Ana M Gómez
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Ana M Gómez has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
- Ana M Ríos
Division of Pediatric Infectious Diseases, Department of Pediatrics, The University of Texas Southwestern Medical Center at Dallas and Children's Medical Center Dallas, Dallas, Texas, USA
1 shared publication - Asuncion Mejias
Department of Infectious Diseases, St. Jude Children’s Research Hospital, Memphis, TN 38105, USA
1 shared publication - Hasan S. Jafri
Medimmune, Gaithersburg, MD, USA
1 shared publication - Kurt D Olsen
Division of Pediatric Infectious Diseases, Department of Pediatrics, The University of Texas Southwestern Medical Center at Dallas and Children's Medical Center Dallas, Dallas, Texas, USA
1 shared publication - Monica Fonseca-Aten
Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, 75390-9063, USA
1 shared publication - Octavio Ramilo
Division of Pediatric Infectious Disease Center for Vaccines and Immunity; The Research Institute at Nationwide Children's Hospital; The Ohio State University College of Medicine Columbus, OH
1 shared publication
Latest Publications
- Open Access
- 25 May 2005
- Published by Springer Nature in Virology Journal
- Vol. 2 (1) , 46
Respiratory syncytial virus-induced acute and chronic airway disease is independent of genetic background: An experimental murine model
Background: Respiratory syncytial virus (RSV) is the leading respiratory viral pathogen in young children worldwide. RSV disease is associated with acute airway obstruction (AO), long-term airway hyperresponsiveness (AHR), and chronic lung inflammation. Using two different mouse strains, this study was designed to determine whether RSV disease patterns are host-dependent. C57BL/6 and BALB/c mice were inoculated with RSV and followed for 77 days. RSV loads were measured by plaque assay and polymerase chain reaction (PCR) in bronchoalveolar lavage (BAL) and whole lung samples; cytokines were measured in BAL samples. Lung inflammation was evaluated with a histopathologic score (HPS), and AO and AHR were determined by plethysmography.Results: Viral load dynamics, histopathologic score (HPS), cytokine concentrations, AO and long-term AHR were similar in both strains of RSV-infected mice, although RSV-infected C57BL/6 mice developed significantly greater AO compared with RSV-infected BALB/c mice on day 5. PCR detected RSV RNA in BAL samples of RSV infected mice until day 42, and in whole lung samples through day 77. BAL concentrations of cytokines TNF-α, IFN-γ, and chemokines MIG, RANTES and MIP-1α were significantly elevated in both strains of RSV-infected mice compared with their respective controls. Viral load measured by PCR significantly correlated with disease severity on days 14 and 21.Conclusion: RSV-induced acute and chronic airway disease is independent of genetic background.
- 25 May 2005
- Published by Springer Nature in Virology Journal
- Vol. 2 (1) , 46
Open AccessRespiratory syncytial virus-induced acute and chronic airway disease is independent of genetic background: An experimental murine model
Background: Respiratory syncytial virus (RSV) is the leading respiratory viral pathogen in young children worldwide. RSV disease is associated with acute airway obstruction (AO), long-term airway hyperresponsiveness (AHR), and chronic lung inflammation. Using two different mouse strains, this study was designed to determine whether RSV disease patterns are host-dependent. C57BL/6 and BALB/c mice were inoculated with RSV and followed for 77 days. RSV loads were measured by plaque assay and polymerase chain reaction (PCR) in bronchoalveolar lavage (BAL) and whole lung samples; cytokines were measured in BAL samples. Lung inflammation was evaluated with a histopathologic score (HPS), and AO and AHR were determined by plethysmography.Results: Viral load dynamics, histopathologic score (HPS), cytokine concentrations, AO and long-term AHR were similar in both strains of RSV-infected mice, although RSV-infected C57BL/6 mice developed significantly greater AO compared with RSV-infected BALB/c mice on day 5. PCR detected RSV RNA in BAL samples of RSV infected mice until day 42, and in whole lung samples through day 77. BAL concentrations of cytokines TNF-α, IFN-γ, and chemokines MIG, RANTES and MIP-1α were significantly elevated in both strains of RSV-infected mice compared with their respective controls. Viral load measured by PCR significantly correlated with disease severity on days 14 and 21.Conclusion: RSV-induced acute and chronic airway disease is independent of genetic background.