Hemorrhagic Fever with Renal Syndrome: Literature Review, Epidemiology, Clinical Picture and Pathogenesis

Tariq, Misbah; Kim, Dong-Min

doi:10.3947/ic.2021.0148

Cited by 35 publications

(30 citation statements)

References 95 publications

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“…While the New World hantaviruses, such as Andes virus and Sin Nombre virus always cause HCPS cases in America ( Ma et al., 2020 ; Mir, 2021 ). HTNV is the etiological agent of HFRS in China ( Tariq and Kim, 2022 ). Annually, 150,000–200,000 clinical cases of hantavirus infection are reported worldwide with mortality rates of HFRS and HCPS up to 15% and 50%, respectively ( Mir, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

IL-15 induced bystander activation of CD8+ T cells may mediate endothelium injury through NKG2D in Hantaan virus infection

Zhang

et al. 2022

Front. Cell. Infect. Microbiol.

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IntroductionHantaan virus (HTNV) can cause endothelium injury in hemorrhagic fever with renal syndrome (HFRS) patients. Bystander activation of CD8+ T cells by virus infection has been shown that was involved in host injury, but it is unclear during HTNV infection. This project aimed to study the effect of bystander-activated CD8+ T cell responses in HTNV infection.MethodsThe in vitro infection model was established to imitate the injury of endothelium in HFRS patients. Flow cytometry was performed to detect the expression of markers of tetramer+ CD8+ T cells and human umbilical vein endothelial cells (HUVECs). The levels of interleukin-15 (IL-15) in serum and supermanant were detected using ELISA kit. The expression of MICA of HUVECs was respectively determined by flow cytometry and western blot. The cytotoxicity of CD8+ T cells was assessed through the cytotoxicity assay and antibody blocking assay.ResultsEBV or CMV-specific CD8+ T cells were bystander activated after HTNV infection in HFRS patients. HTNV-infected HUVECs in vitro could produce high levels of IL-15, which was positively correlated with disease severity and the expression of NKG2D on bystander-activated CD8+ T cells. Moreover, the elevated IL-15 could induce activation of CD122 (IL-15Rβ)+NKG2D+ EBV/CMV-specific CD8+ T cells. The expression of IL-15Rα and ligand for NKG2D were upregulated on HTNV-infected HUVECs. Bystander-activated CD8+ T cells could exert cytotoxicity effects against HTNV-infected HUVECs, which could be enhanced by IL-15 stimulation and blocked by NKG2D antibody.DiscussionIL-15 induced bystander activation of CD8+ T cells through NKG2D, which may mediate endothelium injury during HTNV infection in HFRS patients.

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Section: Introductionmentioning

confidence: 99%

IL-15 induced bystander activation of CD8+ T cells may mediate endothelium injury through NKG2D in Hantaan virus infection

Zhang

et al. 2022

Front. Cell. Infect. Microbiol.

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“…Serum ALT activity and liver section analysis showed that KHF4 and KHF5 infections caused hepatitis; however, glycogen storage reduction and petechial hemorrhage in the presence of viral antigens were detected in mice with KHF5 infection. Significant increases in ALT activity have been frequently reported in HFRS cases, and liver damage is considered important for hantavirus pathology [ 36 , 37 ].…”

Section: Discussionmentioning

confidence: 99%

Pathological Studies on Hantaan Virus-Infected Mice Simulating Severe Hemorrhagic Fever with Renal Syndrome

Wei

Shimizu

Sarii

et al. 2022

Viruses

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Hantaan virus is the causative agent of hemorrhagic fever with renal syndrome (HFRS). The Hantaan virus strain, Korean hemorrhagic fever virus clone-5 (KHF5), causes weight loss and renal hemorrhage in laboratory mice. Clone-4 (KHF4), which has a single E417K amino acid change in its glycoprotein, is an avirulent variant. In this study, KHF4 and KHF5 were compared to evaluate pathological differences in mice in vitro and in vivo. The characteristics of the two glycoproteins were not significantly different in vitro. However, the virulent KHF5 strain targeted the lungs and caused pneumonia and edema in vivo. Both strains induced high infectivity levels in the liver and caused hepatitis; however, petechial hemorrhage and glycogen storage reduction were observed in KHF5-infected mice alone. Renal hemorrhage was observed using viral antigens in the tubular region of KHF5-infected mice. In addition, an increase in white blood cell levels and neutrophilia were found in KHF5-infected mice. Microarray analysis of liver cells showed that CD8+ T cell activation, acute-phase protein production, and neutrophil activation was induced by KHF5 infection. KHF5 infectivity was significantly increased in vivo and the histological and clinicopathological findings were similar to those in patients with HFRS.

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“…Of note, there is no specific treatment available for HFRS, and the treatment of HFRS remains primarily supportive. 20 , 21 Ribavirin, an antiviral drug, has been confirmed to significantly reduce the mortality rate by administration in the first 5 days after the onset of symptoms. Unfortunately, ribavirin treatment is likely ineffective during HTNV pulmonary syndrome progressing to the cardiopulmonary phase.…”

Section: Discussionmentioning

confidence: 99%

Hemorrhagic Fever with Renal Syndrome Complicated with Acute Pancreatitis and Capillary Cholangitis: A Case Report

Liu¹,

Wu²,

Li³

et al. 2022

IDR

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Hemorrhagic fever with renal syndrome (HFRS), caused by hanta viruses (HTNV), can be complicated by severe complications. Seventeen percent of the HFRS patients with abdominal pain had acute pancreatitis (AP). The reported prevalence of AP among HFRS patients has a conspicuous high mortality rate. Of note, acute capillary cholangitis (ACC) among HFRS patients presenting with abdominal pain appears extremely rare, particularly independent of HFRS patients complicated with AP. The main pathophysiological mechanism of HFRS complicated with AP and ACC may be that it preferentially damages the microvascular and induces plasma leakage. To date, the management of severe HFRS cases is mainly based on supportive treatment, including extracorporeal blood purification and mechanical ventilation. Here, we describe an exceptionally rare case of a 34-year man who developed HFRS with AP and ACC while improving from HTNV infection via antiviral and supportive treatment.

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Hemorrhagic Fever with Renal Syndrome: Literature Review, Epidemiology, Clinical Picture and Pathogenesis

Cited by 35 publications

References 95 publications

IL-15 induced bystander activation of CD8+ T cells may mediate endothelium injury through NKG2D in Hantaan virus infection

IL-15 induced bystander activation of CD8+ T cells may mediate endothelium injury through NKG2D in Hantaan virus infection

Pathological Studies on Hantaan Virus-Infected Mice Simulating Severe Hemorrhagic Fever with Renal Syndrome

Hemorrhagic Fever with Renal Syndrome Complicated with Acute Pancreatitis and Capillary Cholangitis: A Case Report

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