Puumala Virus Pulmonary Syndrome in a Romanian Immigrant

Caramello, Pietro; Canta, Francesca; Bonino, L.; Moiraghi, Corrado; Navone, F; Lipani, Filippo; Balbiano, Rosanna; Caputo, Anna Maria; Gai, V

doi:10.2310/7060.2002.30014

Cited by 17 publications

(8 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Despite intensive studies, there are currently no specific therapies for ARDS, especially following virus infection, and model systems are desperately needed. While several viruses are known to cause ARDS, including SARS-CoV and influenza virus (9,11,30,39,42,51), the molecular mechanisms of virus-induced ARDS are not well characterized due to the limited number of available animal models. The recent reconstruction of two lethal SARS-CoV infection models in mice that recapitulate the age-related pathogenic phenotype noted in humans (47) provided us with the novel opportunity to characterize host response kinetics and to more fully develop the model for characterizing the molecular mechanisms of virus-induced ARDS.…”

Section: Discussionmentioning

confidence: 99%

“…This may progress to an organizing-phase DAD that progresses to pulmonary fibrosis, and both occurred following SARS-CoV infection. ARDS has been reported following SARS-CoV or influenza virus infection and is sporadically reported following herpesvirus, respiratory syncytial virus, adenovirus, varicella virus, and hantavirus infections, as well (9,11,30,39,42,51); however, few well-defined ARDS animal models exist. Select SARS-CoV strains and H5N1 influenza virus are robust models for ARDS in rodents (47,56), yet the molecular mechanisms governing ARDS pathogenesis following virus infection are still unclear, especially when placed into the context of aging.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Early Upregulation of Acute Respiratory Distress Syndrome-Associated Cytokines Promotes Lethal Disease in an Aged-Mouse Model of Severe Acute Respiratory Syndrome Coronavirus Infection

Rockx

Baas

Zornetzer

et al. 2009

J Virol

163

101

View full text Add to dashboard Cite

Several respiratory viruses, including influenza virus and severe acute respiratory syndrome coronavirus (SARS-CoV), produce more severe disease in the elderly, yet the molecular mechanisms governing age-related susceptibility remain poorly studied. Advanced age was significantly associated with increased SARS-related deaths, primarily due to the onset of early-and late-stage acute respiratory distress syndrome (ARDS) and pulmonary fibrosis. Infection of aged, but not young, mice with recombinant viruses bearing spike glycoproteins derived from early human or palm civet isolates resulted in death accompanied by pathological changes associated with ARDS. In aged mice, a greater number of differentially expressed genes were observed than in young mice, whose responses were significantly delayed. Differences between lethal and nonlethal virus phenotypes in aged mice could be attributed to differences in host response kinetics rather than virus kinetics. SARS-CoV infection induced a range of interferon, cytokine, and pulmonary wound-healing genes, as well as several genes associated with the onset of ARDS. Mice that died also showed unique transcriptional profiles of immune response, apoptosis, cell cycle control, and stress. Cytokines associated with ARDS were significantly upregulated in animals experiencing lung pathology and lethal disease, while the same animals experienced downregulation of the ACE2 receptor. These data suggest that the magnitude and kinetics of a disproportionately strong host innate immune response contributed to severe respiratory stress and lethality. Although the molecular mechanisms governing ARDS pathophysiology remain unknown in aged animals, these studies reveal a strategy for dissecting the genetic pathways by which SARS-CoV infection induces changes in the host response, leading to death.

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Early Upregulation of Acute Respiratory Distress Syndrome-Associated Cytokines Promotes Lethal Disease in an Aged-Mouse Model of Severe Acute Respiratory Syndrome Coronavirus Infection

Rockx

Baas

Zornetzer

et al. 2009

J Virol

163

101

View full text Add to dashboard Cite

show abstract

“…However, when delivered via the intranasal route, the primary organ affected was the lung and viral RNA was still at high levels at day 14 post-challenge, demonstrating persistence. While many early reports of SEOV disease have described classic HFRS type features, there is growing evidence from human clinical studies of disease for involvement of the pulmonary system [62][63][64][65], confirming overlap between HPS and HFRS disease outcomes. Notably, this evidence underscores that the natural tropism of SEOV observed in this study is recapitulated in A129 mice.…”

Section: Discussionmentioning

confidence: 99%

Hantavirus infection in type I interferon receptor-deficient (A129) mice

Dowall

Graham

Aram

et al. 2020

Journal of General Virology

View full text Add to dashboard Cite

Type I interferon receptor knockout mice (strain A129) were assessed as a disease model of hantavirus infection. A range of infection routes (intramuscular, intraperitoneal and intranasal) were assessed using minimally passaged Seoul virus (strain Humber). Dissemination of virus to the spleen, kidney and lung was observed at 5 days after intramuscular and intraperitoneal challenge, which was resolved by day 14. In contrast, intranasal challenge of A129 mice demonstrated virus tropism to the lung, which was maintained to day 14 post-challenge. These data support the use of the A129 mouse model for future infection studies and the in vivo evaluation of interventions.

show abstract

“…Renal involvement due to PUUV is frequent but pulmonary involvement is quite rare. [ 1 ] Although varying degrees of pulmonary involvement have been previously described in PUUV-infected patients,[ 3 4 5 6 7 8 9 10 ] severe pulmonary manifestations are uncommon, and there is almost always prominent renal involvement. [ 3 4 5 ] The pattern of lung involvement in hantavirus infection is characterized by interstitial edema and alveolar disease with central or bibasilar involvement.…”

Section: Discussionmentioning

confidence: 99%

Bilateral massive pneumonia as an unusual manifestation of Puumala hantavirus infection

Gozdas

Menemenlioğlu²,

Coşgun³

et al. 2018

Journal of Postgraduate Medicine

View full text Add to dashboard Cite

Renal involvement due to European Puumala virus (PUUV) is frequent but pulmonary involvement is quite rare. We present here, a 24-year-old male with atypical clinical presentation of acute PUUV infection with gross pulmonary and minimal renal involvement. Severe pulmonary manifestations of PUUV infection, in this case, highlights that hantavirus infection should be considered in the differential diagnosis of atypical pneumonia.

show abstract

Puumala Virus Pulmonary Syndrome in a Romanian Immigrant

Cited by 17 publications

References 7 publications

Early Upregulation of Acute Respiratory Distress Syndrome-Associated Cytokines Promotes Lethal Disease in an Aged-Mouse Model of Severe Acute Respiratory Syndrome Coronavirus Infection

Early Upregulation of Acute Respiratory Distress Syndrome-Associated Cytokines Promotes Lethal Disease in an Aged-Mouse Model of Severe Acute Respiratory Syndrome Coronavirus Infection

Hantavirus infection in type I interferon receptor-deficient (A129) mice

Bilateral massive pneumonia as an unusual manifestation of Puumala hantavirus infection

Contact Info

Product

Resources

About