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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].
Pulmonary Endothelium in Health and Viral Infections
Published in Sunit K. Singh, Human Respiratory Viral Infections, 2014
Nikolaos Manitsopoulos, Frantzeska Frantzeskaki, Anastasia Kotanidou, Stylianos E. Orfanos
Hantaviruses, RNA viruses belonging to the family Bunyaviridae, are causatively related to a hemorrhagic fever associated with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS).137HPS in North and South America is caused by Sin Nombre virus and Andes virus, included in the New World hantaviruses.138 HPS begins with “flu like illness” and progressively evolves to pulmonary edema and shock. Pulmonary edema is mainly noncardiogenic, in terms of ARDS. However, in fatal cases a cardiopulmonary syndrome might develop, characterized by cardiogenic shock.139 Microvascular endothelium is the prominent target of the hantavirus, and microvascular leakage is the cornerstone of pathology of the relevant syndrome.139
Association Between IL28B, IL29 Gene Polymorphisms and Clinical Manifestations of Behçet’s Disease
Published in Immunological Investigations, 2021
G. Cakmak Genc, S. Karakas Celık, A. Kocaaga, R. Koca, A. Dursun
In this study, we evaluated to association of three SNPs related IL28B and IL29 with BD susceptibility and its clinical characteristics at the first time. When we compared the groups for the genotype distributions of rs8099917 (IL28 G/T) polymorphism between BD patients and controls (Table 3), we found the GG genotype significantly higher in controls in the recessive inheritance model (Table 3). Arpacı et al. found the G allele frequency higher in the controls for rs8099917 (IL28 G/T) polymorphism in HT (Arpaci et al. 2016). Therefore, they suggested that the G allele may have a protective role in HT pathogenesis. Additionally, results of Astudillo et al. revealed that the GG genotype and G allele for SNP rs8099917 (IL28 G/T) linked with a mild respiratory syncytial virus bronchiolitis among hospitalized pediatric patients (Astudillo et al. 2019). Angulo et al. showed that the GG genotype of rs8099917 (IL28 G/T) is associated with a mild phenotype in Andes virus-induced disease (Angulo et al. 2015). Finally, de Sa et al. searched the association between IL28B gene polymorphisms and the development of HTLV associated arthropathy (HAA). Their findings suggest that TT genotype of rs8099917 (IL28 G/T) is associated with poor prognosis of HAA (de Sá et al. 2016). Our results were similar to these studies and we suggest that the GG genotype of rs8099917 (IL28 G/T) might be a protective factor against BD.
Post-exposure prophylactic vaccine candidates for the treatment of human Risk Group 4 pathogen infections
Published in Expert Review of Vaccines, 2020
James Logue, Ian Crozier, Peter B Jahrling, Jens H Kuhn
Orthohantaviruses (Hantaviridae: Orthohantavirus) are separated into Old World viruses, usually causing hemorrhagic fever with renal syndrome, and New World viruses, which generally cause hantavirus pulmonary syndrome associated with a CFR of 30–50%. These zoonoses are maintained in Europe and Asia by murid and cricetid rodents (Old World orthohantaviruses) or in the Americas by cricetid rodents (New World orthohantaviruses) [98,99]. Of the viruses in this genus, Andes virus (ANDV), a New World orthotantavirus, is of highest concern because ANDV, in contrast to most other orthohantaviruses, has been associated with person-to-person transmission [100–102]. Consequently, orthohantavirus PEP vaccine research has largely focused on ANDV, again using the rVSIV platform to express the ANDV glycoprotein. In vivo, this candidate vaccine protected 90% (9 of 10) of golden hamsters when given 1 day after an otherwise lethal ANDV injection [103]. Interestingly, a rVSIV-vectored EBOV vaccine elicited a similar level of protection (6 of 6) against ANDV in golden hamsters, again questioning whether antigen-specificity is necessary for effective PEP. However, only very few reports are available on the development of an orthohantavirus NHP animal model to date (e.g., [104–106]), and these results of PEP in small animal models have yet to be corroborated in an NHP model.
Characterization of clinical features and outcome for human-to-human transmitted severe fever with thrombocytopenia syndrome
Published in Infectious Diseases, 2018
Bei Jia, Weihua Wu, Rui Huang, Guiyang Wang, Peixin Song, Yang Li, Yong Liu, Yali Xiong, Xiaomin Yan, Yingying Hao, Juan Xia, Zhaoping Zhang, Yuxin Chen, Chao Wu
First, our study suggested that secondary infection usually happens among family clusters or medical staffs after close contact with SFTS patients. Specifically, blood samples and bloody secretions are highly contagious [7,9,10,19,20], even after the patient’s death [21]. No obvious evidence thus far has demonstrated that SFTSV transmits through respiratory secretions, urine and feces [7,9,10,19–21]. Of note, the blood contact is not necessary during person-to-person spread of several bunyaviruses, such as CCHF virus and Andes virus, suggesting the transmission mode of SFTS is quite unique among Bunyaviridae family [22,23].