Hantavirus Pulmonary Syndrome in New England and Europe

Le, Brackett; Rotenberg, Joshua S.; Cb, Sherman

doi:10.1056/nejm199408253310813

Cited by 75 publications

(11 citation statements)

References 15 publications

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“…Since hantaviruses are transmitted predominantly via inhalation, studying immunological events in the airways where viral replication is first initiated is of importance to understand the processes leading to immunopathogenesis. Furthermore, pulmonary dysfunction has been reported in HFRS patients [40–42]. Expansion of cytotoxic CD8 + T cells in the airways of hantavirus-infected patients has been described as contributing to disease severity [13, 14].…”

Section: Introductionmentioning

confidence: 99%

Human hantavirus infection elicits pronounced redistribution of mononuclear phagocytes in peripheral blood and airways

et al. 2017

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Hantaviruses infect humans via inhalation of virus-contaminated rodent excreta. Infection can cause severe disease with up to 40% mortality depending on the viral strain. The virus primarily targets the vascular endothelium without direct cytopathic effects. Instead, exaggerated immune responses may inadvertently contribute to disease development. Mononuclear phagocytes (MNPs), including monocytes and dendritic cells (DCs), orchestrate the adaptive immune responses. Since hantaviruses are transmitted via inhalation, studying immunological events in the airways is of importance to understand the processes leading to immunopathogenesis. Here, we studied 17 patients infected with Puumala virus that causes a mild form of hemorrhagic fever with renal syndrome (HFRS). Bronchial biopsies as well as longitudinal blood draws were obtained from the patients. During the acute stage of disease, a significant influx of MNPs expressing HLA-DR, CD11c or CD123 was detected in the patients’ bronchial tissue. In parallel, absolute numbers of MNPs were dramatically reduced in peripheral blood, coinciding with viremia. Expression of CCR7 on the remaining MNPs in blood suggested migration to peripheral and/or lymphoid tissues. Numbers of MNPs in blood subsequently normalized during the convalescent phase of the disease when viral RNA was no longer detectable in plasma. Finally, we exposed blood MNPs in vitro to Puumala virus, and demonstrated an induction of CCR7 expression on MNPs. In conclusion, the present study shows a marked redistribution of blood MNPs to the airways during acute hantavirus disease, a process that may underlie the local immune activation and contribute to immunopathogenesis in hantavirus-infected patients.

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Section: Introductionmentioning

confidence: 99%

Human hantavirus infection elicits pronounced redistribution of mononuclear phagocytes in peripheral blood and airways

et al. 2017

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“…Frequent clinical findings include cough, dyspnoea, interstitial lung infiltrates, pleural effusion and impaired pulmonary function [10–12]. Pronounced lung involvement in HFRS has previously been reported [13–16]. However, none of those reported patients had a fatal outcome that could be attributed to the acute infection, and there is no description of histopathological findings.…”

Section: Introductionmentioning

confidence: 99%

Time to revise the paradigm of hantavirus syndromes? Hantavirus pulmonary syndrome caused by European hantavirus

Rasmuson

Andersson

Norrman

et al. 2011

Eur J Clin Microbiol Infect Dis

106

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Hantaviruses have previously been recognised to cause two separate syndromes: hemorrhagic fever with renal syndrome in Eurasia, and hantavirus pulmonary syndrome (HPS) in the Americas. However, increasing evidence suggests that this dichotomy is no longer fruitful when recognising human hantavirus disease and understanding the pathogenesis. Herein are presented three cases of severe European Puumala hantavirus infection that meet the HPS case definition. The clinical and pathological findings were similar to those found in American hantavirus patients. Consequently, hantavirus infection should be considered as a cause of acute respiratory distress in all endemic areas worldwide.

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“…Although these 2 types of diseases have been characterized, there are many similarities in the clinical picture of the symptoms, which often are incomplete and overlap [4,5,6,7]. Most of the HFRS cases presented in Europe are caused by Puumala hantavirus (PUUV).…”

Section: Introductionmentioning

confidence: 99%

Community Acquired Severe Acute Kidney Injury Caused by Hantavirus-Induced Hemorrhagic Fever with Renal Syndrome Has a Favorable Outcome

Outinen¹,

Mäkelä²,

Clément³

et al. 2015

Nephron

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Background: Puumala hantavirus (PUUV) induces an acute tubulointerstitial nephritis and acute kidney injury (AKI). Our aim was to evaluate the prognosis of severe AKI associated with PUUV infection. Methods: We examined 556 patients who were treated at Tampere University Hospital during 1982-2013 for acute, serologically confirmed PUUV infection. Plasma creatinine was measured during hospitalization, convalescence, and 1, 2, and 5 years after the acute infection. Results: Plasma creatinine concentration was elevated (>100 μmol/l) in 459 (83%) patients, while altogether 189 patients (34%) had severe AKI defined as Kidney Disease: Improving Global Outcomes (KDIGO) stage 3, that is, plasma creatinine ≥353.6 μmol/l (4.0 mg/dl) or need of dialysis. There were no fatal cases during the hospitalization or the following 3 months. Fatality rate during the years following PUUV infection did not differ between patients who had suffered from severe AKI versus those without severe AKI. Post-hospitalization plasma creatinine values were available for 188 (34%) patients. One month after the acute infection, patients with prior severe AKI had higher median plasma creatinine concentration (82 µmol/l, range 54-184) than patients without severe AKI (74 µmol/l, range 55-109, p = 0.005). After 1 year, no significant difference existed in median plasma creatinine concentrations between patients with (71 µmol/l, range 36-123) and without prior severe AKI (72 µmol/l, range 34-116, p = 0.711). After 5 years all but 1 patient had normal creatinine levels. Conclusions: In contrast to the worldwide well-accepted KDIGO criteria, severe AKI associated with PUUV infection is not associated with excess fatality but has a very good prognosis, both in the short and long terms.

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Hantavirus Pulmonary Syndrome in New England and Europe

Cited by 75 publications

References 15 publications

Human hantavirus infection elicits pronounced redistribution of mononuclear phagocytes in peripheral blood and airways

Human hantavirus infection elicits pronounced redistribution of mononuclear phagocytes in peripheral blood and airways

Time to revise the paradigm of hantavirus syndromes? Hantavirus pulmonary syndrome caused by European hantavirus

Community Acquired Severe Acute Kidney Injury Caused by Hantavirus-Induced Hemorrhagic Fever with Renal Syndrome Has a Favorable Outcome

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