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By LARRY NEUMEISTER Associated Press

NEW YORK (AP) - A computer virus that spread to more than a million computers worldwide, including some at NASA, and produced at least $50 million in illegal profits or losses to victims should be a "wake-up call" for banks and consumers unaware of the threat posed by Internet criminals, a prosecutor said Wednesday.

U.S. Attorney Preet Bharara and George Venizelos, head of the New York FBI office, warned of the growing threat to financial and international security as they announced that a 2-year probe had resulted in three arrests, two of them overseas, and the seizure of vast amounts of computer-related evidence that will take months or years to fully analyze. They said the Gozi virus had infected 40,000 computers in the United States since 2005, including 190 at the National Aeronautics and Space Administration, along with computers in Germany, Great Britain, Poland, France, Finland, Italy, Turkey and elsewhere.

"This case should serve as a wake-up call to banks and consumers alike because cybercrime remains one of the greatest threats we face, and it is not going away anytime soon," Bharara said. "It threatens individuals, businesses and governments alike."

He told a news conference that cybercriminals "believe that their online anonymity and their distance from New York render them safe from prosecution, but nothing could be further from the truth."

Venizelos said law enforcement had seized 51 computer servers in Romania, along with laptops, desktops and external hard drives, accumulating more than 250 terabytes of information.

"That vast pile of data is almost certain to aid criminal investigation at FBI offices around the country as well as law enforcement agencies around the world," he said. "It is more than standard boilerplate to say that this investigation is very much ongoing."

So far, the investigation has produced three arrests, including that of Nikita Kuzmin, a 25-year-old Russian who pleaded guilty to computer intrusion and fraud charges in Manhattan in May 2011, admitting his role in creating the virus. The plea by the Moscow resident was followed by the arrest in November of a co-conspirator in Latvia and another in Romania last month. Extradition proceedings are under way against both on various criminal charges, including conspiracy.

The NASA breach occurred from Dec. 14, 2007, to Aug. 9, 2012, with the most damage occurring between May and August last year, according to documents filed in U.S. District Court in Manhattan. The infected computers sent data without user authorization, including login credentials for an eBay account and a NASA email account, details of visited websites and the contents of Google chat messages.

Mihai Ionut Paunescu, 28, who was arrested in Romania, set up online infrastructure that allowed others to distribute destructive viruses and malicious software, including ones dubbed Zeus Trojan, SpyEye and BlackEnergy, according to a criminal complaint filed against him. The document said Paunescu, a Romanian national residing in Bucharest, was also known as "Virus."

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Feds: 3 nabbed for widespread Gozi computer virus

Jan. 20, 2013 A research team led by the La Jolla Institute for Allergy & Immunology has discovered the mechanism that enables CD4 helper T cells to assume the more aggressive role of killer T cells in mounting an immune attack against viruses, cancerous tumors and other damaged or infected cells. The finding, made in collaboration with researchers from the RIKEN Institute in Japan, could enable the development of more potent drugs for AIDS, cancer and many other diseases based on using this mechanism to trigger larger armies of killer T cells against infected or damaged cells.

CD4 helper T cells, which normally assist other cells of the immune system during an infection, and CD8 killer T cells, which directly attack and eliminate infected cells, are two of the body's most important immune cells for defending against diseases. Earlier research studies have shown that helper T cells can become killer cells in some instances. However, the specific mechanism of action that allowed this to occur was not known until now.

"We have identified the molecular switch that enables CD4 T cells to override their programming as helper cells and transform into cytolytic (killer) cells," said La Jolla Institute scientist and study co-leader Hilde Cheroutre, Ph.D. "Our team also showed that these transformed helper T cells represent a separate and distinct population of cells. They are not a subset of TH-1 helper cells as previously thought."

Jay A. Berzofsky, M.D., Ph.D., chief of the Vaccine Branch at the National Cancer Institute's Center for Cancer Research, called the finding "a major advance" that provides new understanding about the cell's lineage and basic mechanisms. Dr. Berzofsky was among the researchers whose work in the 1980s first demonstrated that helper cells could convert to killer cells. "Understanding how these cells derive and what causes them to switch from helper T cells to cytolytic T cells is an important step to learning how to manipulate them in disease," he said, noting it could lead to novel approaches "either to turn these cells off in autoimmune disease or turn them on in infectious diseases."

He added that the finding could also have important implications in cancer. "We need all of the cytolytic machinery that we can get to try to destroy cancers," he said. "If we can learn to turn them on, I think it's reasonable to believe that these cytolytic T cells can play an important role in controlling cancer."

The findings were published January 20 in Nature Immunology in a paper entitled "Transcriptional reprogramming of mature CD4 helper T cells generates distinct MHC class II-restricted cytotoxic T lymphocytes." Dr. Cheroutre is co-senior author on the study together with Dr. Ichiro Taniuchi of the RIKEN Research Center for Allergy and Immunology in Yokohama, Kanagawa, Japan. First authors on the paper are: Mohammad Mushtaq Husain, Ph.D., of the La Jolla Institute; Daniel Mucida, Ph.D., formerly of the La Jolla Institute, now at Rockefeller University; Femke van Wijk, Ph.D., formerly of the La Jolla Institute, now at the University Medical Center Utrecht, The Netherlands, and Sawako Muroi, of the RIKEN Institute.

In the study, the researchers found that a certain transcription factor, which are molecules in the cell nucleus that control the activity of cells, continually suppresses the killer T cell lineage in helper T cells. Using mice, the team showed that turning off this transcription factor (ThPOK) enabled the helper cells in the body's peripheral areas, like the blood, spleen and the intestine, to override their original programming and to become killer T cells. "While our work focused on the intestines, we found that helper T cells in all tissues of the body have the potential to become killer cells in response to recognition of viral, tumor or other antigens in the context of cytokines such as IL-15," said Dr. Cheroutre.

Jonathan Braun, M.D., chair of the Department of Pathology and Laboratory Medicine at UCLA's David Geffen School of Medicine, praised the study as laying the groundwork for using T helper cells in a much more aggressive manner. "Helper T cells are mainly understood for their role in regulating other immune cells," he said. "This work reveals how they themselves can be triggered to become the action cells in the immune response. This opens new possibilities for how to manipulate them therapeutically in disease."

Dr. Cheroutre said the transformation of CD 4 helper T cells into killer cells already occurs in the body naturally. "Our finding could help to explain a number of occurrences that we haven't really understood up to this point, such as why some people can be chronically infected with HIV without developing AIDS." In these instances, Dr. Cheroutre is convinced that CD4 helper T cells must be taking over the role of killer cells after the CD8 T cells become exhausted. "It's like the helper cells can come in as reinforcements to keep the virus under control. If we can develop ways to artificially trigger that process, we may be able to significantly help people with HIV and other chronic infections."

While scientists would want to trigger a larger army of virus-specific killer cells in the case of infections, the opposite would be true in inflammation-fueled autoimmune diseases, like rheumatoid arthritis or multiple sclerosis, said Dr. Cheroutre. "The CD4 T cells are the bad wolves in inflammatory diseases because they often trigger more pro-inflammatory cells which worsen these conditions," she said. "With this knowledge, we may be able to prevent that by coaxing the CD4 killer cells to become regulatory cells instead, which is another one of their potential functions. In regulatory mode, the CD4 T cells suppress the immune system. This suppression reduces inflammatory cells, which is what we want to do in autoimmune diseases."

Original post:
Molecular switch enabling immune cells to better fight disease

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Read more:
DOH reminds public on dengue, chikungunya

-- Finding on Killer Cells Opens New Avenue for Combating AIDS, Cancer and other Diseases

Newswise SAN DIEGO (January 20th, 2013) A research team led by the La Jolla Institute for Allergy & Immunology has discovered the mechanism that enables CD4 helper T cells to assume the more aggressive role of killer T cells in mounting an immune attack against viruses, cancerous tumors and other damaged or infected cells. The finding, made in collaboration with researchers from the RIKEN Institute in Japan, could enable the development of more potent drugs for AIDS, cancer and many other diseases based on using this mechanism to trigger larger armies of killer T cells against infected or damaged cells.

CD4 helper T cells, which normally assist other cells of the immune system during an infection, and CD8 killer T cells, which directly attack and eliminate infected cells, are two of the bodys most important immune cells for defending against diseases. Earlier research studies have shown that helper T cells can become killer cells in some instances. However, the specific mechanism of action that allowed this to occur was not known until now.

We have identified the molecular switch that enables CD4 T cells to override their programming as helper cells and transform into cytolytic (killer) cells, said La Jolla Institute scientist and study co-leader Hilde Cheroutre, Ph.D. Our team also showed that these transformed helper T cells represent a separate and distinct population of cells. They are not a subset of TH-1 helper cells as previously thought.

Jay A. Berzofsky, M.D., Ph.D., chief of the Vaccine Branch at the National Cancer Institutes Center for Cancer Research, called the finding a major advance that provides new understanding about the cells lineage and basic mechanisms. Dr. Berzofsky was among the researchers whose work in the 1980s first demonstrated that helper cells could convert to killer cells. Understanding how these cells derive and what causes them to switch from helper T cells to cytolytic T cells is an important step to learning how to manipulate them in disease, he said, noting it could lead to novel approaches either to turn these cells off in autoimmune disease or turn them on in infectious diseases.

He added that the finding could also have important implications in cancer. We need all of the cytolytic machinery that we can get to try to destroy cancers, he said. If we can learn to turn them on, I think its reasonable to believe that these cytolytic T cells can play an important role in controlling cancer.

The findings were published today in Nature Immunology in a paper entitled Transcriptional reprogramming of mature CD4 helper T cells generates distinct MHC class II-restricted cytotoxic T lymphocytes. Dr. Cheroutre is co-senior author on the study together with Dr. Ichiro Taniuchi of the RIKEN Research Center for Allergy and Immunology in Yokohama, Kanagawa, Japan. First authors on the paper are: Mohammad Mushtaq Husain, Ph.D., of the La Jolla Institute; Daniel Mucida, Ph.D., formerly of the La Jolla Institute, now at Rockefeller University; Femke van Wijk, Ph.D., formerly of the La Jolla Institute, now at the University Medical Center Utrecht, The Netherlands, and Sawako Muroi, of the RIKEN Institute.

Mitchell Kronenberg, Ph.D., La Jolla Institute president & chief scientific officer, said the study reflects the very successful collaboration between the La Jolla Institute and RIKEN in Japan, which have joined efforts on a number of projects over the years.

In the study, the researchers found that a certain transcription factor, which are molecules in the cell nucleus that control the activity of cells, continually suppresses the killer T cell lineage in helper T cells. Using mice, the team showed that turning off this transcription factor (ThPOK) enabled the helper cells in the bodys peripheral areas, like the blood, spleen and the intestine, to override their original programming and to become killer T cells. While our work focused on the intestines, we found that helper T cells in all tissues of the body have the potential to become killer cells in response to recognition of viral, tumor or other antigens in the context of cytokines such as IL-15, said Dr. Cheroutre.

Jonathan Braun, M.D., chair of the Department of Pathology and Laboratory Medicine at UCLAs David Geffen School of Medicine, praised the study as laying the groundwork for using T helper cells in a much more aggressive manner. Helper T cells are mainly understood for their role in regulating other immune cells, he said. This work reveals how they themselves can be triggered to become the action cells in the immune response. This opens new possibilities for how to manipulate them therapeutically in disease.

View original post here:
La Jolla Institute Identifies Molecular Switch Enabling Immune Cells to Better Fight Disease

Human immunodefieciency virus (HIV)

HIV turns against itself and dampens the progress of the killer disease in tests that may pave the way for an Aids cure.

Scientists in Australia have modified a protein of the HIV virus to prevent it from replicating. That stopped progress of the deadly disease in its tracks.

Queensland Institute for Medical Research associate professor David Harris, who took part in the research, called the technique "fighting fire with fire".

He predicted that it could one day wipe out the fatal Acquired Immune Deficiency Syndrome although it would not prevent people contracting the virus.

"What we've done is taken a normal virus protein that the virus needs to grow, and we've changed this protein, so that instead of assisting the virus, it impedes virus replication and does it quite strongly," Harris told ABC.

Prof David Harris

"This therapy is potentially a cure for Aids," he said. "It's not a cure for HIV infection but it potentially could end the disease.

"This protein, present in immune cells, would help to maintain a healthy immune system so patients can handle normal infections.

Aids is the final stage of the HIV virus, which devastates the body's immune system. More than 30 million people have died of Aids since its emergence in the 1980s.

Excerpt from:
Aids Cure Breakthrough Hopes High among Australian Scientists