scholarly journals Contact-dependent transmission of Langat and tick-borne encephalitis virus in type I interferon receptor-1 deficient mice.

2021 ◽  
Author(s):  
Sarah Schreier ◽  
Kristin Cebulski ◽  
Andrea Kröger
Keyword(s):  
Interferon Alpha ◽  
Close Contact ◽  
Encephalitis Virus ◽  
Interferon Α ◽  
Type I ◽  
Milk Products ◽  
Tick Borne Encephalitis ◽  
Contact Transmission ◽  
Tick Borne Encephalitis Virus ◽  
Close Contact Transmission

Tick-borne encephalitis virus (TBEV) is primarily transmitted to humans through tick bites or oral consumption of accordingly contaminated unpasteurized milk or milk products. The detection of TBEV RNA in various body fluids in immunosuppressed human patients is documented. However, the risk of direct contact exposure remains unclear. Interferon-alpha receptor-1 deficient (Ifnar1-/-) mice, which are lacking the interferon-α/β responses, develop neurologic manifestations after infection with TBEV and Langat virus (LGTV). We showed that subcutaneous, intranasal, and peroral infection of LGTV lead to disease, whereas mice with intragastric application of LGTV showed no disease signs. With LGTV infected mice exhibit seroconversion and significant viral RNA levels was detected in saliva, eye smear, feces and urine. As a result, TBEV and LGTV are transmitted between mice from infected to naïve co-caged sentinel animals. Although intranasal inoculation of LGTV is entirely sufficient to establish the disease in mice, the virus is not transmitted by aerosols. These pooled results from animal models highlight the risks of exposure to TBEV contaminants and the possibility for close contact transmission of TBEV in interferon-alpha receptor-1 deficient laboratory mice. Importance Tick-borne encephalitis is a severe disease of the central nervous system caused by the tick-borne encephalitis virus (TBEV). Every year between 10,000-12,000 people become infected with this flavivirus. The TBEV is usually transmitted to humans via the bite of a tick, but infections due to consumption of infectious milk products are increasingly being reported. Since there is no therapy for an TBEV infection and mechanisms of virus persistence in reservoir animals are unclear, it is important to highlight the risk of exposure to TBEV contaminants and know possible routes of transmission of this virus. The significance of our research is in identifying other infection routes of TBEV and LGTV, and the possibility of close contact transmission.

scholarly journals Infection and injury of human astrocytes by tick-borne encephalitis virus

2014 ◽  
Vol 95 (11) ◽  
pp. 2411-2426 ◽  
Author(s):  
Martin Palus ◽  
Tomáš Bílý ◽  
Jana Elsterová ◽  
Helena Langhansová ◽  
Jiří Salát ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Encephalitis Virus ◽  
Ultrastructural Changes ◽  
Interferon Α ◽  
Human Astrocytes ◽  
Tick Borne Encephalitis ◽  
Infected Cells ◽  
Tick Borne Encephalitis Virus ◽  
Tbev Infection ◽  
Pro Inflammatory Cytokines

Tick-borne encephalitis (TBE), a disease caused by tick-borne encephalitis virus (TBEV), represents the most important flaviviral neural infection in Europe and north-eastern Asia. In the central nervous system (CNS), neurons are the primary target for TBEV infection; however, infection of non-neuronal CNS cells, such as astrocytes, is not well understood. In this study, we investigated the interaction between TBEV and primary human astrocytes. We report for the first time, to the best of our knowledge, that primary human astrocytes are sensitive to TBEV infection, although the infection did not affect their viability. The infection induced a marked increase in the expression of glial fibrillary acidic protein, a marker of astrocyte activation. In addition, expression of matrix metalloproteinase 9 and several key pro-inflammatory cytokines/chemokines (e.g. tumour necrosis factor α, interferon α, interleukin (IL)-1β, IL-6, IL-8, interferon γ-induced protein 10, macrophage inflammatory protein, but not monocyte chemotactic protein 1) was upregulated. Moreover, we present a detailed description of morphological changes in TBEV-infected cells, as investigated using three-dimensional electron tomography. Several novel ultrastructural changes were observed, including the formation of unique tubule-like structures of 17.9 ±0.15 nm diameter with associated viral particles and/or virus-induced vesicles and located in the rough endoplasmic reticulum of the TBEV-infected cells. This is the first demonstration that TBEV infection activates primary human astrocytes. The infected astrocytes might be a potential source of pro-inflammatory cytokines in the TBEV-infected brain, and might contribute to the TBEV-induced neurotoxicity and blood–brain barrier breakdown that occurs during TBE. The neuropathological significance of our observations is also discussed.

scholarly journals Alimentary Infections by Tick-Borne Encephalitis Virus

Viruses ◽  
2021 ◽  
Vol 14 (1) ◽  
pp. 56
Author(s):  
Martina Ličková ◽  
Sabína Fumačová Havlíková ◽  
Monika Sláviková ◽  
Boris Klempa
Keyword(s):  
Experimental Data ◽  
Neurological Disease ◽  
Preventive Measures ◽  
Experimental Studies ◽  
Raw Milk ◽  
Encephalitis Virus ◽  
Relevant Factor ◽  
Milk Products ◽  
Tick Borne Encephalitis ◽  
Tick Borne Encephalitis Virus

Tick-borne encephalitis virus (TBEV) causes serious the neurological disease, tick-borne encephalitis (TBE). TBEV can be transmitted to humans by ticks as well as by the alimentary route, which is mediated through the consumption of raw milk products from infected ruminants such as sheep, goats, and cows. The alimentary route of TBEV was recognized in the early 1950s and many important experimental studies were performed shortly thereafter. Nowadays, alimentary TBEV infections are recognized as a relevant factor contributing to the overall increase in TBE incidences in Europe. This review aims to summarize the history and current extent of alimentary TBEV infections across Europe, to analyze experimental data on virus secretion in milk, and to review possible alimentary infection preventive measures.

scholarly journals Tick-Borne Encephalitis Virus Delays Interferon Induction and Hides Its Double-Stranded RNA in Intracellular Membrane Vesicles

2010 ◽  
Vol 84 (17) ◽  
pp. 8470-8483 ◽  
Author(s):  
Anna K. Överby ◽  
Vsevolod L. Popov ◽  
Matthias Niedrig ◽  
Friedemann Weber
Keyword(s):  
Particle Production ◽  
Encephalitis Virus ◽  
Type I Interferons ◽  
Initiation Factor ◽  
Type I ◽  
Intracellular Membrane ◽  
Viral Dsrna ◽  
Double Stranded Rna ◽  
Tick Borne Encephalitis ◽  
Tick Borne Encephalitis Virus

ABSTRACT Tick-borne encephalitis virus (TBEV) (family Flaviviridae, genus Flavivirus) accounts for approximately 10,000 annual cases of severe encephalitis in Europe and Asia. Here, we investigated the induction of the antiviral type I interferons (IFNs) (alpha/beta IFN [IFN-α/β]) by TBEV. Using strains Neudörfl, Hypr, and Absettarov, we demonstrate that levels of IFN-β transcripts and viral RNA are strictly correlated. Moreover, IFN induction by TBEV was dependent on the transcription factor IFN regulatory factor 3 (IRF-3). However, even strain Hypr, which displayed the strongest IFN-inducing activity and the highest RNA levels, substantially delayed the activation of IRF-3. As a consequence, TBEV can keep the level of IFN transcripts below the threshold value that would permit the release of IFN by the cell. Only after 24 h of infection have cells accumulated sufficient IFN transcripts to produce detectable amounts of secreted IFNs. The delay in IFN induction appears not to be caused by a specific viral protein, since the individual expressions of TBEV C, E, NS2A, NS2B, NS3, NS4A, NS4B, NS5, and NS2B-NS3, as well as TBEV infection itself, had no apparent influence on specific IFN-β induction. We noted, however, that viral double-stranded RNA (dsRNA), an important trigger of the IFN response, is immunodetectable only inside intracellular membrane compartments. Nonetheless, the dependency of IFN induction on IFN promoter stimulator 1 (IPS-1) as well as the phosphorylation of the alpha subunit of eukaryotic initiation factor 2 (eIF2α) suggest the cytoplasmic exposure of some viral dsRNA late in infection. Using ultrathin-section electron microscopy, we demonstrate that, similar to other flaviviruses, TBEV rearranges intracellular membranes. Virus particles and membrane-connected vesicles (which most likely represent sites of virus RNA synthesis) were observed inside the endoplasmic reticulum. Thus, apparently, TBEV rearranges internal cell membranes to provide a compartment for its dsRNA, which is largely inaccessible for detection by cytoplasmic pathogen receptors. This delays the onset of IFN induction sufficiently to give progeny particle production a head start of approximately 24 h.

scholarly journals Sequential MAVS- and MyD88/TRIF-signaling triggers anti-viral responses of tick-borne encephalitis virus-infected murine astrocytes

2020 ◽  
Author(s):  
Luca Ghita ◽  
Veronika Breitkopf ◽  
Felix Mulenge ◽  
Andreas Pavlou ◽  
Olivia Luise Gern ◽  
...  
Keyword(s):  
Cell Subset ◽  
Encephalitis Virus ◽  
Type I ◽  
Tick Borne Encephalitis ◽  
Transcriptome Analyses ◽  
Tick Borne Encephalitis Virus ◽  
Viral Responses ◽  
Mitochondrial Antiviral Signaling ◽  
Tbev Infection

AbstractTick-borne encephalitis virus (TBEV), a member of the Flaviviridae family, is typically transmitted upon tick bite and can cause meningitis and encephalitis in humans. In TBEV infected mice, mitochondrial antiviral signaling protein (MAVS), the downstream adaptor of retinoic acid inducible gene I-like receptor (RLR)-signaling, is needed to induce early type I interferon (IFN) responses and to confer protection. To identify the brain resident cell subset that produces protective IFN-β in TBEV infected mice, we isolated neurons, astrocytes and microglia and exposed these cells to TBEV in vitro. Under such conditions, neurons showed the highest percentage of infected cells, whereas astrocytes and microglia were infected to a lesser extent. In the supernatant (SN) of infected neurons, IFN-β was not detectable, while infected astrocytes showed very high and microglia low IFN-β production. Transcriptome analyses of astrocytes implied that MAVS-signaling was needed early after TBEV infection. Accordingly, MAVS-deficient astrocytes showed enhanced TBEV infection and significantly reduced early IFN-β responses. At later time points, moderate amounts of IFN-β were detected in the SN of infected MAVS-deficient astrocytes. Transcriptome analyses indicated that MAVS-deficiency negatively affected the induction of early anti-viral responses, which resulted in significantly increased TBEV replication. Treatment with MyD88 and TRIF inhibiting peptides reduced late IFN-β responses of TBEV infected WT astrocytes and entirely blocked IFN-β responses of infected MAVS-deficient astrocytes. Thus, upon TBEV exposure of brain-resident cells, astrocytes are important IFN-β producers that show biphasic IFN-β induction that initially depends on MAVS- and later on MyD88/TRIF-signaling.

TBE in South Korea

2019 ◽  
Author(s):  
Joon Young Song
Keyword(s):  
South Korea ◽  
Human Case ◽  
Encephalitis Virus ◽  
Surveillance Studies ◽  
Tick Borne Encephalitis ◽  
Tick Borne Encephalitis Virus

Although no human case of tick-borne encephalitis (TBE) has been documented in South Korea to date, surveillance studies have been conducted to evaluate the prevalence of tick-borne encephalitis virus (TBEV) in wild ticks.

TBE in Slovakia

2019 ◽  
Author(s):  
Jana Kerlik
Keyword(s):  
Encephalitis Virus ◽  
Tick Borne Encephalitis ◽  
Tick Borne Encephalitis Virus

The former Czechoslovak Republic was one of the first countries in Europe where the tick-borne encephalitis virus (TBEV) was identified.

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