it was another NFLX debacle.

I said this was crazy! This price bump should only make CSTR earnings estimates go up. And everybody I knew who rented movies the Redbox way would gladly pay another 20 cents. Heck, most people I know would pay another buck and not think twice. Why? Because it's fun to go pick a flick that way - even if you are 'streaming' video at home, which most consumers are not.

I was so convinced about CSTR being a bargain, I told everyone to 'buy it with both hands' under $45. The company was not only executing its core strategy, it was brewing the content distribution deal with Verizon for potential streaming opportunities. As you can see from the chart, CSTR caught a lot of bears by surprise on their last earnings report in early February. I made 24% on my shares.

3) Vertex Pharmaceuticals (NasdaqGS:VRTX - News)

Vertex is not exactly a 'dominator' in biotech when compared to Amgen or Celgene. But it did create something incredible last year that surprised lots of pharma experts and investors. They produced the first incredibly successful drug treatment for the hepatitis-C virus (:HCV). Their drug Incivek topped sales of over $400 million in the third quarter of 2011, while pharma giant Merck could only do about $80 million in sales with their HCV treatment.

Based on this success, the earnings estimates for Vertex soared to above $4 per share for 2012 with projected sales of over $2.5 billion. But the stock was already in a curious collapse before and after those results came out, getting cut in half from $52 to $26 in only two months. I decided to take a closer look at the catalysts.

What I found was that the analyst community and large biotech investors were looking at all kinds of new competition for Incivek coming to market. The VRTX drug used an interferon cocktail regime with nasty side effects and lots of competitors were creating next-generation oral treatments that didn't need interferon. The biggest threat came from Gilead Sciences who had just paid $10 billion for Pharmasett to get their hands on that young biotech's HCV treatment.

The problem was that none of these competitors would have their drugs ready for market until 2014. So with 170 million people worldwide exposed to HCV, and VRTX estimates not coming down, I thought that Incivek still would win in 2012. Plus, VRTX had a cystic fibrosis drug very close to FDA approval.

On the very first day of the Tactical Trader service in early December, we opened the books by buying the VRTX April 30 calls for under $4. We just sold them for a 100% gain last week. Too bad we didn't keep them a little longer as the stock launched above my $40 price target Friday morning.

Catching Falling Knives, or Scooping Fallen Gems?

There's an old adage in trading and investing that one can get really hurt trying to catch a falling knife. But if you do your homework, and you develop sound screening criteria that give you a very favorable risk/reward edge, you can bank sizable profits off the irrationality of other investors.

I may not have the deep pocket and time horizon of a Warren Buffett, but my approach fully capitalizes on the idea to 'be greedy when others are fearful.'

No Need to Pursue These Profits on Your Own If you'd like some help, my private trading group has been re-opened until Saturday to new investors. Its purpose is to go long or short with stock, ETF, and options moves to catch small market swings that others rarely spot and ride them for substantial one to 12-week gains. The number of investors who share the moves from our Zacks Tactical Trader must be limited, and demand to get into the service was so intense that it had to be closed early when introduced last December. Now it's open to you again, but only until 11:59 pm Saturday, February 18. There will be no extensions so I strongly encourage you to look into it now. Click now for details about Tactical Trader >> Good Investing, Kevin Cook Kevin, a Senior Stock Strategist at Zacks, is a recognized authority in global markets. A former market-maker in the $4-trillion-dollar-a-day world of interbank trading, he developed the ability to track the movement of money, and trained his reflexes to take advantage of it. Today he directs the new Zacks Tactical Trader, providing commentary and recommendations.

Read the analyst report on CME

Read the analyst report on CSTR

Read the analyst report on VRTX

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3 Killer Criteria for Super Swing Trades

Public release date: 17-Feb-2012
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Contact: Erin Tornatore
erin.tornatore@childrens.harvard.edu
617-919-3110
Children's Hospital Boston

Boston, Mass. ? Some 90 percent of people are exposed to the Epstein Barr virus (EBV) at some point in their life. Even though it is quickly cleared from the body, the virus can linger silently for years in small numbers of infected B cells. According to researchers at Children's Hospital Boston and the Immune Disease Institute (IDI), the immune system subdues the virus by watching for a single viral protein called LMP1, knowledge that has already helped suggest two new treatments for the EBV-fueled cancers seen in some immunosuppressed patients.

The study team, led by Klaus Rajewksy, MD, and Baochun Zhang, MD, PhD, of the Program in Cellular and Molecular Medicine at Children Hospital Boston and the IDI, reported their results online this week in the journal Cell.

While the immune system's T cells rapidly clear most EBV-infected B cells, about one in a million infected cells escapes destruction. Within these cells, the virus enters a latent phase, kept in check by the watchful eye of so-called memory T cells. This uneasy relationship usually holds steady the rest of a person's life, unless something ? such as infection with HIV or use of anti-rejection drugs following a transplant ? suppresses the immune system and breaks the surveillance. The virus can then reawaken and drive the development of B cell cancers like AIDS-associated B cell lymphoma and post-transplant lymphoproliferative disorder.

To better understand how the immune system maintains its watch and how the virus turns cells cancerous, Rajewsky and his team had generated a model mimicking latent EBV infection by engineering mice whose B cells contained an inducible version of viral LMP1. Researchers have long known that EBV needs LMP1 to turn B cells cancerous, but modeling this relationship in vivo had proven challenging.

"We had previously attempted to develop an animal model of LMP1 transformation of B cells," said Rajewsky, who recently moved to the Max Delbr?ck Center for Molecular Medicine in Germany, "but we had never been able to get the mice in our models to actually produce any mature B cells. The immune response against the LMP1-producing B cells was so robust that the cells were eliminated very early on."

Their breakthrough came when Zhang and colleagues reengineered the model to lack T cells. "The mice were initially fine, but succumbed within two to three months to aggressive B cell lymphomas," Rajewsky said. "The profile mimicked very closely what we see in immunosuppressed lymphoma patients." In additional experiments with Rajewsky's original model, the team eliminated the mice's T cells before activating the viral protein in B cells, sparking a similar but even more rapid fatal disease.

The team also made several observations with possible clinical application. First, they noted that in the mouse model the LMP1 producing B cells were being attacked by a specific kind of T cell called a CD4+ T cell. "Transplant patients who develop B cell lymphomas because they are immunosuppressed by their anti-rejection drugs are often treated with T cells that carry the CD8 marker," Rajewsky noted. "These results would argue for also considering CD4+ T cells for treatment."

Second, they found that tumors in the LMP1 producing mice often displayed targets recognized by another kind of immune cell called a natural killer (NK) cell. Seeing an opportunity, Rajewsky worked with cancer immunologist Glenn Dranoff, MD and colleagues at Dana-Farber Cancer Institute, to test a potential therapeutic agent that uses a portion of the NK cell activating receptor called NKG2D, fused to the stimulatory Fc portion of an antibody, a combination capable of activating and directing immune attack against tumor cells. In a transplantation model of LMP1-fueled lymphomas, the NKG2D-Fc fusion proved quite capable of reducing tumor growth and prolonging survival of the recipients.

"These preclinical results suggest administration of the NKG2D-Fc fusion protein, perhaps combined with treatment with CD4+ T cells, could benefit some patients with EBV-driven lymphomas," Rajewsky said. "What we can say with certainty, though, is that LMP1 is the immune system's primary surveillance trigger following EBV infection and clearance, knowledge that we think will open doors to additional treatment options."

###

This study was supported by the National Cancer Institute, the National Institute of Allergy and Infectious Diseases, the Leukemia and Lymphoma Society, the Japan Society for the Promotion of Science, and the Astellas Foundation for Research on Metabolic Disorders.

Children's Hospital Boston is home to the world's largest research enterprise based at a pediatric medical center, where its discoveries have benefited both children and adults since 1869. More than 1,100 scientists, including nine members of the National Academy of Sciences, 11 members of the Institute of Medicine and nine members of the Howard Hughes Medical Institute comprise Children's research community. Founded as a 20-bed hospital for children, Children's Hospital Boston today is a 395 bed comprehensive center for pediatric and adolescent health care grounded in the values of excellence in patient care and sensitivity to the complex needs and diversity of children and families. Children's also is the primary pediatric teaching affiliate of Harvard Medical School. For more information about research and clinical innovation at Children's, visit: http://vectorblog.org.

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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

Read the original:
A single protein helps the body keep watch over the Epstein-Barr virus

ScienceDaily (Feb. 15, 2012) — A team of scientists from the Charité and German Rheumatism Research Center Berlin and the University of Geneva has found a fundamentally new mechanism how our defense system is ramped up when facing a viral intruder. Exploitation of this mechanism in vaccines sparks new hope for better prevention and therapy of infectious diseases and cancer.

"T killer cells" (CD8 T cells) represent an important element of our body's defense system. They have the capacity to specifically identify and kill cells, which harbor viruses and bacteria or form a cancer. T killer cells would therefore represent an important component of yet unavailable vaccines against infections like HIV/AIDS, hepatitis C virus and malaria, and also for the treatment of cancer.

It has been a longstanding observation that there is no match to the overwhelming T killer cell armada, which is triggered when a viral infection invades our body. Scientists had generally accredited this observation to "pathogen-associated molecular patterns" (PAMPs) on viruses and other microbes. PAMPs, i.e. the "foreign look" of viruses, alert so-called "dendritic cells," which serve as policemen coordinating the T killer cell response.

In a report now published in the journal Science, researchers led by Prof. Max Löhning (Charité-University Medicine & DRFZ Berlin) and Prof. Daniel Pinschewer (University of Geneva) describe an additional general mechanism by which viral infection triggers potent T killer cells: "Dying virus-infected cells themselves ring the alarm bells to T killer cells.," Löhning says. Viruses cause infected cells to die, resulting in the release of cell components, which normally are not be visible to the outside -- analogous to an injured individual loosing blood. Such substances, heralding injury when released, are referred to as "alarmins." The scientists found that T killer cells can sense an alarmin called "interleukin 33" (IL-33). IL-33 is contained in cells, which form the scaffold of the T killer cells' home, the spleen and lymph nodes, and is released when such scaffold cells die.

Mice lacking the gene encoding IL-33 failed to form a large T killer cell army upon viral infection. The few remaining cells had very poor fighting skills. Such mice were therefore exquisitely sensitive to several types of viral infections. Conversely, IL-33 could be used to artificially increase the T killer cell army, which was generated in response to vaccination. As Max Löhning and Daniel Pinschewer explain, PAMPs and alarmins apparently have complementary and non-redundant functions in shaping our T killer cell defense: "The "foreign look" of viruses (PAMPs) activates the "dendritic cell" policemen to engage T killer cells. T killer cells, however, remain lousy fighters unless alerted by a cell death in their neighborhood (alarmins)." These new findings could provide a key to effective vaccination against infectious diseases and cancer.

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The above story is reprinted from materials provided by Deutsches Rheuma-Forschungszentrum Berlin, via AlphaGalileo.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

Journal Reference:

W. V. Bonilla, A. Frohlich, K. Senn, S. Kallert, M. Fernandez, S. Johnson, M. Kreutzfeldt, A. N. Hegazy, C. Schrick, P. G. Fallon, R. Klemenz, S. Nakae, H. Adler, D. Merkler, M. Lohning, D. D. Pinschewer. The Alarmin Interleukin-33 Drives Protective Antiviral CD8 T Cell Responses. Science, 2012; DOI: 10.1126/science.1215418

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

Read more here:
New defense mechanism against viruses and cancer identified

Though Prototype 2 explains why its main character gains the ability to shoot tendrils from his arms, it never touches on why the virus that gives him super powers also turns him into an unrelatable hypocrite, while removing all semblance of morality. All of it. Just wrings it on out. Every drop.

It made more sense in the original game. Beyond being the scapegoat for a massive chemical weapon cover-up, Alex Mercer was also sort of a jerk. He amorally killed thousands of civilians on his rampaging quest for the truth, becoming the monster the government made him out to be. It made sense and happened somewhat organically, as he felt like the entire world had turned against him. It also makes sense that, at least for the opening minutes of Prototype 2, he would be the villain – he sort of already was.

Above: Flying between buildings is always fun

James Heller, the protagonist of the sequel, starts off with the best of intentions: to kill Alex Mercer. He believes Mercer responsible for the virus that destroyed New York City (now called New York Zero for some reason), among the casualties being his daughter and wife.

But it didn’t take long for the new hero to find out the truth about the virus and its origins, and within a few minutes of the game’s opening, he’d already tried to kill Mercer, failed, been injected with the virus, transformed into a powerful super-mutant, and dropped his vendetta almost entirely. In under an hour, Heller had gone from trying to kill Mercer to joining him in an uneasy alliance against the mercenary group responsible for the outbreak.

Above: He could cut Wolverine clean in half with those

And when we say he was given powers, boy do we mean it. Your character in Prototype 2 starts off 10 times stronger than your character ends up in nearly any other game. Right away, we were running up walls, throwing dumpsters at helicopters and slashing apart waves of enemies. Seriously. Spider-Man? Hulk? They’ve got nothing on Heller. Even Infamous's Cole MacGrath looks weak next to Heller an hour into the game.

In fact, we were so powerful right out of the gate that we had problems picking out which skills were new and which ones Mercer flaunted around in the original.  Some stood out – like being able to infect an enemy with the virus and throw him like a grenade (called the bio bomb), and the addition of deadly tendrils, which work like Spider-Man’s webs to let us zip to locations – but it’s hard to figure out what is and isn’t new when you’re so damn powerful. Could we flying kick a helicopter to death in the original game? Could Alex Mercer slam the ground and destroy everything around him with powerful spikes? We just couldn't remember.

Above: We could turn him into a bio-bomb and throw him for hilarious effect

While that might sound negative, it’s actually a compliment to how well the developers weaved the new powers and abilities into the already successful Prototype mold. Controlling Heller is an absolute blast. The sense of power is damn near unparalleled, and the abilities the game threw our way made for a tremendously fun time. He might not feel all that different from Mercer right away, but he feels different enough to make things feel fresh. It even makes sense within the game’s canon. Both characters are infected with the same virus, and viruses mutate. That explains why Mercer’s powers manifested the way they did, while Heller’s gave him tendrils and “viral sonar,” which… well, lets him send out a sonar pulse that points him in the direction of guys he needs to kill.

One thing that confuses us, however, is that shortly after the game began, we felt like Heller had become an insane killer. In Mercer’s case we bought it, as he was sort of an enemy of the state, so we didn’t mind when we were able to slaughter civilians. With Heller… we just don’t get it. He’s a father, a husband, and once he finds out who is responsible for the death of his loved ones ,he sets off on a quest to avenge his wife and daughter by… killing thousands of wives, daughters, sons, and husbands? 

Above: If you don't feel like using powers you can just punch dudes in the jaw

Sure, the game doesn’t “make” you do it, but it’s impossible to fight a battle in Prototype 2 without insane collateral damage. Throwing a car at a helicopter will usually end with that helicopter landing on a pile of meaty humans. In the hour we played we really couldn’t identify with him because his actions didn’t make much sense to us. Maybe the finished product will fix this by providing additional context, or explaining why he doesn't see this as being an issue.

Or maybe the Prototype formula dictates that the hero needs to be a jerk. We don't know. We didn't really think we'd end up liking Mercer all that much, and here we are pining over him.

Then again, as long as we’re still playing a super-human mutant with the ability to slaughter thousands of people at a time ,we doubt we’ll be complaining. Not so long as we’re having fun, at least.

The rest is here:
Prototype 2’s hypocritical protagonist almost gets in the way of our bloody, murderous fun

By Helen Branswell
(Click here for the original article)

A simple math problem lies at the heart of a heated debate over whether scientists should be allowed to publish provocative research into the transmissibility of H5N1 flu. Assuming the avian virus could spread easily among people, just how deadly would an H5N1 pandemic be for humans?

Flu scientists tend to shy away from that question, suggesting that it is not possible to predict how lethal the virus would still be after undergoing the necessary changes to adapt to human physiology. But inevitably, people look for clues to what appears to be the best predictor of the virus's future path—its current behavior. And that appears downright terrifying: as many as 59 percent of people known to have contracted the virus have died from the infection.

More specifically, of the 584 people who have tested positive with what the World Health Organization (WHO) confirms is H5N1, 345 have died. (These numbers are current as of February 8, 2012.)

But what if H5N1 isn't as deadly as the official numbers suggest?

Indeed, two researchers have charged into the already fraught H5N1 publication controversy insisting the numbers are wrong, that the true mortality rate is likely to be much, much lower and that bad policy is being driven by the inflated figures.

Peter Palese, a noted influenza virologist at Mount Sinai School of Medicine in New York City, and Vincent Racaniello, a professor of microbiology at Columbia University Medical Center, also in New York City, are among a vocal group of scientists who vehemently oppose any decision to suppress the details of research conducted by Yoshihiro Kawaoka of the University of Wisconsin–Madison and Ron Fouchier of Erasmus Medical Center in the Netherlands.

Fouchier and Kawaoka had—at the request of the National Institutes of Health—figured out whether the H5N1 virus could become more transmissible in non-avian species. Their efforts reportedly revealed that just a few mutations were all that was needed to create a bird flu virus that is easily transmitted between ferrets. In addition, Fouchier said that his strain remained just as deadly to ferrets as it had been to birds, although Kawaoka later declared that his lab strain was not lethal.

Palese suggested in a perspective article co-authored by Taia Wang and published ahead of print on January 25, 2012 in Proceedings of the National Academy of Sciences that the case fatality rate of H5N1 human was almost certainly "orders of magnitude" too high.

Starting with the current 59 percent rate, if you start pushing the decimal point left, 59 becomes 5.9, which becomes 0.59 or even 0.059. Each adjustment of the decimal corresponds to an order of magnitude. (For comparison's sake, the mortality rate of current seasonal flu is less than 0.1 percent whereas researchers estimate that the mortality rate of the killer 1918 flu pandemic was around 2 percent.)

Racaniello, who did his thesis research under Palese, suggested on his popular Virology Blog in early January that the estimates of H5N1's killing potential were vastly overrated. Citing a recently published study that found what might be H5N1 antibodies in the blood of some villagers in Thailand, he mused that if 9 percent of rural Asians had antibodies to the virus, the perception of how dangerous H5N1 is would change dramatically.

In the flu world, few people would argue that Palese and Racaniello are wrong that the case/fatality rate is too high. It might be difficult, though, to find many who agreed with their conclusion on what that means about the virus.

It is widely accepted that the cases that come to light and get tallied by WHO are only an unknown portion of the total human infections that have occurred. Official case counts are certainly missing some infections—but not enough to morph H5N1 into a benign virus, a number of flu scientists agree in interviews for Scientific American.

"I think all these numbers are flexible, and Peter is undoubtedly right it's not 60 percent. But I don't know what it is. And I don't think he does either," says Robert Krug, chairman of Genetics and Microbiology at the University of Texas at Austin, where his work focuses on the molecular mechanisms at play during influenza infection.

"It's dangerous. How dangerous? I have no idea…. I'm sure it's less than 60 percent but it's still too high for the world to tolerate a (human-to-human) transmissible H5N1 virus," says Krug, who believes both papers should be published in full.

The problem with the case/fatality rate, as Palese pointed out in PNAS, is that human infections with what is still a bird virus generally only come to the attention of medical authorities when someone gets really sick. In fact, in order to count as a case by WHO's definition, a person must have a high fever, known exposure to the virus, and needs to test positive for H5N1. A specimen for a test would generally only be taken at a hospital and that facility would have to have access to a laboratory. If H5N1 is causing mild cases, they are unlikely to come to light under that definition. Is a person living in a remote Cambodian village who feels lousy for a couple of days going to seek that kind of medical care? If there are H5N1 cases like that, the fact they are being missed artificially lowers the denominator.

"If the only cases you know about are the ones who are going to die, then you might believe that the case/fatality rate is very high because you lack surveillance of less symptomatic cases," says John J. Treanor, chief of the Infectious Diseases Division at the University of Rochester Medical Center in New York State.

But what of the numerator, or the number of deaths? For the case/fatality rate to plummet, the numerator must be a smaller fraction of the total cases. But it is clear the numerator is off as well, notes Tim Uyeki, an influenza epidemiologist at the U.S. Centers for Disease Control who has spent a lot of time in the field studying human H5N1 cases and outbreaks.

Uyeki points as an example to the first report in the scientific literature of presumed person-to-person spread of H5N1. It was a cluster of three infections that started with an 11-year-old girl who fell ill in September 2004. She lived with an aunt while her mother worked in a distant city. Both the aunt and the mother, who came home to care for the girl, got sick; the mother and daughter died.

All three clearly had H5N1—a throat swab confirmed it in the aunt and virus was found in tissue from the mother. But the hospital had thought the girl had dengue fever. By the time they realized these were H5N1 cases, the girl had died and her body was cremated. Officially that cluster went down on the books as two cases, not three. There are other cases that were designated as probable infections but which never made the official count, Uyeki says.

Given the limitations of the system for finding human cases, researchers have been conducting what are known as sero-surveys—drawing blood samples from groups of people who were likely exposed to the virus to see if they have antibodies specific to it. That would be a sign that they had been infected and survived. More than 20 such studies have been completed since 1997, when the first known cases of H5N1 infection in humans cropped up. Groups that have been tested included workers who culled infected chickens, health care workers who cared for H5N1 patients, people who worked in live animal markets and people who lived in villages where cases have occurred. The studies have been done in China, Indonesia, Nigeria, Cambodia, Thailand and elsewhere, important because different subfamilies of H5N1 viruses circulate in different parts of the world and some—hypothetically—may cause more severe disease than others.

Most of the sero-surveys have been small; few have contained more than 500 people. Whereas one study—among poultry market workers in Hong Kong in 1997—found around 10 per cent had H5N1 antibodies, most reported either no positives or low rates of people with antibodies. Some were under 1 percent, two were in the 3 to 4 percent range.

The study Racaniello drew on to argue H5N1 infection was more prevalent (and thus less lethal) than official numbers suggest looked for evidence of antibodies in 800 Thai adults living in villages where outbreaks of H5N1 had occurred in birds and where at least one human infection had been reported. The researchers found 5.6 percent had elevated antibodies to one H5N1 virus and 3.5 percent to another.

Not everyone agrees, however, that this particular study can be used to support Racaniello's argument. The threshold used in the Thai research as evidence of antibodies is substantially lower than most studies use. With a cutoff that low, says Malik Peiris, chair of the Department of Microbiology at the University of Hong Kong, one cannot be sure whether what is being detected is antibody-specific to H5N1, or antibodies to other flu viruses that happen to cross-react with the H5N1 test. Having low levels of antibodies that react to—and might even protect against—H5N1 does not prove that the person was infected with H5N1, Peiris says.

The senior author of the Thai study, Gregory Gray, chair of the Department of Environmental and Global Health at the University of Florida, says his group used the low threshold because they know antibody levels wane over time. They were looking for "subtle evidence" of infections that might have occurred years previous. But Gray says the results should not be overinterpreted. "It is a stretch to say this is population-based and also a stretch to say these all represented H5N1 infections," he says.

Although Krug, Treanor, Uyeki and Peiris all agree the official 59 percent H5N1 case fatality rate is not the true number, none takes much comfort from the fact. Krug is agitated that the controversy over the studies is drawing attention away from their key message—this virus can adapt to spread in mammals, which may include humans. And Treanor scoffs at the idea that concern over H5N1 is overblown. "If H5 is not dangerous, why are we even bothering to study it at all?" he asks. "I think it is without a doubt the case that it is not as dangerous as it looks from the cases that we have. But it is still without a doubt an extremely dangerous virus—particularly if it gained the ability to spread from person to person."

As for how far off the case/fatality rate is, there is no way of knowing. Uyeki, who has studied the issue at length, gives his estimate: "Are we missing some [cases]? Yeah, probably we're missing some. But are we missing hundreds of thousands? No, I don't think so. Are we missing tens of thousands? Probably not. Are we missing hundreds? Possibly. It's really hard to know."

Also on HuffPost:

See the rest here:
H5N1 Bird Flu May Be Less Deadly to Humans Than Previously Thought -- Or Not