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If the pigs, people, and birds have died in China from H7N9, it is imperative and urgent that the biological connection be made.

By LAURIE GARRETT

WASHINGTON Heres how it would happen. Children playing along an urban river bank would spot hundreds of grotesque, bloated pig carcasses bobbing downstream. Hundreds of miles away, angry citizens would protest the rising stench from piles of dead ducks and swans, their rotting bodies collecting by the thousands along river banks. And three unrelated individuals would stagger into three different hospitals, gasping for air. Two would quickly die of severe pneumonia and the third would lay in critical condition in an intensive care unit for many days. Government officials would announce that a previously unknown virus had sickened three people, at least, and killed two of them. And while the world was left to wonder how the pigs, ducks, swans, and people might be connected, the World Health Organization would release deliberately terse statements, offering little insight.

It reads like a movie plot I should know, as I was a consultant for Steven Soderberghs Contagion. But the facts delineated are all true, and have transpired over the last six weeks in China.

The events could, indeed, be unrelated, and the new virus, a form of influenza denoted as H7N9, may have already run its course, infecting just three people and killing two.

Or this could be how pandemics begin.

On March 10, residents of Chinas powerhouse metropolis, Shanghai, noticed some dead pigs floating among garbage flotsam in the citys Huangpu River.

The vile carcasses appeared in Shanghais most important tributary of the mighty Yangtze, a 71-mile river that is edged by the Bund, the citys main tourist area, and serves as the primary source of drinking water and ferry travel for the 23 million residents of the metropolis and its millions of visitors.

The vision of a few dead pigs on the surface of the Huangpu was every bit as jarring for local Chinese as porcine carcasses would be for French strolling the Seine, Londoners along the Thames, or New Yorkers looking from the Brooklyn Bridge down on the East River.

And the nightmarish sight soon worsened, with more than 900 animal bodies found by sunset on that Sunday evening.

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Is this the next pandemic? Tale of mystery virus unfolds like a movie plot (Commentary)

Public release date: 1-Apr-2013 [ | E-mail | Share ]

Contact: Karen Richardson krchrdsn@wakehealth.edu 336-716-4453 Wake Forest Baptist Medical Center

WINSTON-SALEM, N.C. April 1, 2013 Using the same strategy that a common virus employs to evade the human immune system, researchers at Wake Forest Baptist Medical Center's Institute for Regenerative Medicine have modified adult stem cells to increase their survival with the goal of giving the cells time to exert their natural healing abilities.

"Basically, we've helped the cells be 'invisible' to the body's natural killer cells, T cells and other aspects of the immune system, so they can survive to promote healing," said Graca Almeida-Porada, M.D., Ph.D., senior author and professor of regenerative medicine at Wake Forest Baptist.

The research, reported in the current issue of PLOS One, a peer-reviewed, open access journal, involves mesenchymal stem cells (MSCs), found in bone marrow, peripheral and cord blood and fetal liver and lung tissue. These cells are known for their ability to migrate to damaged tissues and contribute to healing. However, like all cells, they are susceptible to being killed by the body's complement system, a part of the immune system involved in inflammation and organ rejection.

"These cells have a natural ability to help modulate the immune response, so if we can increase their survival, they theoretically could be a therapy to decrease inflammation and help transplant patients avoid organ rejection," said Almeida-Porada.

In the study, the researchers evaluated the potential of human cytomegalovirus (HCMV), a member of the herpes virus family, to help increase the survival of MSCs. While the HCMN virus infects between 50 percent and 80 percent of people in the U.S., it normally produces no symptoms and remains latent in the body over long periods.

"We wanted to take advantage of the virus' ability to evade the immune system," said Almeida-Porada. "Our strategy was to modify the cells to produce the same proteins as the HCMV virus so they could escape death and help modulate inflammation and promote healing."

MSCs were purified from human fetal liver tissue. They were then engineered to produce specific proteins expressed by the HMCV virus. Through this process, the scientists identified the protein that was most effective at increasing cell survival. Specifically, the team is the first to show that overexpression of the US2 protein made the cells less recognizable to the immune system and increased cell survival by 59 percent (+/- 13 percent).

"The research showed that modifying the cells indeed improves their survival," said Almeida-Porada. "Next, we hope to evaluate the healing potential of these cells in conditions such as bowel disease, traumatic brain injury and human organ transplant."

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Researchers are first to use common virus to 'fortify' adult stem cells

Apr. 1, 2013 Using the same strategy that a common virus employs to evade the human immune system, researchers at Wake Forest Baptist Medical Center's Institute for Regenerative Medicine have modified adult stem cells to increase their survival -- with the goal of giving the cells time to exert their natural healing abilities.

"Basically, we've helped the cells be 'invisible' to the body's natural killer cells, T cells and other aspects of the immune system, so they can survive to promote healing," said Graca Almeida-Porada, M.D., Ph.D., senior author and professor of regenerative medicine at Wake Forest Baptist.

The research, reported in the current issue of PLOS ONE, a peer-reviewed, open access journal, involves mesenchymal stem cells (MSCs), found in bone marrow, peripheral and cord blood and fetal liver and lung tissue. These cells are known for their ability to migrate to damaged tissues and contribute to healing. However, like all cells, they are susceptible to being killed by the body's complement system, a part of the immune system involved in inflammation and organ rejection.

"These cells have a natural ability to help modulate the immune response, so if we can increase their survival, they theoretically could be a therapy to decrease inflammation and help transplant patients avoid organ rejection," said Almeida-Porada.

In the study, the researchers evaluated the potential of human cytomegalovirus (HCMV), a member of the herpes virus family, to help increase the survival of MSCs. While the HCMN virus infects between 50 percent and 80 percent of people in the U.S., it normally produces no symptoms and remains latent in the body over long periods.

"We wanted to take advantage of the virus' ability to evade the immune system," said Almeida-Porada. "Our strategy was to modify the cells to produce the same proteins as the HCMV virus so they could escape death and help modulate inflammation and promote healing."

MSCs were purified from human fetal liver tissue. They were then engineered to produce specific proteins expressed by the HMCV virus. Through this process, the scientists identified the protein that was most effective at increasing cell survival. Specifically, the team is the first to show that overexpression of the US2 protein made the cells less recognizable to the immune system and increased cell survival by 59 percent (+/- 13 percent).

"The research showed that modifying the cells indeed improves their survival," said Almeida-Porada. "Next, we hope to evaluate the healing potential of these cells in conditions such as bowel disease, traumatic brain injury and human organ transplant." The research was supported by National Institutes of Health grants HL73737 and HL97623.

Almeida-Porada's co-researchers were Melisa A. Soland, Ph.D., and Christopher Porada, Ph.D., Wake Forest Baptist; Mariana Bego, Ph.D., Institut de Recherches Cliniques de Montreal, Canada; and Evan Colletti, Ph.D, Esmail Zanjani, Ph.D., and Stephen S. Jeor, Ph.D., University of Nevada.

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Researchers first to use common virus to 'fortify' adult stem cells

By Maureen Salamon HealthDay Reporter

WEDNESDAY, March 27 (HealthDay News) -- An experimental therapy for hepatitis C -- a "silent killer" linked to liver cancer and cirrhosis -- has shown promise in tamping down virus levels in early trials.

Experts caution, however, that it's too soon to know if the injectable drug will someday gain a standing among emerging oral medications against the disease.

New research suggests that the drug, miravirsen, could potentially be part of a drug "cocktail" that manages the hepatitis C virus in much the same way as similar combinations have transformed HIV/AIDS from a death sentence into a chronic, manageable condition.

Miravirsen suppresses molecules the hepatitis C virus needs to reproduce. The drug decreased viral loads by about 500-fold at the highest doses used in a small, phase 2 study by an international group of researchers. Drug resistance, a common problem with other hepatitis C medications, did not develop among patients taking miravirsen.

A phase 2 trial evaluates a drug's effectiveness while continuing to assess its safety.

"This is the first real clinical study of this approach and the results are encouraging," said Dr. Judy Lieberman, chairwoman of cellular and molecular medicine at Boston Children's Hospital. "What's exciting to me is that there doesn't seem to be any drug resistance developing. If there's a way to develop a drug cocktail that doesn't require a half a year of treatment ... that would be really exciting, but it's too early to tell."

Lieberman was not involved in the research but co-wrote an editorial accompanying the new study in the March 27 issue of the New England Journal of Medicine.

Hepatitis C is one form of liver disease and affects about 170 million people worldwide, according to study background information. It's transmitted by shared needles or, less frequently, through sex. Often symptomless, the infection is a major cause of liver cancer and cirrhosis, or scarring of the liver.

Led by Dr. Harry Janssen, a professor of medicine at the University of Toronto and Erasmus University Rotterdam in the Netherlands, researchers split 36 patients with hepatitis C into four groups. Nine patients in each of the first three groups received a dose of either 3 milligrams (mg), 5 mg or 7 mg of miravirsen per kilogram of body weight for 29 days, while the last nine patients received a placebo. All were followed for 18 weeks.

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Experimental Drug May Work Against Hepatitis C

Treatment in asymptomatic individuals may speed up the development of deadlier virus strains

Even as researchers creep closer toeliminating the human immunodeficiency virus (HIV)in some patients via intense multi-drug therapies and early treatment, researchers at theUniversity of Southern Californiawarn that the responsible treatment may give rise to new killer strains that resist drugs.

The USC study hits close to home as the Los Angeles county targetsmen who have sex with men (MSM) -- a high-risk group for HIV/AIDS -- with a so-called "test and treat" strategy. The strategy pushes foruniversal testing-- particularly between MSM and other high-risk groups. It calls forearly retroviral drug treatmentin individuals who test HIV positive.

The approach has thus far lowered the death rates and decreased the number of cases.

The USC researchers dug into data on MSM infections, which account for 82 percent of total known HIV infections nationwide. Using data from theCenters for Disease Control, internal data, and knowledge of drug resistance, the researchers modeled the occurrence of drug resistant viral strains if the "test and treat" strategy was aggressively followed over the next several years.

The study suggests that the rates ofmultiple-drug-resistantHIV (MDR) could jump from 4.79 percent to 9.06 percent.

USC ProfessorNeeraj Sood, who was a lead author on the study, suggests that much of the benefit comes from the knowledge of infection status. Hecomments, "Were not saying that testing everybody and treating everybody is bad. All were saying is that you should proceed with caution and closely monitor the prevalence of multi-drug-resistant HIV as you scale up the test and treat model. Prior studies show a dramatic reduction inrisk-taking behaviorby individuals once they know their HIV-positive status."

The research was funded by theEunice Kennedy Shriver National Institute of Child Healthand Human Developmentandpublishedin an edition of this month'sClinical Infectious Diseasesjournal.

Sources: USC [press release], Clinical Infectious Diseases [abstract]

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Study: Early HIV Drug Treatment May Lead to Drug-Resistant Strains