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Order Bunyavirales
Published in Paul Pumpens, Peter Pushko, Philippe Le Mercier, Virus-Like Particles, 2022
Paul Pumpens, Peter Pushko, Philippe Le Mercier
The 1.6 Å crystal structure of the RVFV hexameric ring-shaped protein N forming a functional RNA binding site and expressed in E. coli was determined (Ferron et al. 2011). This structure explained the switch from an intra- to an intermolecular interaction mode of the N-terminal arm as a general principle that underlies multimerization and RNA encapsidation by bunyaviruses. Next, the crystal structure of the protein N of an emerging phlebovirus, namely human severe fever with thrombocytopenia syndrome phlebovirus (SFTSV), was resolved (Zhou H et al. 2013). Then, the crystal structure of the RVFV glycoprotein Gc followed and demonstrated an important but unanticipated evolutionary link between bunyavirus and flavivirus envelopes (Dessau and Modis 2013; Rusu et al. 2012), namely, the gained structure was similar to that described earlier for the alphavirus E1-E2 proteins.
Ticks
Published in Gail Miriam Moraru, Jerome Goddard, The Goddard Guide to Arthropods of Medical Importance, Seventh Edition, 2019
Gail Miriam Moraru, Jerome Goddard
In the last decade, several new tick-borne viruses have been identified. Severe fever with thrombocytopenia syndrome (SFTS) was first described in rural areas of China, Japan, and Korea in 2011–2012. This disease, caused by a Phlebovirus, has thus far produced at least 2,500 human cases,92 and is believed to be transmitted by Haemaphysalis longicornis ticks.93 Heartland virus (a Phlebovirus) is associated with the Lone Star tick, Amblyomma americanum and has been recognized in Missouri, Oklahoma, Kentucky, and Tennessee.94,95 Only about 30 cases of heartland virus have been identified. A few cases of a new Thogotovirus called bourbon virus have been identified in the Midwest and southern United States, also with A. americanum as the vector. 9698
COVID-19 and cardiovascular disease: manifestations, pathophysiology, vaccination, and long-term implication
Published in Current Medical Research and Opinion, 2022
Adel Abdel Moneim, Marwa A. Radwan, Ahmed I. Yousef
More prevalent COVID-19 symptoms include dry cough, fever, and fatigue17. Consequently, to prevent extremely high body temperatures from interfering with normal physiological functions, the sympathetic nerves are stimulated, causing an elevated heart rate and heart output80. Most disorders with fever, such as severe fever with thrombocytopenia syndrome (TTS), might be worsened by myocarditis81. Liem et al. observed that prolonged fever is associated with the development of pericarditis after MI. Temperature sensitivity varied according to diseases, with distinct patterns for acute and chronic ischemic cardiac dysfunction. Temperature-induced injury is hypothesized to be associated with increased sympathetic activation, which is accompanied by sympathetic nervous system stimulation, renin-angiotensin system stimulation, dehydration, and systemic inflammation82,83. It is important to note that cardiac damage in coronavirus infection may be accompanied by fever. Several factors, such as fever, may cause or worsen arrhythmias in patients with COVID-19. Specifically, fever can indicate the presence of cardiac channelopathies including Brugada syndrome and long QT syndrome 63 (Figure 1).
TANK-binding kinase 1 as a novel therapeutic target for viral diseases
Published in Expert Opinion on Therapeutic Targets, 2019
Nonstructural protein (NS) of heartland virus (HRTV) [89], dengue virus (DENV) serotype 4 (DENV4) [90] and West Nile virus (WNV) [90] can directly prevent the autophosphorylation of TBK and thus attenuate antiviral innate immune responses. In addition, NS of HRTV directly binds to TBK1 and thus blocks the association between TBK1 and IRF3 [91]. The NSs of severe fever with thrombocytopenia syndrome bunyavirus (SFTSV) escape the host immune system by inducing the formation of cytoplasmic inclusion bodies (IBs) [92,93]. The IBs are characterized as dynamic and functional structures that benefit to the virus to accomplish their life cycle [92,93]. The viral NSs bind to the TBK1/IKKε complex and relocate them into IBs, leading to the spatial separation of TBK1 complexes from other adaptors [92,93]. However, recently Moriyama and colleagues presented that the NS of SFTSV could impair the autophosphorylation of TBK by direct interaction, leading the mechanism of NS to the mist [94].
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
Severe fever with thrombocytopenia syndrome (SFTS) is an emerging hemorrhagic fever-like illness, first identified in central and northeast China in 2009 and later in Japan and Korea in 2012 [1–3]. In 2013, a similar disease was reported in United States [4]. The cause of this potential life-threatening disease was further identified as SFTS bunyavirus (SFTSV), a new member of family Bunyaviridae. SFTSV infection leads to a wide variety of clinical manifestations that range from asymptomatic infection to various grades of severe disease. Severe SFTS is characterized by fever, thrombocytopenia, gastrointestinal symptoms and multi-organ dysfunction syndrome (MODS). The average case fatality of SFTSV infection is about 12%, ranging from 6.3% to 30.0% [5,6]. SFTSV has been widely isolated and identified from tick species (Haemaphysalis longicornis and Rhipicephalus microplus) in mountain-hill area. Further, poultry and livestock are also the reservoirs for SFTSV, as SFTSV-specific antibodies were present in domestic animals. Therefore, it is considered that most cases acquired infection via tick bites and livestock [5]. However, there is a small percentage of patients who denied the presence of tick bite or livestock contact before illness onset.