Tick-Borne Encephalitis Virus Infection of Cultured Mouse Macrophages

Ahantarig, Arunee; Růžek, Daniel; Vancová, Marie; Janowitz, Anna; Šťastná, Hana; Tesařová, Martina; Grubhoffer, Libor

doi:10.1159/000235741

Cited by 12 publications

(5 citation statements)

References 37 publications

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“…We have demonstrated that TBEV is able to adhere from the virus containing liquid to the surface of the neutrophils and resident macrophages, penetrate into the cells, and reproduce in these cells. Similar data on selective adsorption to monocytes/macrophages were obtained while studying the interaction of these cells with TBEV (Ahantarig et al, 2009). Morphological examination of the cell culture infected by virulent strains TBEV revealed the features of the cytopathic action of this virus on the macrophages in contrast with the cells infected by avirulent strains.…”

Section: Resultssupporting

confidence: 66%

The Cells of Innate Systems in Tick-Borne Encephalitis

Плехова¹,

Сомова²,

Lyapun³

et al. 2011

Flavivirus Encephalitis

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Section: Resultssupporting

confidence: 66%

The Cells of Innate Systems in Tick-Borne Encephalitis

Плехова¹,

Сомова²,

Lyapun³

et al. 2011

Flavivirus Encephalitis

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“…Intradermal injection followed by ex vivo analysis revealed a primary infection of local dendritic cells, neutrophils, and monocytes (36). Furthermore, cell culture experiments showed that macrophages are infectible and produce large amounts of viral titers (37). Our results in vivo show that LGTV is indiscriminate and that it can target different hematopoietic and nonhematopoietic cell types in the peripheral and CNS tissues.…”

Section: Discussionmentioning

confidence: 67%

Type I Interferon Protects Mice from Fatal Neurotropic Infection with Langat Virus by Systemic and Local Antiviral Responses

Weber

Finsterbusch

Lindquist

et al. 2014

J Virol

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Vector-borne flaviviruses, such as tick-borne encephalitis virus (TBEV), West Nile virus, and dengue virus, cause millions of infections in humans. TBEV causes a broad range of pathological symptoms, ranging from meningitis to severe encephalitis or even hemorrhagic fever, with high mortality. Despite the availability of an effective vaccine, the incidence of TBEV infections is increasing. Not much is known about the role of the innate immune system in the control of TBEV infections. Here, we show that the type I interferon (IFN) system is essential for protection against TBEV and Langat virus (LGTV) in mice. In the absence of a functional IFN system, mice rapidly develop neurological symptoms and succumb to LGTV and TBEV infections. Type I IFN system deficiency results in severe neuroinflammation in LGTV-infected mice, characterized by breakdown of the blood-brain barrier and infiltration of macrophages into the central nervous system (CNS). Using mice with tissue-specific IFN receptor deletions, we show that coordinated activation of the type I IFN system in peripheral tissues as well as in the CNS is indispensable for viral control and protection against virus induced inflammation and fatal encephalitis. IMPORTANCEThe type I interferon (IFN) system is important to control viral infections; however, the interactions between tick-borne encephalitis virus (TBEV) and the type I IFN system are poorly characterized. TBEV causes severe infections in humans that are characterized by fever and debilitating encephalitis, which can progress to chronic illness or death. No treatment options are available. An improved understanding of antiviral innate immune responses is pivotal for the development of effective therapeutics. We show that type I IFN, an effector molecule of the innate immune system, is responsible for the extended survival of TBEV and Langat virus (LGTV), an attenuated member of the TBE serogroup. IFN production and signaling appeared to be essential in two different phases during infection. The first phase is in the periphery, by reducing systemic LGTV replication and spreading into the central nervous system (CNS). In the second phase, the local IFN response in the CNS prevents virus-induced inflammation and the development of encephalitis.

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“…However, POWV directly infects macrophages (Fig. 2 ) at an early stage in the tick-feeding site [ 53 , 54 ], which potentially triggers the activation of NK and NKT cells to produce IFNγ causing a cytotoxic response in POWV virions (Fig. 2 ).…”

Section: Introductionmentioning

confidence: 99%

Potential molecular mechanisms of chronic fatigue in long haul COVID and other viral diseases

Gottschalk

Peterson²,

Armstrong³

et al. 2023

Infect Agents Cancer

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Historically, COVID-19 emerges as one of the most devastating diseases of humankind, which creates an unmanageable health crisis worldwide. Until now, this disease costs millions of lives and continues to paralyze human civilization's economy and social growth, leaving an enduring damage that will take an exceptionally long time to repair. While a majority of infected patients survive after mild to moderate reactions after two to six weeks, a growing population of patients suffers for months with severe and prolonged symptoms of fatigue, depression, and anxiety. These patients are no less than 10% of total COVID-19 infected individuals with distinctive chronic clinical symptomatology, collectively termed post-acute sequelae of COVID-19 (PASC) or more commonly long-haul COVID. Interestingly, Long-haul COVID and many debilitating viral diseases display a similar range of clinical symptoms of muscle fatigue, dizziness, depression, and chronic inflammation. In our current hypothesis-driven review article, we attempt to discuss the molecular mechanism of muscle fatigue in long-haul COVID, and other viral diseases as caused by HHV6, Powassan, Epstein–Barr virus (EBV), and HIV. We also discuss the pathological resemblance of virus-triggered muscle fatigue with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). Graphical Abstract

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Tick-Borne Encephalitis Virus Infection of Cultured Mouse Macrophages

Cited by 12 publications

References 37 publications

The Cells of Innate Systems in Tick-Borne Encephalitis

The Cells of Innate Systems in Tick-Borne Encephalitis

Type I Interferon Protects Mice from Fatal Neurotropic Infection with Langat Virus by Systemic and Local Antiviral Responses

Potential molecular mechanisms of chronic fatigue in long haul COVID and other viral diseases

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