Three Big Books

Tuesday, December 16, 2014

Hemispherx's Ampligen(R) Provides Anti-Tumor Activity

Cytokine expression in CFS and GWS: A distinction without a difference?

Cytokine expression provides clues to the pathophysiology of Gulf War illness and myalgic encephalomyelitis

Chronic Fatigue Syndrome and Exercise

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Julian Lake's The Chronic Fatigue Syndrome Follies: Cartoons about an epidemic of lies. Now in print or on Kindle and free on Kindle Unlimited.

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The title of this collection of cartoons by Julian Lake was inspired by the The March of Folly, a stunning work by the late Barbara Tuchman. To try and explain why certain political disasters in history have occurred, Tuchman uses the very apt construct of "folly," which she defines as the "pursuit of policy contrary to the self-interest of the constituency or state involved." Tuchman analyzes four periods in history that are characterized by enormous folly. Julian Lake's collection is in many ways about a fifth example of such a phenomenon. Surely the last two decades in which so-called "Chronic Fatigue Syndrome" has been called "mysterious" over and over in a cult-like manner (and in the manner of the Big Lie) qualifies as another period of egregious folly. Anyone who has read the lucid journalism of Neenyah Ostrom and Hillary Johnson on "Chronic Fatigue Syndrome" knows precisely what this is  alluding to. And if you don't know, you should find out, lest you be caught aiding and abetting this great folly. That an epidemic as serious as "Chronic Fatigue Syndrome," and so obviously connected to the AIDS epidemic, could be treated to this very day as a "mystery" by the government, by researchers, by the media, and even by most of the patients, has not reduced Julian Lake to tears, for like most humorists, this great tragedy--and folly--is at times, downright funny. Morbid maybe, perhaps dark, and maybe of the gallows school of comedy, but still funny. Julian Lake has tried to capture the folly of two decades of an obvious Chronic Fatigue Syndrome coverup in a manner that is surprisingly three-dimensional, given his hostility to the medical establishment that has been playing deadly political games with CFS. While trying to use humor to capture the horrific plight of CFS patients, in Julian Lake’s democratically mischievous world view, some of the CFS patients have themselves become little emperors without you-know-what. In this collection of cartoons, Julian Lake has given us a rich universe of CFS folly. Unless your easily offended and suffer from CFS political correctness (a new CFS symptom?), don't be afraid to enter Julian Lake’s zany world and have a few laughs. After all, laughter boosts your immune system. And maybe from a political viewpoint, the best antidote to folly is hum

Herpes virus rearranges telomeres to improve viral replication

 Herpesvirus Genome Integration into Telomeric Repeats of Host Cell Chromosomes


It is well known that numerous viruses integrate their genetic material into host cell chromosomes. Human herpesvirus 6 (HHV-6) and oncogenic Marek's disease virus (MDV) have been shown to integrate their genomes into host telomeres of latently infected cells. This is unusual for herpesviruses as most maintain their genomes as circular episomes during the quiescent stage of infection. The genomic DNA of HHV-6, MDV, and several other herpesviruses harbors telomeric repeats (TMRs) that are identical to host telomere sequences (TTAGGG). At least in the case of MDV, viral TMRs facilitate integration into host telomeres. Integration of HHV-6 occurs not only in lymphocytes but also in the germline of some individuals, allowing vertical virus transmission. Although the molecular mechanism of telomere integration is poorly understood, the presence of TMRs in a number of herpesviruses suggests it is their default program for genome maintenance during latency and also allows efficient reactivation.

Findings lead to better understanding of how viruses replicate and role of telomeres in stopping viruses

IMAGE: This is Paul Lieberman, Ph.D., of The Wistar Institute.

Click here for more information.
PHILADELPHIA - (Dec. 11, 2014) - A team of scientists, led by researchers at The Wistar Institute, has found that an infection with herpes simplex virus 1 (HSV-1) causes rearrangements in telomeres, small stretches of DNA that serve as protective ends to chromosomes. The findings, which will be published in the Dec. 24 edition of the journal Cell Reports, show that this manipulation of telomeres may explain how viruses like herpes are able to successfully replicate while also revealing more about the protective role that telomeres play against other viruses.
"We know that telomeres play a very important part in the lifespan of a cell," said Paul M. Lieberman, Ph.D., Hilary Koprowski, M.D., Endowed Professor and Professor and Program Leader of the Gene Expression and Regulation Program at The Wistar Institute. "We wanted to know whether they also play a role in either viral replication or protection from viruses, and our findings suggest - at least in the case of the herpes simplex virus - that this may indeed be the case."
Telomeres are often compared to the clear tips of shoelaces because they protect the end of chromosomes - the keepers of our vital genetic information - and prevent them from fraying and breaking, thus preserving their ability to pass on necessary genetic information. Previously, Lieberman's lab at Wistar has shown that viral DNA replication and maintenance share some common features with telomeres.
"Telomeres may serve as a barrier to viral replication," Lieberman said. "We wanted to explore whether that protection was at a physical level or a more molecular level."
Among the viruses Lieberman and his lab have decided to study is HSV-1, a particularly aggressive virus that replicates in the nucleus of a healthy cell where chromosomes and their telomeres reside. HSV-1 is a common virus that causes cold sores but can also cause more serious diseases including blindness and encephalitis. In the United States, approximately 65 percent of the population has antibodies to this particular strain of the virus as well as latent infections that can periodically reactivate to cause clinical symptoms. There is no vaccine for preventing HSV-1 infection and reactivation, and only a few effective treatments for the virus are available.
As detailed in the study, the Lieberman lab found that HSV-1 is able to induce the transcription of telomere repeat-containing RNA (TERRA). This is followed by the virus degrading a telomere protein called TPP1 - part of a complex of proteins responsible for protection called "telomere sheltering" - which results in the loss of the telomere repeat DNA signal. When TPP1 becomes inhibited, the virus is able to increase its ability to replicate, suggesting that TPP1 normally provides some sort of protective function against this virus. HSV-1 is able to replicate more efficiently by disabling this protection. Finally, the virus uses a replication protein called ICP8 that works with the manipulated telomeric proteins to promote viral genomic replication.
"This study expands our knowledge of telomeres further in two very important ways," Lieberman said. "First, it gives us an indication that some viruses are able to manipulate telomeres specifically in order to replicate. Second, it appears that proteins like TPP1 provide very specific protective functions. These findings allow us to ask additional questions and better understand just how telomeres may protect cells from viral infection."
This work was supported by an American Heart Association grant (11SDG5330017) and a National Institutes of Health grant (RO1CA140652). This work was also supported by the Institute's National Cancer Institute Cancer Center Support Grant (P30CA010815) and the Commonwealth Universal Research Enhancement Program, Pennsylvania Department of Health.
Members of the Lieberman laboratory who co-authored this study include Zhong Deng, Olga Vladimirova, Jayaraju Dheekollu, and Zhuo Wang. Other authors from The Wistar Institute included Scott E. Hensley, Susan Janicki, Jaclyn L. Myers, and Alyshia Newhart. Other authors included Eui Tae Kim and Matthew D. Weitzman from the Department of Pathology and Laboratory Medicine at the University of Pennsylvania Perelman School of Medicine and The Children's Hospital of Philadelphia; Dongmei Liu and Jennifer Moffat from the Department of Microbiology and Immunology at State University of New York Upstate Medical University; Nigel W. Fraser from the Department of Microbiology at the Perelman School of Medicine at the University of Pennsylvania; and David M. Knipe from the Department of Microbiology and Immunobiology at Harvard Medical School.
The Wistar Institute is an international leader in biomedical research with special expertise in cancer research and vaccine development. Founded in 1892 as the first independent nonprofit biomedical research institute in the country, Wistar has long held the prestigious Cancer Center designation from the National Cancer Institute. The Institute works actively to ensure that research advances move from the laboratory to the clinic as quickly as possible. The Wistar Institute: Today's Discoveries - Tomorrow's Cures. On the Web at

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Everyone needs to know what the CDC is hiding about CFS and HHV-6. NEW YORK NATIVE contains both volumes of THE CHRONIC FATIGUE SYNDROME EPIDEMIC COVER-UP. The print version is $23. Only $7.98 in Kindle.

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