Recovery of Cytopathogenic Agent from Chimpanzees with Goryza

Morris, J. A.; Blount, R. E.; Savage, Russelle .

doi:10.3181/00379727-92-22538

Cited by 441 publications

(135 citation statements)

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“…RSV was first identified in 1956 as the agent that caused chimpanzee coryza [6]. The virus belongs to the Paramyxoviridae family, where it has been assigned a genus of its own, Pneumovirus.…”

Section: The Virusmentioning

confidence: 99%

Relationship between respiratory syncytial virus bronchiolitis and future obstructive airway diseases

Wennergren¹,

Kristjánsson²

2001

Eur Respir J

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Relationship between respiratory syncytial virus bronchiolitis and future obstructive airway diseases. G. Wennergren, S. Kristjánsson. #ERS Journals Ltd 2001. ABSTRACT: Evidence from a large number of prospective case-control studies shows that respiratory syncytial virus (RSV) bronchiolitis in infancy is often associated with recurrent wheezing and asthma during subsequent years. However, wheezing tends to diminish and most studies show no significant increase in wheezing compared to controls by school age or adolescence. An unresolved question is whether severe RSV infection during infancy causes the respiratory sequelae or inherent abnormalities predispose an infant to develop severe respiratory infection and sequelae, i.e. RSV is associated with the development of pulmonary sequelae.Studies on long-term outcome of RSV bronchiolitis are reviewed from an evidencebased perspective.The majority of prospective placebo-controlled studies do not show any long-term beneficial effects of corticosteroid treatment, i.e. the risk of subsequent wheezing is not diminished by the treatment. The evidence for an increased risk of allergic sensitization after RSV bronchiolitis is not nearly as strong as the evidence for an increased risk of subsequent wheezing. In fact, most studies do not show any significant increase in atopy after RSV bronchiolitis. This suggests that the increased risk of wheezing after RSV is not linked to an increased risk of atopy. There are some indications that infants who develop severe RSV and subsequent wheezing may have aberrations that predate the RSV infection.To decide whether respiratory syncytial virus bronchiolitis causes, or is associated with the respiratory sequelae (or with subsequent allergy), it will be necessary to conduct prospective, randomized studies, where the cytokine profile prior to bronchiolitis onset is known. Such studies should preferably include some form of intervention against respiratory syncytial virus. A more complete understanding of the risk factors for severe respiratory syncytial virus infection and the role of respiratory syncytial virus infection in the initiation of asthma is needed as a basis for large-scale and cost-effective programmes to prevent respiratory syncytial virus-related morbidity. Eur Respir J 2001; 18: 1044-1058. Respiratory syncytial virus (RSV) bronchiolitis is the most common, severe lower respiratory tract infection in infancy. It now seems well established that RSV bronchiolitis in infancy is associated with recurrent wheezing and asthma during the first decade of life. In some children, wheezing after early lower airway infection with RSV is transient, but in many of the children RSV-induced bronchiolitis represents the onset of asthma. In fact, there are results which indicate that severe RSV bronchiolitis in the young infant may shift the T-helper (Th)1/Th2 balance in favour of a Th2 cytokine pattern, leading to development of allergic sensitization and persistent asthma [1,2]. However, the association with risk of development of atopy...

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Section: The Virusmentioning

confidence: 99%

Relationship between respiratory syncytial virus bronchiolitis and future obstructive airway diseases

Wennergren¹,

Kristjánsson²

2001

Eur Respir J

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“…Respiratory syncytial virus (RSV), named by its ability to induce fusion of infected epithelial cells (49), is a leading cause of epidemic respiratory tract illness in children (28). Spread primarily by contact with contaminated secretions, RSV replicates in the nasopharyngeal epithelium and spreads to the lower respiratory tract via epithelial cell-to-cell transfer along intracytoplasmic bridges (27).…”

mentioning

confidence: 99%

Expression of Respiratory Syncytial Virus-Induced Chemokine Gene Networks in Lower Airway Epithelial Cells Revealed by cDNA Microarrays

Zhang¹,

Luxon²,

Casola³

et al. 2001

J Virol

209

223

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Respiratory syncytial virus (RSV), named by its ability to induce fusion of infected epithelial cells (49), is a leading cause of epidemic respiratory tract illness in children (28). Spread primarily by contact with contaminated secretions, RSV replicates in the nasopharyngeal epithelium and spreads to the lower respiratory tract via epithelial cell-to-cell transfer along intracytoplasmic bridges (27). Although only two RSV serotypes, A and B, circulate in RSV epidemics (29), immunity to naturally acquired infection is incomplete, resulting in repeated infections through adulthood (24; reviewed in reference 28). In humans, RSV infection produces a spectrum of airway involvement ranging from otitis media to lower tract infection.Clinically severe RSV infections involving the lower respiratory tract are primarily seen in young children with naïve immune systems and/or genetic predispositions (32), patients with suppressed T-cell immunity (such as heart transplant recipients [41]), and the elderly (48). In autopsy studies of fatal disease, RSV infection is characterized by the presence of cytoplasmic eosinophilic inclusion bodies, characteristic of viral replication, in airway epithelial cells; sloughing and necrosis of the epithelial surface; and concomitant mucous plugging of the airways with trapping of air (1,18,19). In addition to these manifestations of direct epithelial involvement, RSV infection produces a pronounced perivascular infiltrate of mononuclear cells and lymphocytes (1, 18) and a neutrophil-rich exudate detected by bronchoalveolar lavage (16). Finally, the presence of eosinophil cationic protein (20,30) and histamine (64) in nasal secretions at concentrations that correlate with disease severity suggests the participation of eosinophils and basophils in the pathology of RSV infection.The mechanisms responsible for recruitment of circulating leukocytes, mononuclear cells, and lymphocytes into the lung as a consequence of RSV infection are largely unknown. Cellular recruitment into inflamed tissues is a multistep process in which circulating leukocytes first demarginate, adhere to stimulated endothelial cells, and subsequently become activated. Activated leukocytes then migrate through the vascular endothelium toward chemical gradients of chemoattractant peptides or antigens (reviewed in reference 58). Recent attention has focused on the important role of chemokines in mediat-* Corresponding author. Mailing address: Division of Endocrinology, MRB 8.138, The University of Texas Medical Branch, 301 University Blvd., Galveston, TX 77555-1060.

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“…In 1956, respiratory syncytial virus (RSV) was discovered in chimpanzees [158]. According to Dr. Viera Scheibner, who studied more than 30,000 pages of medical papers dealing with vaccination, RSV viruses "formed prominent contaminants in polio vaccines, and were soon detected in children [159]."…”

Section: More Animal Virusesmentioning

confidence: 99%

The polio vaccine: a critical assessment of its arcane history, efficacy, and long-term health-related consequences

Miller¹

2004

Medical Veritas

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Polio (poliomyelitis) is a potentially dangerous viral ailment. To combat this disease, researchers developed two polio vaccines (inactivated and live) grown in cultures made from monkey kidneys. Beginning in the 1950s, these vaccines were administered to millions of people in the United States and throughout the world. Officially, the polio vaccine is considered safe and effective, and has been credited with singularly reducing the incidence of this disease. These tenets are not supported by the data.A cancer-causing monkey virus-SV-40-was discovered in polio vaccines administered to millions of people. SV-40 has been found in brain tumors, bone cancers, lung cancers and leukemia. SV-40 is transmitted through sexual intercourse, and from mother to child in the womb. Monkeys that were used to make polio vaccines were infected with simian immunodeficiency virus (SIV), a virus closely related to human immunodeficiency virus (HIV), the infectious agent associated with AIDS. Some researchers question whether HIVs may simply be SIVs "residing in and adapting to a human host." Polio vaccines also contain calf serum, glycerol and other parts of the cow that may have been infected with bovine spongiform encephalopathy (BSE), or mad cow disease, a fatal brain-wasting ailment that some researchers link to Cruetzfeldt-Jakob disease (CJD), its human equivalent.Current disease reduction techniques that emphasize short-term gains over long-term health consequences need to be reevaluated and discontinued while new and safer health paradigms are researched and implemented.

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Recovery of Cytopathogenic Agent from Chimpanzees with Goryza

Cited by 441 publications

References 0 publications

Relationship between respiratory syncytial virus bronchiolitis and future obstructive airway diseases

Relationship between respiratory syncytial virus bronchiolitis and future obstructive airway diseases

Expression of Respiratory Syncytial Virus-Induced Chemokine Gene Networks in Lower Airway Epithelial Cells Revealed by cDNA Microarrays

The polio vaccine: a critical assessment of its arcane history, efficacy, and long-term health-related consequences

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