Dr. Kuan-Teh Jeang (born 1958)

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Born - 1958 [HW002W][GDrive]

Died - Jan 27, 2013

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2013 (Jan 31) - In remembrance of Dr Kuan-Teh Jeang ( by Srimathy Sriskantharajah )

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Dr Kuan-Teh Jeang, Editor-in-Chief of Retrovirology, passed away on 27th January. We understand that Teh was well known and well liked by his friends and colleagues, so we would like to invite you share your memories and add your messages of condolences to this post. Below is a message about Teh from Dr Gottesman of NIH.

Dear colleagues,

Some of you have now heard the tragic news about Kuan-Teh Jeang of NIAID, who died suddenly and unexpectedly late Sunday night, on January 27. The cause of his death has not been verified, and I do not have the full details to relay.

I am sure you share my sense of shock and grief. Teh was 54 years old, had a remarkably productive scientific career, and was broadly admired on the NIH campus and in the field of virology and, in particular, retroviruses. I still can’t believe, more than a full day after his death, that I am sending this kind of message about him to the NIH staff.

In my introduction for Teh for the George Khoury Lecture that he delivered in October 2012, I described him as a dynamo. He was chief of the Molecular Virology Section in NIAID’s Laboratory of Molecular Microbiology, where he was a major figure in the fields of HIV and HTLV-1. In his 27 years at the NIH, he co-authored more than 300 publications and edited six books. He was the editor-in-chief of the journal Retrovirology, editor at Cell & Bioscience, associate editor of Cancer Research, and on the editorial board of numerousother scientific journals, including the Journal of Virology. He also was the recent past-president of the Society of Chinese Bioscientists in America, where he was outspoken in his desire for increased representation in leadership positions for Asian American scientists.

Teh’s recent awards include the International Retrovirology Association Dale McFarlin Award in 2011, Biomed Central’s Open Access “Editor of the Year” in 2010, and several Gates Foundation grant awards.

Teh’s lab studies host factors that influence the pathogenesis of human retroviruses HIV-1 and HTLV-I. Some of his group’s notable recent findings include: new insights into RNA modification and RNA-binding factors that affect HIV-1 post-transcriptional gene expression; successful genome-wide characterization of 252 human host cell factors in Jurkat T cells that are contributory to HIV-1 replication; and characterization of several oncogenic microRNAs and their contributions to HTLV-1 oncogenesis.

Teh had a colorful childhood. He was born in Taiwan, spent his childhood in Libya, came to the United States at age 12, and was accepted to the Massachusetts Institute of Technology at age 16. He arrived at the NIH in 1985 upon earning MD and PhD degrees from Johns Hopkins University. He was a postdoc in the lab of George Khoury, another great NIHer who tragically died young, for whom an NIH Wednesday Afternoon Lecture is named.

Teh’s death is a blow to the NIH and the retrovirus research community; and our thoughts and condolences are with Teh’s family: his wife Diane, a veterinarian with the FDA’s Office of Regulatory Affairs, and his children David, John and Diana. We will keep you informed about any planned funeral or memorial arrangements.

Michael Gottesman, M.D.

Deputy Director for Intramural Research, NIH

Image of Teh provided by Jean-Luc Darlix

2013 Obituary: Kuan-Teh Jeang (Retrovirology volume 10, Article number: 28 (2013))

Note : Downloadable PFD is here : [HW002V][GDrive]

Source of below : [HW002W][GDrive]

Authors - Ben Berkhout, Monsef Benkirane, Andrew Lever, Mark Wainberg, Ariberto Fassati, Persephone Borrow, Masahiro Fujii, Srimathy Sriskantharajah & Matthew Cockerill

Dear colleagues

Our loyal friend Kuan-Teh Jeang, “Teh” to friends and colleagues, passed away unexpectedly at the age of 54 on the evening of January 27, 2013. Great shock and sorrow was apparent in the avalanche of email messages by the very many international colleagues with whom Teh interacted over the years. Many of us came to know Teh as an energetic and gifted scientist for whom we had much respect and affection.

Teh was born in 1958 in Taichung, Taiwan and was the youngest to his two older brothers. Teh spent his childhood in Libya and came to the US in 1970. At age 16, he began college at the Massachusetts Institute of Technology, and after two years, started medical school at Johns Hopkins University, receiving both his M.D. and Ph.D. degrees by age 25. His Ph.D. thesis was on the regulation of gene expression in cytomegalovirus with Dr. Gary S. Hayward as advisor. During his time at Hopkins, Teh met his wife, Diane, a graduate student in the same laboratory. They married in 1984 in Iowa, where Teh completed his medical internship. The next year, Teh started his post-doctoral work at the National Institutes of Health (NIH) in the laboratory of Dr. George Khoury at the National Cancer Institute. Dr. Khoury died much too early at the age of 43 in 1987, but he was Teh’s role model and influenced him greatly in his professional life. As a recognition of his scientific achievements, Teh was recently selected to deliver the 2012 George Khoury Lecture at NIH on cellular transformation by the human T cell leukemia virus (HTLV-I).

Teh had been working at the NIH in Bethesda for 27 years, exactly half of his life, and was chief of the Molecular Virology Section in the Laboratory of Molecular Microbiology. His major research interest was around the human immunodeficiency virus (HIV-1) and HTLV-I, with an abundant production of more than 300 scientific publications on the molecular details of virus replication and relevant disease-causing mechanisms of viral pathogenesis. Teh was a true experimentalist with an interest in the implementation of new technologies to get to the next level of understanding of the biology of human pathogenic viruses. He only stopped bench work in 2004 when he became editor-in-chief of Retrovirology.

HTLV-1 is linked to the development of adult T-cell leukemia and a variety of inflammatory manifestations including HTLV-1 associated myelopathy. Teh was the first to show that HTLV-1 transcription is regulated through the cAMP signaling pathway implicating roles for CREB and CBP before these proteins were clearly identified and cloned. His research team also contributed to our understanding of how the viral Tax oncoprotein activates the pro-inflammatory factor NF-kB. More recently, he proposed a role for deubiquitinases in the regulation of TRAF6–mediated NF-kB signaling. Teh’s work has also advanced our understanding of genetic damage in virus-cellular transformation. In 1990, he first reported that the HTLV-1 Tax oncoprotein repressed DNA-repair. Thereafter, he characterized the important roles of dysregulated mitotic checkpoint and AKT activation in cellular transformation. His work has contributed to the elucidation of the role played by the spindle assembly checkpoint in oncogenesis, helping to explain how the loss of multiple checkpoints alters cancer tropism in vivo.

Teh had a long standing interest in understanding the viral and cellular factors that govern HIV-1 gene expression in infected human cells. In the late 1980s, Teh’s lab showed that HIV-1 uses an unprecedented mechanism of transcription that is dictated by an RNA-binding protein, Tat, which binds a nascent viral RNA target (TAR), the first RNA enhancer element ever described. Subsequently, Teh’s group characterized cellular RNA-binding proteins that regulate HIV-1 replication, including the TAR RNA binding protein (TRBP) that later became known as an important factor of the cellular RNA interference machinery. In recent work, his lab completed a genome-wide screening for human cell factors that are needed for HIV-1 replication. Using novel technology, Teh extended his interests in RNA-biology through the identification of small RNAs (i.e. siRNAs and miRNAs) that have biologically important roles in viral infection, cellular metabolism and virus-induced pathogenesis.

In addition to all these accomplishments, one of Teh’s greatest contributions to science probably lies in his role as mentor for young scientists. Teh trained 37 international postdoctoral fellows and 7 more are currently working in his group at the NIH. He has been a fantastic mentor of young scientists who have since spread across the globe, from Taiwan to China, from France to the Netherlands, from Canada to many places in the United States. Many flew into Washington DC to attend the funeral ceremony on February 9th. Teh was attentive, supportive and kind, but at the same time, demanding to his postdocs. Importantly, he set himself as an unselfish role model for them, working essentially 7 days per week and regular working days ran from 7 am to 7 pm. But, also during the evening and at night, one never had to wait long for reply emails. He was truly interested and at many times influenced the future careers of those who were lucky enough to have spent some time in his laboratory. In fact, his words of advice reached many more individuals with whom he came across in his professional and private life. His mentoring commitment is also reflected in his service to many professional societies. For instance, Teh was a standing member of the AIDS Molecular and Cellular Biology (AMCB) Study Section, where he had a reputation for being strongly supportive of new investigators.

Teh always had a special interest in the area of scientific publication. For instance, in 1994 he joined the editorial board of the Journal of Biomedical Science (JBS) of the National Science Council of Taiwan, the country in which he was born. He was an avid advocate for ways to improve the journal’s Impact Factor. He left this journal in 2004 to free himself for an important new activity: the launch of the journal Retrovirology, where he served as Editor-in-Chief since the journal’s inception. From the earliest years, Teh was an advocate of the Open Access publishing format. In particular, at the helm of Retrovirology, Teh witnessed much skepticism in regard to Open Access publishing during the early years and indomitably championed the new publishing format while overcoming initial prejudice. Teh often referred to himself and his Editorial Board members as the ‘Young Turks’ of virology, pioneering a new and exciting publishing format. Unsurprisingly, his talent for kicking off new initiatives paid off and Retrovirology is currently among the highest cited journals in the field of virology, and all of this was achieved in less than 10 years. In addition, he served on the editorial board of numerous journals, including the Journal of Virology and the Journal of Biological Chemistry.

Teh – as all who knew him will attest – would never rest on his laurels and although Retrovirology had become a leader in its field, he pushed for more journal involvement with the retroviral community .… and Frontiers in Retrovirology was born in 2009. It was the first conference organized by a BioMed Central journal – another example of Teh taking the lead – and proved to be such a universal success that the 3rd conference in the series will take place in September 2013 in the UK in Cambridge.

Teh was a scientist with a vision and a broad interest in all aspects of scientific endeavor. He also was a true scientific leader, initiating scientific debate, writing editorials, sitting on many committees, orchestrating new book volumes and organizing international meetings on diverse topics. For instance, he was president of the Society of Chinese Bioscientists in America (SCBA) in 2010 and voiced the strong opinion that the representation of Asian-American scientists in leadership positions should be increased. He was instrumental in the decision to take the 2011 SCBA conference to China.

He was the recipient of an extraordinary number of awards, most recently the International Retrovirology Association’s Dale McFarlin Award in 2011, BioMed Central’s Open Access “Editor of the Year” in 2010 and the John’s Hopkins University Woodrow Wilson Award in 2009. Teh was also elected to membership of prestigious societies such as the Academia Sinica in Taiwan, Fellowship in the American Academy of Microbiology, and Fellowship in the American Association for the Advancement of Science.

Teh had an infectious enthusiasm and winner’s mentality both at work and play. He was a skilled tennis and chess player, a gifted writer, and a great debater with strong opinions on virtually all subjects of science and life in general. Additionally, he had a passion for current events and a love of travel, movies, food and music.

Teh’s death is a blow to the retrovirus research community and we will sorely miss his scientific leadership. He has been central to so much of what we have accomplished together as well as being a supportive and generous friend to many of us individually. Teh’s life was much too short, but his legacy and our memories of him will last forever. Our hearts and condolences are with his wife Diane and his three children David (23), Diana (20), and John (15).

A note from the Publisher

  • Kuan-Teh Jeang was one of BioMed Central’s first academic Editors-in-Chief, launching Retrovirology on our platform in 2004. From the very beginning, his level of enthusiasm and energy was extraordinary, and the results he achieved in developing Retrovirologyshowed he was just as much of a dynamo as an Editor as he was in the laboratory.

  • Teh was a friend and close colleague to many at BioMed Central, past and present. His passing at such a young age caused shock and great sadness. He was simultaneously one of our most solid friends and supporters, while also being a tireless force driving change and improvement, reminding us not to sit on our laurels, and always ready with forthright but constructive criticism when he thought we needed to do better.

  • Teh took a “24x7” approach, and he encouraged those he worked with at BioMed Central to do the same. In return, he was generous with praise and each Christmas he would recognize the BioMed Central team which supported Retrovirology with thanks and gifts. Teh’s determination to make Retrovirology the leading journal in its field was striking, and his journal’s continuing progress up the impact factor rankings gave him huge satisfaction and pride, culminating in June 2012 when Retrovirology overtook Journal of Virology.

  • Teh recognized that, for open access to the results of scientific research to become a reality, a viable business model was crucial, and so he was always supportive of BioMed Central’s growth as a publisher. Introductions made by Teh helped BioMed Central to build its journal portfolio, especially in Asia, with Journal of Biomedical Science and Cell and Bioscience.

  • The success of Retrovirology demonstrated that a strong Editor-in-Chief could build a scientific community around an open access journal. Teh encouraged BioMed Central to take this community-building into the physical realm by arranging a scientific conference in association with the journal. The 3rd Frontiers of Retrovirology conference will be held this year, and the event has provided a template for BioMed Central’s growing number of successful journal-associated conferences.

  • Teh was a deserved winner of our 2010 Editor of the Year award, which he celebrated in London at BioMed Central’s 10th anniversary party (Figure 2). He will be sadly missed by all of us.

Teh's Affiliations

    1. Department of Medical Microbiology, Laboratory of Experimental Virology, Center for Infection and Immunity Amsterdam (CINIMA), Academic Medical Center, University of Amsterdam, Meibergdreef 15, Amsterdam, 1105 AZ, The Netherlands

      • Ben Berkhout

    2. Laboratoire de Virologie Moléculaire, Institut de Génétique Humaine, CNRS-UPR 1142, 141 rue de la Cardonille, 34296, Montpellier, cedex 5, France

      • Monsef Benkirane

    3. Department of Medicine, University of Cambridge, Addenbrooke's Hospital, Cambridge, CB2 0QQ, UK

      • Andrew Lever

    4. McGill University AIDS Centre, Lady Davis Institute, Jewish General Hospital, Montreal, Québec, Canada

      • Mark Wainberg

    5. The Wohl Virion Centre and MRC Centre for Medical & Molecular Virology, Division of Infection and Immunity, University College London, Cruciform Building, 90 Gower Street, London, WC1E 6BT, UK

      • Ariberto Fassati

    6. Nuffield Department of Clinical Medicine, University of Oxford, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Headington, Oxford, OX3 9DS, UK

      • Persephone Borrow

    7. Division of Virology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan

      • Masahiro Fujii

    8. BioMed Central, 236 Gray’s Inn Road, London, WC1X 8HB, UK

      • Srimathy Sriskantharajah

      • & Matthew Cockerill


J Biomed Sci. 2013; 20(1): 7.

Published online 2013 Feb 13. doi: 10.1186/1423-0127-20-7

PMCID: PMC3599596

PMID: 23406502

A Community Mourn The Death Of Dr. Kuan-Teh Jean

Dear colleagues,

Our loyal friend Dr. Kuan-Teh Jeang passed away unexpectedly on the evening of January 27, 2013. The following night and day an avalanche of emails went across the Retrovirus research community, starting in Australia, then Asia, Europe and America. Great shock and sorrow was apparent in the messages by the very many colleagues with whom Teh interacted over the years. Many of us came to know Teh (Additional file 1) as an energetic and gifted scientist for whom we had much respect and affection.

Teh was chief of the Molecular Virology Section in the Laboratory of Molecular Microbiology at the National Institutes of Health in Bethesda, USA. His major research interest was around the human immunodeficiency virus (HIV-1) and human T-cell leukemia virus (HTLV-I), with an abundant production of more than 300 scientific publications on the molecular details of virus replication and the disease-causing mechanisms. He trained over 30 postdoctoral fellows and had been a fantastic mentor of young scientists who have since spread across the globe, from Taipei to Hong Kong, from Montpellier to Amsterdam and from Montreal to Los Angeles.

Teh was a very dynamic and internationally oriented scientist and he always felt a special bond with the scientific community in Taiwan. He was born and spent his early childhood in Taiwan, and later learned to speak Mandarin fluently. He actively participated in the scientific review processes in the National Science Council and the National Health Research Institute and various universities, often travelling long distances to Taiwan to offer comments and suggestions on various aspects of science. He had deep affection towards his home land Taiwan and hence contacted the founding editor Prof. C.C. Chang and volunteered his service for the Journal of Biomedical Science (JBS) of the National Science Council of Taiwan, which was the only international journal sponsored by Taiwan government at that time. He joined the editorial board of JBS in 1994 and had been very influential since then. Teh was a stabilizing force during the formative years of JBS when the biomedical community in Taiwan was somewhat skeptical of an international journal with its Editorial Office based in Taiwan. After JBS was listed in the Journal citation Index in 1999, he was also an avid advocate for ways to improve its impact factor. It is largely due to his suggestions and sometimes unorthodox ideas that JBS jumped in the annual Impact Factor ranking. The creation of Vignettes, which was well-received by our readers, was one of those suggestions.

He left our board in 2004 to free himself for an important new activity: the launch of the Retrovirology journal, where he had been editor-in-chief since then. Again his talent to kick off new initiatives paid off and Retrovirology is currently among the highest cited journals in the field of virology, all achieved in less than 10 years. Since the early years, he had been an advocate of the Open Access publishing format. He was invited for the JBS editorial board meeting last September to present his current views on this topic and gave his most insightful suggestions. Teh always kept a special interest in Taiwan and its research activities, which led to several productive collaborations. He was also a champion for advocacy of the rights of Taiwanese scientists in international scientific organizations. He was elected as Academician of the Academia Sinica in 2008.

Teh was a scientist with a vision and a broad interest in all aspects of the scientific endeavors. He also was a true scientific leader, starting scientific debate, writing editorials, sitting on many committees, orchestrating new book volumes and organizing international meetings on diverse topics. For instance, he was president of the Society of Chinese Bioscientists in America (SCBA) in 2010 and voiced a strong opinion to increase the representation of Asian-American scientists in leadership positions.

Teh's death is a blow to the retrovirus research community and we will sorely miss his scientific leadership. He has been central to so much of what we have done together as well as being a supportive and generous friend to many of us individually. In his spirit, several initiatives have been proposed over the last couple of days by his students and colleagues to honor his legacy. Teh was only 54 years old and the loss is devastating for the Jeang family. Our thoughts and condolences are with his wife Diane and his children David, John and Diana.

Present and past members of the Editorial Board

Journal of Biomedical Science

2010 (June 30) - Chronic-Fatigue Link to Virus Disputed : Wall Street Journal - "One Research Group Finds Virus XMRV in the Blood of Syndrome Sufferers, One Does Not; Papers Held From Publication"

Source - [HN00SW][GDrive]

Two groups of researchers studying a potential link between chronic-fatigue syndrome and a virus called XMRV have reached contradictory conclusions, according to people familiar with the findings.

One group found a link, and the other didn't.

Their reports were held from publication after being accepted by two science journals—a rare move that has caused a stir among scientists in the field.

A paper published in October in the journal Science first identified XMRV in people with chronic-fatigue syndrome. Studies published later by other groups produced conflicting results on whether there was a link, leading to intense scientific debate over the Science report's meaning.

The Centers for Disease Control and Prevention estimates that between one million and four million people in the U.S. have chronic-fatigue syndrome, which is characterized by debilitating fatigue and chronic pain. Doctors tend to treat the symptoms, but there are no established, specific treatments.

Many patients, desperate for answers as to the cause of the condition, pinned a great deal of hope on the original findings.

Scientists at the Food and Drug Administration and the National Institutes of Health, including NIH infectious-disease specialist Harvey Alter, recently finished research that came to a conclusion similar to that of the Science paper—that XMRV, or xenotropic murine leukemia virus-related virus, is found in the blood of chronic-fatigue syndrome patients.

The paper was accepted for publication in the journal Proceedings of the National Academy of Sciences of the United States of America but is on hold, according to Ashley Truxon, media coordinator for the journal. She had no further comment.

Separately, scientists at the CDC, led by microbiologist William Switzer, concluded in a paper in another journal, Retrovirology, that they couldn't find XMRV in the blood of people with chronic-fatigue syndrome, according to people familiar with the situation.

Kuan-Teh Jeang, editor-in-chief of Retrovirology, said the Switzer paper went through peer review and was accepted for publication when he got a call from the authors earlier this month. They asked that the Retrovirology paper be held.

"My understanding was HHS [Department of Health and Human Services] wanted to get it straightened out. Both reports are from different branches of the government," Dr. Jeang said.

In an email between scientists familiar with the situation, viewed by the Wall Street Journal, a researcher said the two teams were asked to put their papers on hold because senior public-health officials wanted to see consensus—or at least an explanation of how and why the papers reached different conclusions, said the people familiar with the situation.

A spokesman for Department of Health and Human Services said the research was being reviewed. "All of these activities need to be completed in order to ensure HHS's commitment to the accuracy and relevancy of the scientific information it reports.''

Dr. Switzer and representatives of the FDA, CDC and NIH said they couldn't comment until the papers were published. Dr. Alter couldn't be reached for comment.

Publication of results is considered a critical part of the scientific process, and researchers familiar with the situation said they were puzzled by the move. It is unusual for a paper to be held after it has already gone through the formal peer-review process and been accepted for publication, say scientists who publish frequently.

"It's fair to say it's not a usual kind of thing," said John M. Coffin, a special adviser to the National Cancer Institute and a professor at Tufts University in Boston who wrote an editorial alongside the Science report in October. Dr. Coffin said he couldn't comment specifically on the XMRV papers, but that scientists often come up with conflicting data, especially when a virus is new and not well understood as is the case of XMRV.

Fred Friedberg, who has chronic-fatigue syndrome and is president of the International Association for Chronic Fatigue Syndrome, said that because the science on XMRV and the illness wasn't yet clear, it is crucial that data on XMRV be published.



Publication of XMRV papers should not be blocked

30 JUNE 2010

The findings by the NIH and FDA that XMRV is associated with chronic fatigue syndromehas been accepted for publication by the Proceedings of the National Academy of Sciences (PNAS). Release of the article has been blocked by PNAS due to work carried out by the US Centers for Disease Control and Prevention (CDC). That study, which was submitted to Retrovirology, failed to find a link between XMRV and CFS. Its publication has also been placed on hold. According to ScienceInsider:

The contradiction has caused “nervousness” both at PNAS and among senior officials within the Department of Health and Human Services, of which all three agencies are part, says one scientist with inside knowledge.

It is senseless to block publication because the two papers reach different conclusions. If both manuscripts were subjected to proper peer-review, and were deemed acceptable by the referees, then they should be published. The journal editorial offices must respect the opinions of the reviewers. By overriding their decisions, they have compromised the entire peer reviewer process.

Blocking publication also sends the wrong message to CFS patients, to the public, and scientists. Not only does this action raise suspicions about their motives – are they trying to publish only the result they believe is correct? – but it ignores the very important fact that science is self correcting. Scientists are humans, and they make mistakes. But eventually the right answer will come to the surface. And that is why PNAS and Retrovirology should respect peer review, publish the XMRV papers, and let science correct itself.

Author links open overlay panelMark A.Wainberg1Kuan-TehJeang2

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https://doi.org/10.1016/j.chom.2011.04.001Get rights and content

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Xenotropic murine leukemia virus-related virus (XMRV) has been proposed to be associated with prostate cancer and chronic fatigue syndrome (CFS). This proposition has been controversial because many investigators have failed to replicate the reported associations. Here, we explore whether XMRV is an authentic human pathogen in the light of recent findings that indicate otherwise.

Main Text


Xenotropic murine leukemia virus-related virus (XMRV) is a recently described gammaretrovirus that was originally detected in and molecularly cloned from a human prostate cancer (Urisman et al., 2006). A later paper reported that XMRV was present in the blood of 67% of patients with chronic fatigue syndrome (CFS) and in 4% of healthy controls (Lombardi et al., 2009). Since these publications, some investigators have detected XMRV in human prostate cancer samples while others have not (Silverman et al., 2010, Aloia et al., 2010). Aside from a single study that reported finding polytropic murine leukemia virus sequences (a virus related to but different from XMRV) in 87% of CFS samples (Lo et al., 2010), all other reports (at least seven) have failed to detect XMRV in CFS patients from Europe, China, and the U.S. (van der Kuyl et al., 2011).

The current state of XMRV as a human pathogen is controversial and remains confounding even to the most knowledgeable retrovirology aficionados. In this context, it is important to frame two separate issues for consideration. First, is XMRV a physiologically prevalent pathogen in humans? Second, based on where the virus has been detected in humans, is XMRV a passenger microbe or is it causal for prostate cancer and/or CFS?

XMRV Can Infect Human Cells

The receptor for XMRV is XPR1, a cell-surface protein ubiquitously expressed in many human and animal cells. Although XMRV was originally described as infecting human prostate stromal cells (Urisman et al., 2006), in vitro assays show that the virus can infect and replicate in various human, feral mouse, mink, monkey, and bovine cell lines (Stieler et al., 2010). A recent intravenous infection study of eight adult Indian rhesus macaques (five infected and three mock-infected controls) used immunohistochemical staining and in situ hybridization-based assays to show that the virus was widely disseminated in vivo. Infected tissues included lymphoid organs (CD4-positive cells) as well as the prostatic epithelium and reproductive tract (Onlamoon et al., 2011). These results show that XMRV has the capability to infect humans. Nevertheless, some of the controversy surrounding XMRV centers on the possibility that detection of this virus in human samples is due to contamination from mouse cells (Smith, 2010). A significant argument against this stance was the identification of 14 XMRV integrated proviral sequences in 9 human prostate cancers (Kim et al., 2008). However, a recent report showed that 2 of these 14 integrated proviral sequences were contaminants from an experimentally infected cell line that was propagated in the laboratory, raising the question of whether the other 12 reported XMRV prostate-cancer integration sequences may not also be erroneously tainted results (Garson et al., 2011).

Unlike other human pathogenic/oncogenic viruses such as human T cell leukemia virus (HTLV-1) or human papilloma virus (HPV) (Table 1), there is currently no conclusively reproducible epidemiological link for an XMRV-related human disease (prostate cancer or CFS) or a natural XMRV reservoir in humans, mice or other animals (Figure 1). In contrast to other “newly discovered” viral infections such as the severe acute respiratory syndrome (SARS) coronavirus or avian influenza virus, the infection source of XMRV for humans has remained elusive. Indeed, some investigators have argued that the high conservation of XMRV genome sequences reported from different geographic locales by multiple laboratories are inconsistent with significant infection or extensive replication of this virus in humans (Hué et al., 2010).

2011 (August)


Equal versus equivalent access to the scientific literature

Retrovirology volume 8, Article number: 83 (2011) Cite this article

The concepts of equal versus equivalent access to the scientific literature are discussed

In 1954, the United States Supreme Court in a landmark decision of Brown vs. Board of Education of Topeka, Kansas sharply repudiated the "separate but equal" principle of public education. The Court concluded that racially segregated education is "inherently unequal". In scientific publishing today, there exist two segregated means of knowledge dissemination --- the subscription journals and the Open Access (OA) journals. For those who can pay, there is immediate access to scientific papers published in both subscription and OA journals; those who cannot pay can access only OA journals. The status quo is thus an "inherently unequal" playing field between the "haves" and the "have nots".

How unequal is the current situation? In an August 1, 2011 posting on the Nature Newswebsite, Richard Van Noorden reported that "the proportion of research papers freely available is slowly and steadily creeping upwards... in 2009, it's above 28%. (Some of this literature is not immediately available at the time that it is published, because of journal policies that impose embargo periods on when material can become free)". The good news is that approximately 30% of published papers can be accessed freely. The bad news is that 70% of published, publicly funded research remains off-limits to those who cannot pay.

Can equal access be had by the "haves" and the "have nots"? To the extent that the subscription and OA tracks will likely co-exist, the foreseeable future is a "separate and unequal" reality. Without equal access, the next best goal is perhaps to achieve equivalent access.

What is equivalent access? Imagine two very similar papers reaching essentially the same conclusions; one is published in a subscription journal and the other published in an OA journal. The paying reader can read both papers; the non-paying person can read only the OA paper. This is "unequal" access. However, if the OA paper sufficiently conveys the same information as the subscription paper, then it is possible that "equivalent" knowledge is conveyed to both the can-pay and cannot-pay audiences.

The equivalent access concept works only if subscription and OA journals can attract and publish, in chronological proximity, similar articles of comparable quality and impact. Practically speaking, for this to occur, OA journals need to achieve quality metrics (e.g. Impact Factor numbers) that match their subscription counterparts. The Retrovirologyexperience suggests that such benchmark can be achieved (Figure 1).

Assorted Notes


Molecular Mechanisms Of Human Immunodeficiency Virus Trans-regulatory Proteins

Jeang, Kuan-Teh National Institute of Allergy and Infectious Diseases

This project focuses on HIV-1 replication in cultured cells to develop understandings of viral pathogenesis and the cellular factors that influence viral gene expression. Examples of important scientific advances that we have achieved in the 2011 to 2012 period are outlined below. RNA helicases are ubiquitous in plants and animals and function in many cellular processes. Retroviruses, such as human immunodeficiency virus (HIV-1), encode no RNA helicases in their genomes and utilize host cellular RNA helicases at various stages of their life cycle. We have continued our study of RNA helicases in HIV-1 replication. We have identified several novel RNA helicases that activate HIV-1 post-transcriptional gene expression and an RNA helicase that represses HIV-1 replication through the interferon pathway. HIV-1 Tat protein recruits host cell factors including CDK9/cyclin T1 to HIV-1 TAR RNA and thereby induces HIV-1 transcription. An interaction with host Ser/Thr protein phosphatase-1 (PP1) is critical for this function of Tat. PP1 binds to a Tat sequence, Q(35)VCF(38), which resembles the PP1-binding """"""""RVxF"""""""" motif present on PP1-binding regulatory subunits. We have found that expression of PP1 binding peptide, a central domain of Nuclear Inhibitor of PP1, disrupted the interaction of HIV-1 Tat with PP1 and inhibited HIV-1 transcription and replication. We have identified small molecule compounds that target the """"""""RVxF""""""""-binding cavity of PP1 to disrupt the interaction of PP1 with Tat and inhibit HIV-1 replication. One of the compounds, 1H4, inhibited HIV-1 transcription and replication at non-cytotoxic concentrations. Our study shows that HIV- inhibition can be achieved through using small molecules to target a non-catalytic site of PP1. We have constructed several HIV-1 molecular clones, each containing a discrete cellular miRNA positioned in Nef. These retroviral genomes express the inserted miRNA and are generally replication competent in T-cells. The inserted intragenomic miRNA was observed to elicit two different consequences for HIV-1 replication. First, the expression of miRNAs with predicted target sequences in the HIV-1 genome was found to reduce viral replication. Second, in one case, where an inserted miRNA was unusually well-processed by Drosha, this processing event inhibited viral replication. Our work is the first study to examine in detail the replication competence of HIV-1 genomes that express cis-embedded miRNAs. The results indicate that a replication competent retroviral genome is not precluded from encoding and expressing a viral miRNA. In FY 2013, we published our findings that NEAT1 long noncoding RNA and paraspeckle bodies modulate HIV-1 posttranscriptional expression. Most of the human genome is transcribed into protein-noncoding RNAs (ncRNAs), including small ncRNAs and long ncRNAs (lncRNAs). Over the past decade, rapidly emerging evidence has increasingly supported the view that lncRNAs serve key regulatory and functional roles in mammal cells. HIV-1 replication relies on various cell functions. To date, while the involvement of host protein factors and microRNAs (miRNAs) in the HIV-1 life cycle has been extensively studied, the relationship between lncRNAs and HIV-1 remains uncharacterized. Here, we have profiled 83 disease-related lncRNAs in HIV-1-infected T cells. We found NEAT1 to be one of several lncRNAs whose expression is changed by HIV-1 infection, and we have characterized its role in HIV-1 replication. We reported that the knockdown of NEAT1 enhances virus production through increased nucleus-to-cytoplasm export of Rev-dependent instability element (INS)-containing HIV-1 mRNAs.