Mucosal inoculation with an attenuated mouse pneumovirus strain protects against virulent challenge in wild type and interferon-gamma receptor deficient mice

Ellis, John; Martin, Brittany V; Waldner, Cheryl L.; Dyer, Kimberly D.; Domachowske, Joseph B.; Rosenberg, Helene F.

doi:10.1016/j.vaccine.2006.09.081

Cited by 21 publications

(26 citation statements)

References 51 publications

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“…We observed no differences in the kinetics of virus replication, and no differences in responses to mucosal vaccination between the wild type and IFNγR gene-deleted mouse strains. Reprinted with permission from Ellis JA et al, [15]. Improved survival resulted from treatment with ribavirin and met-RANTES (* p< 0.05) compared individually to the groups treated with Met-RANTES alone, ribavirin alone, or PBS.…”

Section: Discussionmentioning

confidence: 99%

“…In our hands, PVM strain 15 from Dr. Andrew Easton's laboratory (PVM strain 15 Warwick) is highly attenuated and elicits a minimal inflammatory response in the highly susceptible BALB/c strain of mice [14]. In contrast, PVM strain 15 from the American Type Culture collection (PVM strain 15 ATCC) is pathogenic in BALB/c mice (unpublished findings), but results in little to no disease in the less susceptible C57BL/6 strain at similar inoculating doses (<100 pfu/mouse [15]). Krempl and colleagues [16] likewise found PVM strain 15 (ATCC) to be highly pathogenic in the BALB/c strain.…”

Section: Pathogenic and Attenuated Strains Of Pvmmentioning

confidence: 98%

“…Neutralizing antibodies were detected at 14 days after inoculation in mice receiving live attenuated virus (but not heatinactivated virus), which correlated with protection against subsequent challenge with the highly pathogenic strain J3666 [15]. Among the interesting questions, we are not certain of the duration of protective immunity.…”

Section: Immunity To Pvm Generated Via Mucosal Inoculationmentioning

confidence: 98%

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Pneumonia virus of mice: severe respiratory infection in a natural host

Rosenberg

Domachowske

2008

Immunology Letters

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Pneumonia virus of mice (PVM; family Paramyxoviridae, genus Pneumovirus) is a natural mouse pathogen that is closely related to the human and bovine respiratory syncytial viruses. Among the prominent features of this infection, robust replication of PVM takes place in bronchial epithelial cells in response to a minimal virus inoculum. Virus replication in situ results in local production of proinflammatory cytokines (MIP-1α, MIP-2, MCP-1 and IFNγ) and granulocyte recruitment to the lung. If left unchecked, PVM infection and the ensuing inflammatory response ultimately lead to pulmonary edema, respiratory compromise and death. In this review, we consider the recent studies using the PVM model that have provided important insights into the role of the inflammatory response in the pathogenesis of severe respiratory virus infection. We also highlight several works that have elucidated acquired immune responses to this pathogen, including T cell responses and the development of humoral immunity. Finally, we consider several immunomodulatory strategies that have been used successfully to reduce morbidity and mortality when administered to PVM infected, symptomatic mice, and thus hold promise as realistic therapeutic strategies for severe respiratory virus infections in human subjects.

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Section: Discussionmentioning

confidence: 99%

Section: Pathogenic and Attenuated Strains Of Pvmmentioning

confidence: 98%

Section: Immunity To Pvm Generated Via Mucosal Inoculationmentioning

confidence: 98%

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Pneumonia virus of mice: severe respiratory infection in a natural host

Rosenberg

Domachowske

2008

Immunology Letters

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“…Primers, probes, and standard curves for PVM small hydrophobic (SH) and mouse GAPDH genes were reported in previous publications. 31,32 Reactions were performed in an ABI 7500 Sequence detector, cycling parameters including 50°C for 2 minutes, 95°C for 10 minutes, followed by 40 cycles of 95°C for 15 seconds and 60°C for 1 minute. PVM titer is reported as copies PVM genome per copy mouse GAPDH, based on quantitative detection of the virus SH gene (SH PVM /GAPDH).…”

Section: Determination Of Virus Titer By Q-rt-pcrmentioning

confidence: 99%

Pneumoviruses infect eosinophils and elicit MyD88-dependent release of chemoattractant cytokines and interleukin-6

Dyer

Percopo

Fischer³

et al. 2009

Blood

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Eosinophils are recruited to the lung in response to infection with pneumovirus pathogens and have been associated with both the pathophysiologic sequelae of infection and, more recently, with accelerated virus clearance. Here, we demonstrate that the pneumovirus pathogens, respiratory syncytial virus (RSV) and pneumonia virus of mice (PVM), can infect human and mouse eosinophils, respectively, and that virus infection of eosinophils elicits the release of diseaserelated proinflammatory mediators from eosinophils. RSV replication in human eosinophils results in the release of infectious virions and in the release of the proinflammatory mediator, interleukin-6 (IL-6). PVM replication in cultured bone marrow eosinophils (bmEos) likewise results in release of infectious virions and the proinflammatory mediators IL-6, IP-10, CCL2, and CCL3. In contrast to the findings reported in lung tissue of RSVchallenged mice, PVM replication is accelerated in MyD88 gene-deleted bmEos, whereas release of cytokines is dimin- IntroductionEosinophils are unique proinflammatory leukocytes that are easily recognized but poorly understood. Although eosinophil expansion in the bone marrow and recruitment from the bloodstream to peripheral tissues are prominent findings that are clearly associated with asthma, allergic diseases, and infection with helminthes, there is no full consensus about the physiologic or pathophysiologic roles played by eosinophils in any of these disease states. [1][2][3] Interestingly, among the many points that have emerged from the clinical studies featuring therapeutic administration of antiinterleukin 5 (IL-5) monoclonal antibody (mepolizumab), 4-7 it has become evident that we have a very limited understanding of the subtleties of eosinophil recruitment and function; this limited understanding may relate to a long-standing focus on numbers of eosinophils recruited rather than on the nature, quality, and extent of eosinophil activation.With this in mind, we have focused our studies on the role of eosinophils and of eosinophil activation in acute respiratory virus infections, 8 specifically, infections with respiratory syncytial virus (RSV) and pneumonia virus of mice (PVM), a mouse pneumovirus pathogen that replicates the sequelae of the more severe forms of RSV infection in inbred strains of mice. 9,10 Several converging lines of evidence suggest that eosinophils recruited to the lungs in response to pneumovirus infection may have a direct effect on the outcome of disease. Among these findings, several groups have detected immunoreactive eosinophil degranulation products in bronchial washings of patients with the most severe forms of RSV infection, 11,12 and we and others have reported direct recruitment of eosinophils to the lungs of PVM-infected mice. 13-15 RSV and PVM infections of their respective target cells result in the production of numerous proinflammatory cytokines, including the eosinophil chemoattractants RANTES and macrophage inflammatory protein-1␣/CCL3, [16][17][18][19] and RSV-infected tar...

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“…Standard concentrations of the full-length sh gene and gapdh decatemplate (Ambion, Foster City, CA) were used for quantitation. Results are expressed as copies of PVM-sh per 10 9 copies of gapdh (19). All PCR assays were run in triplicates.…”

Section: Measurementsmentioning

confidence: 99%

Role of the Fas/FasL system in a model of RSV infection in mechanically ventilated mice

Berg

Woensel

Bos

et al. 2011

American Journal of Physiology-Lung Cellular and Molecular Phys

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Infection with respiratory syncytial virus (RSV) in children can progress to respiratory distress and acute lung injury necessitating mechanical ventilation (MV). MV enhances apoptosis and inflammation in mice infected with pneumonia virus of mice (PVM), a mouse pneumovirus that has been used as a model for severe RSV infection in mice. We hypothesized that the Fas/Fas ligand (FasL) system, a dual proapoptotic/proinflammatory system involved in other forms of lung injury, is required for enhanced lung injury in mechanically ventilated mice infected with PVM. C57BL/6 mice and Fas-deficient ("lpr") mice were inoculated intratracheally with PVM. Seven or eight days after PVM inoculation, the mice were subjected to 4 h of MV (tidal volume 10 ml/kg, fraction of inspired O(2) = 0.21, and positive end-expiratory pressure = 3 cm H(2)O). Seven days after PVM inoculation, exposure to MV resulted in less severe injury in lpr mice than in C57BL/6 mice, as evidenced by decreased numbers of polymorphonuclear neutrophils in the bronchoalveolar lavage (BAL), and lower concentrations of the proinflammatory chemokines KC, macrophage inflammatory protein (MIP)-1α, and MIP-2 in the lungs. However, when PVM infection was allowed to progress one additional day, all of the lpr mice (7/7) died unexpectedly between 0.5 and 3.5 h after the onset of ventilation compared with three of the seven ventilated C57BL/6 mice. Parameters of lung injury were similar in nonventilated mice, as was the viral content in the lungs and other organs. Thus, the Fas/FasL system was partly required for the lung inflammatory response in ventilated mice infected with PVM, but attenuation of lung inflammation did not prevent subsequent mortality.

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Mucosal inoculation with an attenuated mouse pneumovirus strain protects against virulent challenge in wild type and interferon-gamma receptor deficient mice

Cited by 21 publications

References 51 publications

Pneumonia virus of mice: severe respiratory infection in a natural host

Pneumonia virus of mice: severe respiratory infection in a natural host

Pneumoviruses infect eosinophils and elicit MyD88-dependent release of chemoattractant cytokines and interleukin-6

Role of the Fas/FasL system in a model of RSV infection in mechanically ventilated mice

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