Erratum: Primary infection of mice with high titer inoculum respiratory syncytial virus: characterization and response to antiviral therapy

2005 ◽  
Vol 83 (3) ◽  
pp. 319-319
Author(s):  
Gordon Bolger ◽  
Nicole Lapeyre ◽  
Nathalie Dansereau ◽  
Lisette Lagacé ◽  
Gerald Berry ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Antiviral Therapy ◽  
Primary Infection ◽  
High Titer ◽  
Syncytial Virus

Primary infection of mice with high titer inoculum respiratory syncytial virus: characterization and response to antiviral therapy

2005 ◽  
Vol 83 (2) ◽  
pp. 198-213 ◽  
Author(s):  
Gordon Bolger ◽  
Nicole Lapeyre ◽  
Nathalie Dansereau ◽  
Lisette Lagacé ◽  
Gerald Berry ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Antiviral Therapy ◽  
Virus Disease ◽  
High Titer ◽  
Lavage Fluid ◽  
Whole Body ◽  
Dependent Manner ◽  
Syncytial Virus ◽  
Dose Dependent

Intranasal infection of BALB/c mice with respiratory syncytial virus (RSV)-A2 (0.5 × 108– 2.0 × 108plaque-forming units, PFU) produced disease characterized by weight loss (2–3 g) and mortality (60%–100%) with the mean day of death ranging from 6–7 d after infection. The extent of RSV disease was inoculum titer-dependent and required a replication competent virus. Lung titers of virus peaked at 0.5-1 × 106PFU/g wet weight. Bronchoalveolar lavage fluid (BALF) levels of IL-1β, TNF-α, INF-γ IL-12, IL-6, MIP-1α, RANTES, and protein were elevated, whereas IL-2, IL-4, IL-5, IL-13, and IL-10 were unchanged. Histological assessment of lungs revealed marked inflammatory pathology characterized by bronchiolitis, vasculitis, and interstitial pneumonia. Whole-body plethysmography revealed significant disease-associated deficits of respiratory function. Therapy with ribavirin administered either by the intranasal, subcutaneous, or oral route significantly reduced disease in a dose-dependent manner. Delaying the initiation of therapy resulted in a loss of activity for ribavirin. Synagis®administered either intramuscularly as a single dose in prophylaxis or intranasally in prophylaxis, followed by therapy, also significantly reduced disease in a dose-dependent manner. Infection of mice with a high titer inoculum of RSV-A2 resulted in severe and fatal pulmonary disease that was responsive to treatment. This model may be useful to characterize the in vivo activity of experimental therapies for RSV infection.Key words: respiratory syncytial virus, disease, mortality, antiviral therapy.

scholarly journals Detection of Influenza A and B Viruses and Respiratory Syncytial Virus by Use of Clinical Laboratory Improvement Amendments of 1988 (CLIA)-Waived Point-of-Care Assays: a Paradigm Shift to Molecular Tests

2018 ◽  
Vol 56 (7) ◽  
Author(s):  
Marwan M. Azar ◽  
Marie L. Landry
Keyword(s):  
Respiratory Syncytial Virus ◽  
Antiviral Therapy ◽  
Influenza A ◽  
Clinical Laboratory ◽  
Point Of Care ◽  
The United States ◽  
Nucleic Acid Amplification ◽  
Molecular Tests ◽  
Syncytial Virus ◽  
Clinical Laboratory Improvement Amendments

ABSTRACT An accurate laboratory diagnosis of influenza, respiratory syncytial virus (RSV), and other respiratory viruses can help to guide patient management, antiviral therapy, infection prevention strategies, and epidemiologic monitoring. Influenza has been the primary driver of rapid laboratory testing due to its morbidity and mortality across all ages, the availability of antiviral therapy, which must be given early to have an effect, and the constant threat of new pandemic strains. Over the past 30 years, there has been an evolution in viral diagnostic testing, from viral culture to rapid antigen detection, and more recently, to highly sensitive nucleic acid amplification tests (NAAT), as well as a trend to testing at the point of care (POC). Simple rapid antigen immunoassays have long been the mainstay for POC testing for influenza A and B viruses and respiratory syncytial virus (RSV) but have been faulted for low sensitivity. In 2015, the first POC NAAT for the detection of influenza was approved by the Food and Drug Administration (FDA), ushering in a new era. In 2017, the FDA reclassified rapid influenza diagnostic tests (RIDTs) from class I to class II devices with new minimum performance standards and a requirement for annual reactivity testing. Consequently, many previously available RIDTs can no longer be purchased in the United States. In this review, recent developments in Clinical Laboratory Improvement Amendments of 1988 (CLIA)-waived testing for respiratory virus infections will be presented, with the focus on currently available FDA-cleared rapid antigen and molecular tests primarily for influenza A and B viruses and RSV.

scholarly journals Prophylactic Treatment with a G Glycoprotein Monoclonal Antibody Reduces Pulmonary Inflammation in Respiratory Syncytial Virus (RSV)-Challenged Naïve and Formalin-Inactivated RSV-Immunized BALB/c Mice

2010 ◽  
Vol 84 (18) ◽  
pp. 9632-9636 ◽  
Author(s):  
Gertrud U. Radu ◽  
Hayat Caidi ◽  
Congrong Miao ◽  
Ralph A. Tripp ◽  
Larry J. Anderson ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Respiratory Syncytial Virus ◽  
Inflammatory Response ◽  
G Protein ◽  
Primary Infection ◽  
Prophylactic Treatment ◽  
Pulmonary Inflammation ◽  
Rsv Infection ◽  
Pulmonary Inflammatory Response ◽  
Syncytial Virus

ABSTRACT We examined whether prophylactically administered anti-respiratory syncytial virus (anti-RSV) G monoclonal antibody (MAb) would decrease the pulmonary inflammation associated with primary RSV infection and formalin-inactivated RSV (FI-RSV)-enhanced disease in mice. MAb 131-2G administration 1 day prior to primary infection reduced the pulmonary inflammatory response and the level of RSV replication. Further, intact or F(ab′)2 forms of MAb 131-2G administered 1 day prior to infection in FI-RSV-vaccinated mice reduced enhanced inflammation and disease. This study shows that an anti-RSV G protein MAb might provide prophylaxis against both primary infection and FI-RSV-associated enhanced disease. It is possible that antibodies with similar reactivities might prevent enhanced disease and improve the safety of nonlive virus vaccines.

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