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Order Blubervirales: Core Protein
Published in Paul Pumpens, Peter Pushko, Philippe Le Mercier, Virus-Like Particles, 2022
Paul Pumpens, Peter Pushko, Philippe Le Mercier
Rainer G. Ulrich and his colleagues generated a set of putative vaccine candidates against hantavirus infection (Ulrich et al. 1998, 1999; Koletzki et al. 1997, 1999, 2000; Krüger et al. 2001; Geldmacher et al. 2004, 2005). The previously mentioned ingenious SplitCore methodology has led to a prospective vaccine against Lyme disease caused by Borrelia burgdorferi (Walker et al. 2008, 2011).
Severe Non-influenza Viral Pneumonia in the Critical Care Unit
Published in Cheston B. Cunha, Burke A. Cunha, Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
David Waldner, Thomas J. Marrie, Wendy Sligl
Hantaviruses are enveloped single-stranded RNA viruses within the family Bunyaviridae and are capable of causing two distinct illnesses, hemorrhagic fever with renal syndrome (HFRS) and hantavirus cardiopulmonary syndrome (HCPS), which occur primarily in the Old and New Worlds, respectively [84]. These viruses were named after the prototypic Hantaan virus, which was isolated from a striped field mouse near the Hantaan river in South Korea and is now known to have been the causative agent of an outbreak of HFRS among thousands of UN troops during the Korean War [84]. Since this outbreak, several other viruses have been identified as causes of HFRS throughout Europe and Asia and are collectively referred to as Old World hantaviruses [84]. Hantavirus infection was largely unrecognized in the New World prior to an outbreak of HCPS in the Four Corners region of the United States during the spring of 1993 [85]. Sin Nombre virus was the agent responsible for this outbreak and remains the predominant cause of HCPS in North America. In addition to SNV, several other New World hantaviruses have been identified as causes of HCPS, of which Andes virus (ANDV) is the most notable, accounting for most cases in South America [84].
Hemorrhagic Fever with Renal Syndrome: A Historical Perspective and Review of Recent Advances
Published in James H. S. Gear, CRC Handbook of Viral and Rickettsial Hemorrhagic Fevers, 2019
Outbreaks of HFRS in the Soviet Union,141,178,188 Japan,147,192,193 Korea,194 Belgium,155,156 and the U.K.164 (Table 4) underscore the risk of laboratory-acquired HFRS among investigators working with experimentally or naturally infected wild or laboratory rodents. Infection has also been reported among individuals engaged in the trapping of rodents in HFRS-endemic regions.55,177 Widespread outbreaks of HFRS at multiple medical institutions in Japan147,192,193 stress the need for laboratory animal suppliers to be certain that their rodent colonies are not infected and to employ the caesarean-obtained, barrier-sustained system of breeding. In addition, rat-associated cases of HFRS at a university in Belgium and a research laboratory in England indicate the importance of routine screening for hantavirus infection before exportation or importation of live animals, their unfixed tissues or cell lines derived from rodents.115,155,164,195 Recently, all cell lines of rat origin, including rat-mouse hybridomas, held in the repository of the American Type Culture Collection, were found not to harbor Hantaan-like viruses, but this does not diminish the need for continued vigilance.195
The role of glomerular lesions in the prognosis of patients with acute kidney injury during hemorrhagic fever with renal syndrome
Published in Renal Failure, 2023
Min Min, Meiling Liu, Chunyu Lu, Lina Zhu, Jiong Zhang, Jinquan Wang
Hantavirus infection is linked to the working and living environment of patients. Humans are not the natural host of Hantavirus, and infection occurs in most cases due to accidental inhalation of virus-containing aerosols in rodent feces. Living or working in an environment with rodents has a high risk of infection [18]. In our study, the patients’ main occupation was farmer or worker, and most of them had experience working outdoors before the onset of HFRS. Additionally, the majority of the patients in this study were male, which is in accordance with the previously reported epidemiological characteristics of HFRS [19]. Rodent control is still the primary measure of prevention of HFRS. Epidemiological surveillance and vaccination are also important measures to protect susceptible populations. Unfortunately, no FDA-approved vaccines or drugs are available. More efforts are needed to develop a usable vaccine or targeted drugs for HFRS. According to previous clinical trials, intravenous ribavirin in the treatment of HFRS significantly reduced the risk of developing severe illness and the risk of mortality, but other studies have not proven these benefits [20].
Logistic regression analysis of risk factors for hemorrhagic fever with renal syndrome complicated with acute pancreatitis
Published in Annals of Medicine, 2023
Wenjie Wang, Dongqing Fan, Bin Quan, Weishun Hou, Jinsun Yang
Hantavirus infection causes rodent-borne zoonotic illness hemorrhagic fever with renal syndrome (HFRS), which is mostly spread to people by aerosolized viral particles found in rodent urine, feces, and saliva [1]. China has the greatest incidence of HFRS worldwide, with Asia and Europe having the highest prevalence rates [2]. In mainland China, 209,209 HFRS cases and 1855 related fatalities were documented from 2004 to 2019. This represents a considerable illness burden [3]. One of the most severely afflicted regions in China is the province of Anhui, home to more than 60 million people. The southern regions of Anhui, including Xuancheng City and Wuhu City, are the most hit. Fever, bleeding, renal failure, thrombocytopenia, and shock are among the clinical signs of HFRS [4]. Currently, there is no effective antiviral treatment for HFRS; consequently, the mortality rate in critically ill patients is high.
Defibrotide: potential for treating endothelial dysfunction related to viral and post-infectious syndromes
Published in Expert Opinion on Therapeutic Targets, 2021
Edward Richardson, David García-Bernal, Eleonora Calabretta, Rubén Jara, Marta Palomo, Rebecca M. Baron, Gregory Yanik, Jawed Fareed, Israel Vlodavsky, Massimo Iacobelli, Maribel Díaz-Ricart, Paul G. Richardson, Carmelo Carlo-Stella, Jose M. Moraleda
The severity of the Hantavirus infection also ranges from mild to severe, with reported case fatality rates up to 35%. HCPS is marked by lung edema and acute hypoxic respiratory failure which may require supplemental oxygen, intubation with mechanical ventilation or extracorporeal membrane oxygenation. HFRS, on the other hand, presents with renal impairment requiring hemodialysis in severe cases [74]. Additional severe manifestations of Hantavirus infection include shock and diffuse hemorrhage due to increased vascular permeability. Vascular endothelial growth factor (VEGF) has been identified as a key factor in Hantavirus infection, as pathogenic hantaviruses augment endothelial permeability in response to VEGF signals [75]. Hantavirus targets beta-integrins, which normally form complexes with VEGF receptors, thereby interfering with the normal regulation of VEGF signaling at the endothelial cell surface through this mechanism [67]. The resultant increase in VEGF signaling contributes to widespread vascular leakage in hantavirus-related diseases. In vitro studies have demonstrated reduced production of VEGF by stromal cells in response to the DF treatment [10], a potentially advantageous effect in the treatment of hantavirus infection. Hantaviruses also binds VE-cadherins on the surface of ECs as one route of cell entry, disrupting inter-endothelial adherens junctions [65]. In vitro studies with DF have also shown that DF can suppress the VE-cadherin expression on ECs [8], and DF may thereby limit the infectivity of hantavirus by decreasing its binding target on ECs. In the context of hantavirus infection, however, this effect of DF may stand to further destabilize adherent junctions.