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Whole-Exome Sequencing of Patients With Recurrent HSV-2 Lymphocytic Mollaret Meningitis

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Harvard

Hait, AS, Thomsen, MM, Larsen, SM, Helleberg, M, Mardahl, M, Barfod, TS, Christiansen, M, Brandt, C & Mogensen, TH 2021, 'Whole-Exome Sequencing of Patients With Recurrent HSV-2 Lymphocytic Mollaret Meningitis', The Journal of infectious diseases, bind 223, nr. 10, s. 1776-1786. https://doi.org/10.1093/infdis/jiaa589

APA

Hait, A. S., Thomsen, M. M., Larsen, S. M., Helleberg, M., Mardahl, M., Barfod, T. S., Christiansen, M., Brandt, C., & Mogensen, T. H. (2021). Whole-Exome Sequencing of Patients With Recurrent HSV-2 Lymphocytic Mollaret Meningitis. The Journal of infectious diseases, 223(10), 1776-1786. https://doi.org/10.1093/infdis/jiaa589

CBE

MLA

Vancouver

Author

Hait, Alon Schneider ; Thomsen, Michelle M ; Larsen, Simon M ; Helleberg, Marie ; Mardahl, Maibritt ; Barfod, Toke S ; Christiansen, Mette ; Brandt, Christian ; Mogensen, Trine H. / Whole-Exome Sequencing of Patients With Recurrent HSV-2 Lymphocytic Mollaret Meningitis. I: The Journal of infectious diseases. 2021 ; Bind 223, Nr. 10. s. 1776-1786.

Bibtex

@article{6902a7a50bee49a2977d6f022b709812,
title = "Whole-Exome Sequencing of Patients With Recurrent HSV-2 Lymphocytic Mollaret Meningitis",
abstract = "Recurrent lymphocytic meningitis, also referred to as Mollaret meningitis, is a rare neurological disease characterized mainly by reactivation of herpes simplex virus 2 (HSV-2) from sensory ganglia. However, the underlying host immune determinants and viral factors rendering some individuals unable to maintain HSV-2 latency are largely unknown. We collected a cohort of 15 patients diagnosed with Mollaret meningitis. By whole-exome sequencing we identified rare host genetic variants predicted to be deleterious in molecules involved in (1) ubiquitin-proteasome pathways, (2) the autophagy machinery, and (3) cell proliferation/apoptosis. Moreover, infection of patient cells with HSV-2 or stimulation by virus-derived double-stranded DNA ligands revealed reduced antiviral interferon responses in most patients. These findings may contribute to a better understanding of disease pathogenesis and protective immunity to HSV in the central nervous system, and may ultimately be of importance for identification of targets for development of improved prophylaxis and treatment of this disease.",
keywords = "autophagy, interferon, recurrent HSV-2 meningitis, whole-exome sequencing",
author = "Hait, {Alon Schneider} and Thomsen, {Michelle M} and Larsen, {Simon M} and Marie Helleberg and Maibritt Mardahl and Barfod, {Toke S} and Mette Christiansen and Christian Brandt and Mogensen, {Trine H}",
note = "{\textcopyright} The Author(s) 2020. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.",
year = "2021",
month = may,
day = "28",
doi = "10.1093/infdis/jiaa589",
language = "English",
volume = "223",
pages = "1776--1786",
journal = "Journal of Infectious Diseases",
issn = "0022-1899",
publisher = "University of Chicago Press",
number = "10",

}

RIS

TY - JOUR

T1 - Whole-Exome Sequencing of Patients With Recurrent HSV-2 Lymphocytic Mollaret Meningitis

AU - Hait, Alon Schneider

AU - Thomsen, Michelle M

AU - Larsen, Simon M

AU - Helleberg, Marie

AU - Mardahl, Maibritt

AU - Barfod, Toke S

AU - Christiansen, Mette

AU - Brandt, Christian

AU - Mogensen, Trine H

N1 - © The Author(s) 2020. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.

PY - 2021/5/28

Y1 - 2021/5/28

N2 - Recurrent lymphocytic meningitis, also referred to as Mollaret meningitis, is a rare neurological disease characterized mainly by reactivation of herpes simplex virus 2 (HSV-2) from sensory ganglia. However, the underlying host immune determinants and viral factors rendering some individuals unable to maintain HSV-2 latency are largely unknown. We collected a cohort of 15 patients diagnosed with Mollaret meningitis. By whole-exome sequencing we identified rare host genetic variants predicted to be deleterious in molecules involved in (1) ubiquitin-proteasome pathways, (2) the autophagy machinery, and (3) cell proliferation/apoptosis. Moreover, infection of patient cells with HSV-2 or stimulation by virus-derived double-stranded DNA ligands revealed reduced antiviral interferon responses in most patients. These findings may contribute to a better understanding of disease pathogenesis and protective immunity to HSV in the central nervous system, and may ultimately be of importance for identification of targets for development of improved prophylaxis and treatment of this disease.

AB - Recurrent lymphocytic meningitis, also referred to as Mollaret meningitis, is a rare neurological disease characterized mainly by reactivation of herpes simplex virus 2 (HSV-2) from sensory ganglia. However, the underlying host immune determinants and viral factors rendering some individuals unable to maintain HSV-2 latency are largely unknown. We collected a cohort of 15 patients diagnosed with Mollaret meningitis. By whole-exome sequencing we identified rare host genetic variants predicted to be deleterious in molecules involved in (1) ubiquitin-proteasome pathways, (2) the autophagy machinery, and (3) cell proliferation/apoptosis. Moreover, infection of patient cells with HSV-2 or stimulation by virus-derived double-stranded DNA ligands revealed reduced antiviral interferon responses in most patients. These findings may contribute to a better understanding of disease pathogenesis and protective immunity to HSV in the central nervous system, and may ultimately be of importance for identification of targets for development of improved prophylaxis and treatment of this disease.

KW - autophagy

KW - interferon

KW - recurrent HSV-2 meningitis

KW - whole-exome sequencing

UR - http://www.scopus.com/inward/record.url?scp=85106859346&partnerID=8YFLogxK

U2 - 10.1093/infdis/jiaa589

DO - 10.1093/infdis/jiaa589

M3 - Journal article

C2 - 32946550

VL - 223

SP - 1776

EP - 1786

JO - Journal of Infectious Diseases

JF - Journal of Infectious Diseases

SN - 0022-1899

IS - 10

ER -

ID: 60905399