Viral neuronotropism is important in the pathogenesis of <scp>M</scp>urray <scp>V</scp>alley encephalitis

Fu, Tzeh Long; Ong, Kien Chai; Tran, Yang David; McLean, Catriona; Wong, Kum Thong

doi:10.1111/nan.12285

Cited by 5 publications

(4 citation statements)

References 12 publications

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“…3A ). This histopathological manifestation has been previously reported during WNV brain invasion ( 27 , 28 ) and other neurovirulent flavivirus infections ( 29 ). However, spongiosis appeared to be more prominent in αβR −/− λR −/− mice ( Fig.…”

Section: Resultssupporting

confidence: 81%

Type III Interferon-Mediated Signaling Is Critical for Controlling Live Attenuated Yellow Fever Virus Infection In Vivo

Douam

Albrecht

Hrebikova

et al. 2017

mBio

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Yellow fever virus (YFV) is an arthropod-borne flavivirus, infecting ~200,000 people worldwide annually and causing about 30,000 deaths. The live attenuated vaccine strain, YFV-17D, has significantly contributed in controlling the global burden of yellow fever worldwide. However, the viral and host contributions to YFV-17D attenuation remain elusive. Type I interferon (IFN-α/β) signaling and type II interferon (IFN-γ) signaling have been shown to be mutually supportive in controlling YFV-17D infection despite distinct mechanisms of action in viral infection. However, it remains unclear how type III IFN (IFN-λ) integrates into this antiviral system. Here, we report that while wild-type (WT) and IFN-λ receptor knockout (λR−/−) mice were largely resistant to YFV-17D, deficiency in type I IFN signaling resulted in robust infection. Although IFN-α/β receptor knockout (α/βR−/−) mice survived the infection, mice with combined deficiencies in both type I signaling and type III IFN signaling were hypersusceptible to YFV-17D and succumbed to the infection. Mortality was associated with viral neuroinvasion and increased permeability of the blood-brain barrier (BBB). α/βR−/− λR−/− mice also exhibited distinct changes in the frequencies of multiple immune cell lineages, impaired T-cell activation, and severe perturbation of the proinflammatory cytokine balance. Taken together, our data highlight that type III IFN has critical immunomodulatory and neuroprotective functions that prevent viral neuroinvasion during active YFV-17D replication. Type III IFN thus likely represents a safeguard mechanism crucial for controlling YFV-17D infection and contributing to shaping vaccine immunogenicity.

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Section: Resultssupporting

confidence: 81%

Type III Interferon-Mediated Signaling Is Critical for Controlling Live Attenuated Yellow Fever Virus Infection In Vivo

Douam

Albrecht

Hrebikova

et al. 2017

mBio

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“…20 Unfortunately, despite some autopsy reports 5,17,18,[22][23][24][25] , we and others 16 believe that acute DENV encephalitis in immunocompetent patients still has not been well characterised unlike the other flaviviral encephalitidies. [10][11][12][13][14][15] However, a recent autopsy report of chronic DEN panencephalitis in an immunocompromised patient demonstrated DENV in inflamed neuroglial tissues 19 confirming that DENV is neurotropic.…”

Section: Discussionmentioning

confidence: 99%

“…Perhaps DENV encephalitis should best be defined as pathological demonstration of typical viral encephalitic changes in brain tissues such as perivascular cuffing and parenchymal infiltration by inflammatory cells, oedema and necrosis together with in situ demonstration of viral antigens and/or viral genome. Other flaviviral encephalitides caused by such Japanese encephalitis virus (JEV) 10,11 West Nile virus 12 , St Louis encephalitis virus 13 , tick-borne encephalitis virus 14 , and Murray Valley encephalitis virus 15 have indeed been pathologically confirmed to be encephalitic and neurotropic. In our opinion and opinions from other authors 16 , typical acute encephalitic changes and cellular localisation of viral antigens and/or viral RNA have not been convincingly demonstrated in DEN studies despite some autopsy cases reported by Chimelli et al and Miagostovich et al 17,18 Nonetheless, an interesting case of chronic DEN encephalitis in which virus has been demonstrated in infected CNS tissues in an immunocompromised patient has been recently reported.…”

Section: Introductionmentioning

confidence: 99%

Dengue virus encephalitis: A systematic review and critique

Fong¹,

Tan²,

Wong³

2022

NeuroAsia

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Background & Objective: Neurological manifestations were reported in dengue fever. We hypothesize that the diagnosis of DEN virus (DENV) encephalitis based on current clinical diagnostic criteria has been made too liberally. We conducted a systematic review of the literature to clarify this, and to characterize DENV encephalitis better. Methods: We systematically review the literature using MEDLINE and PubMed databases papers published from 1st January 1960 to 31st March 2020. We grouped the cases into definite and probable DENV encephalitis. Definite DENV encephalitis required demonstration of DENV (live virus, viral antigens, RNA) in the central nervous system or CSF whereas probable DENV encephalitis required positive anti-DENV IgM in the CSF and evidence of virus or anti-DENV IgM in the serum. Results: Of the 230 publications obtained from literature search, 121 case reports and series appeared relevant to DENV encephalitis. After applying our inclusion criteria, only 42 cases (34.7%) were acceptable as DENV encephalitis: 30 (24.8%) definite and 12 (9.9%) probable cases. Our findings suggest that DENV encephalitis is more uncommon than previously thought. Part of the reason for non-inclusion may be because many studies relied solely on DENV serology for diagnosis. Cross-reactivities of anti-DENV with anti-JE virus immunoglobulins in serum or CSF occur and this limits their usefulness to distinguish DENV encephalitis from JE. Conclusions: The majority of DENV encephalitis cases reported in the literature did not satisfy a more stringent inclusion criteria. Further investigations including autopsy studies are warranted to better characterize and to understand the pathology and pathogenesis of DENV encephalitis.

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“…Virus byl poprvé izolován během epidemie v roce 1951. Dosud nebyla vyvinuta vakcína ani léky, které by byly specificky použitelné proti tomuto viru [49][50][51].…”

Section: Boštíková a Kol: Zajímavosti Ze Světa Arbovirových Nákazunclassified

Zajímavosti Ze Světa Arbovirových Nákaz

Boštíková¹,

Boštíková²,

Boštík³

2017

Mil. Med. Sci. Lett.

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Viral neuronotropism is important in the pathogenesis of Murray Valley encephalitis

Cited by 5 publications

References 12 publications

Type III Interferon-Mediated Signaling Is Critical for Controlling Live Attenuated Yellow Fever Virus Infection In Vivo

Type III Interferon-Mediated Signaling Is Critical for Controlling Live Attenuated Yellow Fever Virus Infection In Vivo

Dengue virus encephalitis: A systematic review and critique

Zajímavosti Ze Světa Arbovirových Nákaz

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