The Prevalence of Common Respiratory Viruses in Human Lungs

Hogg, James C.; Macek, V; Dakhama, Azzeddine; Hayashi, Shizu; Hegele, Richard G.

doi:10.1016/b978-012473340-4/50027-8

Cited by 6 publications

(5 citation statements)

References 37 publications

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“…The specimens obtained for analysis came directly from the lower airways after the lung had been removed from the thorax at autopsy to minimize the potential for upper airway contamination. Because these viral PCR results are similar to the results of our preliminary study of viral nucleic acid detection in surgically resected lung specimens (15), it is unlikely that specimens of lower airway secretions were contaminated by pathogens from the upper respiratory tract. A PCR-based panel for detection of viral nucleic acid was used because it provided a sensitive, practical way to screen for large numbers and serotypes of the nine viruses examined.…”

Section: Discussionsupporting

confidence: 77%

“…Our laboratory previously reported a three-virus PCR panel (14) that established that PCR had over 90% sensitivity to viral culture of clinical respiratory specimens and was especially useful for detecting fastidious RNA pathogens such as HRV, respiratory syncytial virus (RSV), and parainfluenza virus (PIV). We have since expanded our PCR panel to test for nine common respiratory viruses, and have recently used this panel to document viral nucleic acid in surgically resected lung specimens (15).…”

Section: Détection Par Pcr D'acide Nucléique Viral Dans L'asthme Fatamentioning

confidence: 99%

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PCR Detection of Viral Nucleic Acid in Fatal Asthma: Is the Lower Respiratory Tract a Reservoir for Common Viruses?

Macek

Dakhama

Hogg

et al. 1999

Canadian Respiratory Journal

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Section: Discussionsupporting

confidence: 77%

Section: Détection Par Pcr D'acide Nucléique Viral Dans L'asthme Fatamentioning

confidence: 99%

PCR Detection of Viral Nucleic Acid in Fatal Asthma: Is the Lower Respiratory Tract a Reservoir for Common Viruses?

Macek

Dakhama

Hogg

et al. 1999

Canadian Respiratory Journal

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“…Previous work in allergy-susceptible CH has shown that RSV can cause a persistent lung infection associated with AHR and airway inflammation (7,8,14), consistent with a possible role of RSV persistence in the pathogenesis of post-bronchiolitis sequelae. In contrast, other studies have implicated RSV persistence in the lungs but without a clear relationship to a particular clinical phenotype (9,10,12,13). Because Th1 responses are considered important for antiviral immunity, we hypothesized that a host genetic background for allergy susceptibility, manifested by Th2 skewing, would confer more severe consequences of RSV persistence.…”

Section: Discussionmentioning

confidence: 56%

T Helper 1 Background Protects Against Airway Hyperresponsiveness and Inflammation in Guinea Pigs With Persistent Respiratory Syncytial Virus Infection

et al. 2007

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A family history of allergy has been implicated in children who develop post-bronchiolitis wheezing and asthma. In a guinea pig model of respiratory syncytial virus (RSV) lung infection, we evaluated the role of host Th1 background (either genetic or induced) on the development of a persistent infection, nonspecific airway hyperresponsiveness (AHR) and airway inflammation. Allergy resistant/T helper 1 (Th1)-skewed strain 2 guinea pigs (STR2) and cytosine phosphate guanine oligodeoxynucleotides (CpG-ODN) (Th1 stimuli) pretreated Cam Hartley guinea pigs (CH) were inoculated with RSV and compared with virus-inoculated allergysusceptible/Th2-skewed CHs and to sham-inoculated STR2 and CH, 60 d post-inoculation. We measured titers of intrapulmonary RSV, lung interferon (IFN)-␥ and interleukin (IL)-5 mRNA expression, AHR and airway T cells and eosinophils. All virus-inoculated groups of animals showed evidence of persistent RSV lung infection; however, Th2-skewed guinea pigs had virus-associated AHR and significantly greater levels of airway T cells and eosinophils. In conclusion, RSV can establish persistent infection of the guinea pig lung regardless of host Th1/Th2 background; however; a host Th1 background limits the extent of virus-associated AHR and airway inflammation. Heterogeneity in virus-host interactions may be relevant to understanding why some children hospitalized for RSV bronchiolitis go on to develop recurrent wheezing/asthma symptoms. R SV is the most common cause of acute bronchiolitis, the leading cause of infant hospitalization in the developed world (1). A proportion of children hospitalized with acute bronchiolitis develop sequelae of recurrent wheezing and features of asthma for which allergic mechanisms (2-5) or a family history of allergy (6) have been implicated. In addition, studies in animal models have reported that RSV can establish a persistent, low-level infection in the lungs (7,8), and results of several cross-sectional (9 -11) and longitudinal studies (12) suggest that RSV can persistently infect the human lung.However, the consequences of chronic intrapulmonary RSV persistence are unclear (13).We have developed a guinea pig model of experimental RSV infection in which lung function and airway inflammation have been studied in association with RSV persistence (8,14). In this model, intranasal RSV inoculation of juvenile CH results in a productive lung infection that is associated with nonspecific AHR and airway inflammation by lymphocytes and granulocytes, including T cells and eosinophils (8,15,16). After resolution of the acute infection, CH develop a persistent lung infection characterized by ongoing, low-level RSV replication, AHR, and airway eosinophilia (8,14,15). These findings in guinea pigs suggest a possible role for RSV persistence in the pathogenesis of AHR and airway inflammation that have features similar to asthma (17).Importantly, CH are a genetically outbred strain that is highly susceptible to allergic sensitization relative to inbred STR2 or STR13 (18). S...

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“…We have recently performed polymerase chain reaction experiments in surgically resected and postmortem human lung specimens, to test for the presence of nucleic acid from nine common respiratory viruses [30]. The polymerase chain reaction results showed that over 90% of these human lung specimens contained nucleic acid from at least one virus, in marked contradistinction to the concept of the human lung being a sterile environment.…”

Section: Persistent Viral Infectionsmentioning

confidence: 99%

Role of viruses in the onset of asthma and allergy: lessons from animal modelsSupported by the Medical Research Council of Canada (MT‐13766).

Hegele

1999

Clin Experimental Allergy

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There are several potential mechanisms by which viral respiratory tract infections in childhood might trigger the onset of sensitization to allergens and asthma. To study these potential mechanisms, researchers have developed a number of animal models. In this paper, results of animal experiments are discussed under three headings: (i) chronic sequelae of acute viral infections; (ii) viral infections and sensitization to aeroallergens; and (iii) persistent viral infections. The use of animal models to study the role of viral infections in the induction of allergic sensitization and airway responsiveness has provided intriguing new insights that may be relevant to the pathogenesis of human disease.

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The Prevalence of Common Respiratory Viruses in Human Lungs

Cited by 6 publications

References 37 publications

PCR Detection of Viral Nucleic Acid in Fatal Asthma: Is the Lower Respiratory Tract a Reservoir for Common Viruses?

PCR Detection of Viral Nucleic Acid in Fatal Asthma: Is the Lower Respiratory Tract a Reservoir for Common Viruses?

T Helper 1 Background Protects Against Airway Hyperresponsiveness and Inflammation in Guinea Pigs With Persistent Respiratory Syncytial Virus Infection

Role of viruses in the onset of asthma and allergy: lessons from animal modelsSupported by the Medical Research Council of Canada (MT‐13766).

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