Regulatory T cell response correlates with the severity of human hantavirus infection

Koivula, Tuisku-Tuulia; Tuulasvaara, Anni; Hetemäki, Iivo; Mäkelä, Satu; Mustonen, Jukka; Sironen, Tarja; Vaheri, Antti; Arstila, T. Petteri

doi:10.1016/j.jinf.2013.11.007

Cited by 24 publications

(25 citation statements)

References 48 publications

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“…Recently, Prescott et al suggested that an adaptive immune response has no influence on hantavirus replication or disease pathogenesis, based on studies using a hamster model of HPS (54). However, clinical studies indicate the potential role of innate and adaptive immune responses in disease pathogenesis (55–58). Our data support the role of adaptive immune responses in the pathogenesis of hantavirus infection.…”

Section: Discussionmentioning

confidence: 99%

Serum Cytokine Profiles Differentiating Hemorrhagic Fever with Renal Syndrome and Hantavirus Pulmonary Syndrome

et al. 2017

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Hantavirus infection is an acute zoonosis that clinically manifests in two primary forms, hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS). HFRS is endemic in Europe and Russia, where the mild form of the disease is prevalent in the Tatarstan region. HPS is endemic in Argentina, as well as other countries of North and South American. HFRS and HPS are usually acquired via the upper respiratory tract by inhalation of virus-contaminated aerosol. Although the pathogenesis of HFRS and HPS remains largely unknown, postmortem tissue studies have identified endothelial cells as the primary target of infection. Importantly, cell damage due to virus replication, or subsequent tissue repair, has not been documented. Since no single factor has been identified that explains the complexity of HFRS or HPS pathogenesis, it has been suggested that a cytokine storm may play a crucial role in the manifestation of both diseases. In order to identify potential serological markers that distinguish HFRS and HPS, serum samples collected during early and late phases of the disease were analyzed for 48 analytes using multiplex magnetic bead-based assays. Overall, serum cytokine profiles associated with HPS revealed a more pro-inflammatory milieu as compared to HFRS. Furthermore, HPS was strictly characterized by the upregulation of cytokine levels, in contrast to HFRS where cases were distinguished by a dichotomy in serum cytokine levels. The severe form of hantavirus zoonosis, HPS, was characterized by the upregulation of a higher number of cytokines than HFRS (40 vs 21). In general, our analysis indicates that, although HPS and HFRS share many characteristic features, there are distinct cytokine profiles for these diseases. These profiles suggest a strong activation of an innate immune and inflammatory responses are associated with HPS, relative to HFRS, as well as a robust activation of Th1-type immune responses. Finally, the results of our analysis suggest that serum cytokines profiles of HPS and HFRS cases are consistent with the presence of extracellular matrix degradation, increased mononuclear leukocyte proliferation, and transendothelial migration.

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Section: Discussionmentioning

confidence: 99%

Serum Cytokine Profiles Differentiating Hemorrhagic Fever with Renal Syndrome and Hantavirus Pulmonary Syndrome

et al. 2017

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“…Different infection outcomes in humans and rodents could be explained by the fact that T-CD8+ attracted by infected endothelium would be damaging in humans, while in rodents, these T cells will be inactivated by the induction of Tregs. However, this picture is an over simplification because increased severity of PUUV-induced nephropathia epidemica correlates with higher levels of FoxP3+ Treg [106]. …”

Section: Interaction Of Hantaviruses With the Immune Systemmentioning

confidence: 99%

What Do We Know about How Hantaviruses Interact with Their Different Hosts?

Ermonval

Baychelier

Tordo

2016

Viruses

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Hantaviruses, like other members of the Bunyaviridae family, are emerging viruses that are able to cause hemorrhagic fevers. Occasional transmission to humans is due to inhalation of contaminated aerosolized excreta from infected rodents. Hantaviruses are asymptomatic in their rodent or insectivore natural hosts with which they have co-evolved for millions of years. In contrast, hantaviruses cause different pathologies in humans with varying mortality rates, depending on the hantavirus species and its geographic origin. Cases of hemorrhagic fever with renal syndrome (HFRS) have been reported in Europe and Asia, while hantavirus cardiopulmonary syndromes (HCPS) are observed in the Americas. In some cases, diseases caused by Old World hantaviruses exhibit HCPS-like symptoms. Although the etiologic agents of HFRS were identified in the early 1980s, the way hantaviruses interact with their different hosts still remains elusive. What are the entry receptors? How do hantaviruses propagate in the organism and how do they cope with the immune system? This review summarizes recent data documenting interactions established by pathogenic and nonpathogenic hantaviruses with their natural or human hosts that could highlight their different outcomes.

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“…Interleukin-10 and tumor necrosis factor (TNF)-alpha are both increased in patients with a severe course of PUUV and Dobrava infection. In addition, Koivula et al have shown that there is a strong correlation between FOXP3 + regulatory T cells and disease severity in patients with PUUV infection [15]. …”

Section: Introductionmentioning

confidence: 99%

Determination of Procalcitonin Levels in Patients with Nephropathia Epidemica - A Useful Tool or an Unnecessary Diagnostic Procedure?

Latus

Kitterer²,

Segerer³

et al. 2015

Kidney Blood Press Res

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Background/Aims: Puumala virus causes nephropathia epidemica (NE), a milder form of hemorrhagic fever with renal syndrome that occurs in Central and Northern Europe. Several studies have sought to identify risk factors for severe NE. However, elevated procalcitonin (PCT) levels have not previously been investigated as a predictive marker for a severe course of NE. Methods: A cross-sectional prospective survey of 456 adults with serologically confirmed NE was performed. Results: PCT levels at the time of diagnosis were available for 43 out of 456 patients, and in 24 of these patients (56%) PCT levels were elevated (“PCT positive”). C-reactive protein (CRP) levels at admission to hospital and peak CRP levels during the acute course of the disease were higher in the PCT-positive compared with the PCT-negative group (p<0.05). Severe acute kidney injury (AKI) (RIFLE I and F) was present in similar numbers of PCT-positive and -negative patients (p=0.7), but antibiotics were more frequently used in the PCT-positive than the PCT-negative group (p<0.05). Within the PCT-positive group, PCT levels were similar among those receiving and not receiving antibiotics (p=0.13), and neither the duration of hospital stay nor CRP peak levels were lower in those treated with antibiotics (p=0.12 and p=0.13, respectively). Conclusions: Elevated PCT levels are common in patients with acute NE. There was no association between PCT levels and severity of disease, including AKI or thrombocytopenia. It is important to distinguish Puumala virus infection from other causes of AKI with thrombocytopenia. However, PCT might not be useful in differentiating hantavirus infection from bacterial infection.

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Regulatory T cell response correlates with the severity of human hantavirus infection

Cited by 24 publications

References 48 publications

Serum Cytokine Profiles Differentiating Hemorrhagic Fever with Renal Syndrome and Hantavirus Pulmonary Syndrome

Serum Cytokine Profiles Differentiating Hemorrhagic Fever with Renal Syndrome and Hantavirus Pulmonary Syndrome

What Do We Know about How Hantaviruses Interact with Their Different Hosts?

Determination of Procalcitonin Levels in Patients with Nephropathia Epidemica - A Useful Tool or an Unnecessary Diagnostic Procedure?

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