Upregulation of IFN-γ and IL-12 is associated with a milder form of hantavirus hemorrhagic fever with renal syndrome

Khaiboullina, Svetlana F.; Martynova, Ekaterina; Khamidullina, Z. L.; Lapteva, E. V.; Nikolaeva, I. V.; Anokhin, V. V.; Lombardi, Vincent; Rizvanov, Albert A.

doi:10.1007/s10096-014-2176-x

Cited by 21 publications

(26 citation statements)

References 53 publications

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“…Our data support previous observations that chemokines promoting mononuclear leukocyte migration are upregulated in hantavirus-infected patients (28). In this study, upregulation of CXCL9 and CXCL10 were characteristic for both HPS and HFRS throughout the course of the disease.…”

Section: Discussionsupporting

confidence: 93%

“…For example, Saksida et al demonstrated that the level of serum pro-inflammatory cytokines was higher in HFRS patients infected with Dobrava virus as compared to PUUV-infected patients (30). Additionally, our previous report points out the potential role of Th1-type immune response in the severity of NE (28). PUUV infection presents with a milder form of the disease and lower mortality rate when compared to Dobrava virus infections.…”

Section: Introductionmentioning

confidence: 92%

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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: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 92%

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

et al. 2017

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“…We have demonstrated that increased serum IFN- γ and IL-12 are associated with the mild form of NE [24]. These data confirm this observation, with a lower NE severity score being associated with higher levels of these cytokines.…”

Section: Discussionsupporting

confidence: 66%

“…Upregulation of these cytokines in female NE suggests that there is activation of Th1 lymphocytes. Previously, we have shown an association between the mild form of NE and elevated serum IFN- γ and IL-12 [24]. Therefore, these data suggest that lower severity scores in female cases are associated with activation of Th1 type immune response.…”

Section: Resultssupporting

confidence: 51%

High Triglycerides Are Associated with Low Thrombocyte Counts and High VEGF in Nephropathia Epidemica

Martynova

Valiullina

Gusev

et al. 2016

Journal of Immunology Research

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Nephropathia epidemica (NE) is a mild form of hemorrhagic fever with renal syndrome. Several reports have demonstrated a severe alteration in lipoprotein metabolism. However, little is known about changes in circulating lipids in NE. The objectives of this study were to evaluate changes in serum total cholesterol, high density cholesterol (HDCL), and triglycerides. In addition to evaluation of serum cytokine activation associations, changes in lipid profile and cytokine activation were determined for gender, thrombocyte counts, and VEGF. Elevated levels of triglycerides and decreased HDCL were observed in NE, while total cholesterol did not differ from controls. High triglycerides were associated with both the lowest thrombocyte counts and high serum VEGF, as well as a high severity score. Additionally, there were higher levels of triglycerides in male than female NE patients. Low triglycerides were associated with upregulation of IFN-γ and IL-12, suggesting activation of Th1 helper cells. Furthermore, levels of IFN-γ and IL-12 were increased in patients with lower severity scores, suggesting that a Th1 type immune response is playing protective role in NE. These combined data advance the understanding of NE pathogenesis and indicate a role for high triglycerides in disease severity.

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“…Variations then depends on the phase and severity of the disease, with IFN-γ and IL-12 relating to mild forms [112]. An up-regulation of uPAR has also been described in PUUV patients.…”

Section: Activation Of Host Cell Factors By Hantavirusesmentioning

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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Upregulation of IFN-γ and IL-12 is associated with a milder form of hantavirus hemorrhagic fever with renal syndrome

Cited by 21 publications

References 53 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

High Triglycerides Are Associated with Low Thrombocyte Counts and High VEGF in Nephropathia Epidemica

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

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