Adenoviruses Cause COPD

It has always been obvious merely from looking at the scatter plots in old studies of lung function that, among both smokers and nonsmokers, certain individuals were distinctly abnormal. They had much higher rates of loss than the others. There was a higher proportion of abnormal individuals among the smokers, and, by ignoring these individual differences and lumping together all smokers versus all nonsmokers, the anti-smoking ideologues falsely implicated tobacco as the cause of chronic obstructive pulmonary disease (COPD).

Adenoviruses were first discovered in 1953 (Isolation of a cytopathic agent from human adenoids undergoing spontaneous degeneration in tissue culture. WP Rowe, RJ Huebner*, LK Gilmore, RH Parrott. Proc Soc Exp Biol Med 1953;84:570-573; and: Recovery of new agents from patients with acute respiratory illness. MR Hilleman, JH Werner. Proc Soc Exp Biol Med 1954;85:183-188). (*This is our old "friend" Robert J Huebner of the National Cancer Institute's Cancer Virus Program, who failed to find any despite the vast sums of money at his disposal, see "The Lasker Syndicate.") For over 40 years, investigation of the role of adenoviruses in chronic diseases has been superficial or nonexistent. Only recently, particularly since the successful lynching of the tobacco companies, has a tiny trickle of this kind of research begun to appear, always with the politically correct anti-smoker spin, and under the supervision of big shots in the ALA's American Thoracic Society, particularly JC Hogg.

Latent adenoviral infection in the pathogenesis of chronic airways obstruction. T Matsuse, S Hayashi, K Kuwano, H Keunecke, WA Jefferies, JC Hogg. Am Rev Respir Dis 1992 Jul;146(1):177-184. The American Review of Respiratory Disease and its successor, the American Review of Critical Care Medicine, is the organ of the American Thoracic Society, which was formed as a division of the American Lung Association.

Endotoxin-specific NF-kappa-B activation in pulmonary epithelial cells harboring adenovirus E1A. N Keicho, Y Higashimoto, GP Bondy, WM Elliot, JC Hogg, S Hayashi. Am J Physiol 1999;277(Lung Cell Mol Physiol 21):L523-L532. "Studies from our laboratory showed that greater copy numbers of the E1A DNA from Group C adenovirus are found in the lungs of smokers with chronic obstructive pulmonary disease than in smokers without airways obstruction and that E1A proteins are detected in lung epithelial cells of these patients."

Effect of adenovirus E1A on ICAM-1 promoter activity in human alveolar and bronchial epithelial cells. Y Higashimoto, N Keicho, WM Elliot, JC Hogg, S Hayashi. Gene Expr 1999;8(5-6):287-297. "Because adenovirus E1A gene products are known to regulate the expression of many genes by interacting with cellular transcription factors, we postulated that E1A enhances the production of inflammatory mediators and exacerbates the inflammatory process in smokers' lungs." This is pure Political Correctness, because contrary to the lies we've been brainwashed with, most smokers don't have any such "inflammatory process" and some nonsmokers do.

New treatments proposed for chronic obstructive pulmonary disease. Lisa Melton, The Lancet Interactive 2000 Feb 5. "James Hogg (St. Paul's Hospital, Vancouver, Canada) believes that, in patients with COPD, latent adenoviral infection might amplify the inflammation that cigarettes trigger in all smokers. His team has detected large amounts of an adenoviral protein in lung samples from patients with COPD, localised to areas of inflammation and emphysema."

Amplification of inflammation in emphysema and its association with latent adenoviral infection. I Retamales, WM Elliott, B Meshi, HO Coxson, PD Pare, FC Sciurba, RM Rogers, S Hayashi, JC Hogg. Am J Respir Crit Care Med 2001 Aug 1;164(3):469-473. These charlatans compare "patients with similar smoking histories and either no (n=7), mild (n=7), or severe emphysema (n=7), and illogically conclude that "cigarette smoke-induced lung inflammation [which most smokers don't have -cast] is amplified in severe emphysema and that latent expression of the adenoviral E1A protein expressed by alveolar epithelial cells influenced this amplification process."

(Comment on Retamales et al.) End-stage chronic obstructive pulmonary disease: the cigarette is burned out but inflammation rages on. SD Shapiro. Am J Respir Crit Care Med 2001 Aug 1;164(3):339-340.

[Latent adenovirus infection in chronic obstructive pulmonary disease.] B He, M Zhao, X Li. Zhonghua Jie He He Hu Xi Za Zhi 2001 Sep;24(9):520-523. "The E1A region of adenovirus was found in the epithelial cells of COPD and chronic bronchitis patients (27%), not found in the patients with asthma and normal volunteers. Furthermore, E1A DNA was much more commonly in the COPD patients (50%) than in the patients with chronic bronchitis (8%) (P<0.05). CONCLUSIONS: Latent adenoviral infection was present in the stable stage of COPD and may be related to the pathogenesis of the disease."

Role of latent viral infections in chronic obstructive pulmonary disease and asthma. JC Hogg. Am J Respir Crit Care Med 2001 Nov 15;164(10 Pt 2):S71-S75. A propaganda study with guinea pigs. Quoth Hogg: "Acute viral respiratory tract infections are well known to precipitate asthma attacks and acute exacerbations of chronic obstructive pulmonary disease, but their role in the pathogenesis of chronic disease is poorly designed." And why is this this case, Dr. Hogg? Haven't you and your ATS cronies known about the disintegrating effects of adenoviruses since the 1950s? And purposely stifled the research so you could blame smoking?

Emphysematous lung destruction by cigarette smoke. The effects of latent adenoviral infection on the lung inflammatory response. B Meshi, TZ Vitalis, D Ionescu, WM Elliot, C Liu, XD Wang, S Hyashi, JC Hogg. Am J Respir Cell Mol Biol 2002 Jan;26(1):52-57. Another rehash of Hogg's guinea pig study. Another question: Why does it seem as if James C. Hogg and his friends are the only ones allowed to investigate and/or publish on this subject, at least in the western literature?

COPD Prevalence in Lifetime Nonsmokers

While admitting that COPD occurs in only "15-20% of heavy, long-term cigarette smokers," they fail to acknowledge that 4 to 6% of lifelong nonsmokers have physician-diagnosed COPD as well (Chronic obstructive pulmonary disease in lifelong nonsmokers: results from NHANES. AS Whittemore, SA Perlin, Y DiCiccio. Am J Public Health 1995 May;85(5):702-706), with COPD defined as chronic bronchitis or emphysema. The lie the health establishment has been pounding into us for decades that COPD is "vanishingly rare" in lifelong nonsmokers is explicitly rejected by Whittemore et al. While spin-doctoring their work with the specious reservation that it failed to measure exposure to environmental tobacco smoke, they nevertheless admit that "Despite these reservations, some conclusions seem warranted. In particular, the disease is not vanishingly rare in nonsmokers. The overall prevalence in [never-smoking] adults aged 18 to 74 is about 4% to 6%."

Airway obstruction in never smokers: results from the Third National Health and Nutrition Examination Survey. BR Celli, RJ Halbert, RJ Nordyke, B Schau. Am J Med 2005 Dec;118(12):1364-1372. "Never smokers represented 42% of the Third National Health and Nutrition Examination Survey population aged 30 to 80 years, with obstruction prevalence of 91 per 1000. Never smokers accounted for 4.56 million cases of obstruction, or 23% of the total burden."

COPD and Social Class

It has long been known that adenovirus infection is more common in the lower socioeconomic classes, just as Whittemore et al. found in their study of lifelong nonsmokers, where the percentages of physician-diagnosed COPD by income ranged from 2.7% to 5.6% in men, and 3.8% to 6.9% among women. Since smokers are more likely to be from the lower socioeconomic classes, smokers are more likely to be exposed to this infection. Exposure to infection, not ETS, is the most important confounder, and socioeconomic class is only an inadequate proxy for this true confounder. Furthermore, it has been known since 1962 that certain strains of adenovirus, notably Ad12, are known to be carcinogenic in animals, and the main difference between the carcinogenic and noncarcinogenic strains is in their ability to escape immune detection to cause a chronic infection. It has also long been known that adenoviruses interact with other oncogenic viruses, inlcuding polyoma, papilloma, and hepatitis viruses. The health establishment has purposely eschewed research of the appropriate level of sophistication in order to falsely blame smoking and passive smoking.

James C. Hogg

Meanwhile, the central investigator in these studies of adenoviruses and COPD, James C. Hogg, MD, of St. Paul's Hospital and professor of pathology at the University of British Columbia in Vancouver, has been the focus of defamatory propaganda. Dr. Terry Polevoy, who bills his website as the biggest anti-smoker site in Canada, attacks Hogg for accepting tobacco industry funding. But Polevoy fails to mention Hogg's long history of Politically Correct studies on both active and passive smoking, not to mention Hogg's listing in "Who's Who in ATS" of August 1997. Furthermore, Polevoy's supposed exposé of Hogg's long involvement with the tobacco companies, dating back to 1979 in Stanton Glantz's tobacco documents, actually implicates the tobacco lawyers in a long-term conspiracy with the anti-smokers. They could have been funding research on infection all along, but they didn't. In 1979, Hogg was "dosing guinea pigs with antigens to create inflammatory processes in the airways," in order to bolster the anti-smokers' claims.

In 1983, Hogg was an International Advisor of the Aspen Lung Conference, sponsored by the Skull & Bones-controlled Webb-Waring Institute for Medical Research.

Polevoy also fails to mention the money that Hogg has gotten for this research from the US National Institutes of Health: "Emphysema research gets $1.26 million boost (November 2000). Pulmonary researcher Jim Hogg has received $1.26 million Cdn over four years from the US funding agency, National Institutes of Health, to pursue his groundbreaking research on the causes of emphysema...."

Since Hogg is clearly a powerful member in good standing of the anti-smoker health establishment, Polevoy's attacks will have no effect on his professional status. Only ignorant members of the public (and media) would be influenced to believe that Hogg is a tobacco industry stooge so his work should be dismissed. And this enables the health establishment to maintain the two-faced system of science that it has nurtured over many decades: A public science of official lies and propaganda, versus a secret science that is known by only a tiny educated elite.

Adenovirus Mechanisms

Pulmonary Immunity to Viral Infection: Adenovirus Infection of Lung Dendritic Cells Renders T Cells Nonresponsive to Interleukin-2. AT Thiele, TL Sumpter, JA Walker, Q Xu, C-H Chang, RL Bacallao, R Kher, DS Wilkes. J Virol. 2006 Feb;80(4):1826-1836. "Results suggest that Ad-infected DCs induce T cells to be nonresponsive to IL-2 during primary coculture, as the addition of IL-2 in secondary cultures recovered T-cell proliferation. In vivo studies supported in vitro results showing that Ad infection resulted in lung T cells with decreased proliferative ability. This study demonstrates that Ad infection induces local immunoincompetence by altering DC-T-cell interactions."

Other Viruses

Respiratory Viruses Augment the Adhesion of Bacterial Pathogens to Respiratory Epithelium in a Viral Species- and Cell Type-Dependent Manner. V Avadhanula, CA Rodriguez, JP DeVincenzo, Y Wang, RJ Webby, GC Ulett, EE Adderson.
J Virol 2006 Feb;80(4):1629-1636. "All viruses enhanced bacterial adhesion to primary and immortalized cell lines. RSV and HPIV-3 infection increased the expression of several known receptors for pathogenic bacteria by primary bronchial epithelial cells and A549 cells but not by primary small airway epithelial cells. Influenza virus infection did not alter receptor expression. Paramyxoviruses augmented bacterial adherence to primary bronchial epithelial cells and immortalized cell lines by up-regulating eukaryotic cell receptors for these pathogens, whereas this mechanism was less significant in primary small airway epithelial cells and in influenza virus infections. Respiratory viruses promote bacterial adhesion to respiratory epithelial cells, a process that may increase bacterial colonization and contribute to disease. These studies highlight the distinct responses of different cell types to viral infection and the need to consider this variation when interpreting studies of the interactions between respiratory cells and viral pathogens."

Miscellaneous

"Patients who are prescribed long term oxygen for chronic chest disease have usually been heavy smokers and many continue to smoke. Indeed research in the United States shows that half such patients are in rooms where someone is smoking within 10-15 feet of the machine--so the relative rarity of fire calamities (Respiratory Care 1983; 28: 906-12) reflects the fact that oxygen is neither explosive nor combustible. The plastic delivery tubing, however, will burn furiously if ignited while carrying pure oxygen." (News and Notes. British Medical Journal, 1983 Sep 17;287(6395):842.)

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cast 06-24-08