Lymphocytic choriomeningitis virus (LCMV) infection of macaques: A model for Lassa fever

► History of LCMV infections of primates (from mice to monkeys and man). ► Comparison of outcomes in murine and primate infections. ► Description of findings from LCMV-infected rhesus macaques. ► Utility of the model for testing host-response antivirals over virus-specific antivirals. Arenaviruses s...

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Vydáno v:Antiviral research Ročník 92; číslo 2; s. 125 - 138
Hlavní autoři: Zapata, Juan C., Pauza, C. David, Djavani, Mahmoud M., Rodas, Juan D., Moshkoff, Dmitry, Bryant, Joseph, Ateh, Eugene, Garcia, Cybele, Lukashevich, Igor S., Salvato, Maria S.
Médium: Journal Article
Jazyk:angličtina
Vydáno: Kidlington Elsevier B.V 01.11.2011
Elsevier
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ISSN:0166-3542, 1872-9096, 1872-9096
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Abstract ► History of LCMV infections of primates (from mice to monkeys and man). ► Comparison of outcomes in murine and primate infections. ► Description of findings from LCMV-infected rhesus macaques. ► Utility of the model for testing host-response antivirals over virus-specific antivirals. Arenaviruses such as Lassa fever virus (LASV) and lymphocytic choriomeningitis virus (LCMV) are benign in their natural reservoir hosts, and can occasionally cause severe viral hemorrhagic fever (VHF) in non-human primates and in human beings. LCMV is considerably more benign for human beings than Lassa virus, however certain strains, like the LCMV-WE strain, can cause severe disease when the virus is delivered as a high-dose inoculum. Here we describe a rhesus macaque model for Lassa fever that employs a virulent strain of LCMV. Since LASV must be studied within Biosafety Level-4 (BSL-4) facilities, the LCMV-infected macaque model has the advantage that it can be used at BSL-3. LCMV-induced disease is rarely as severe as other VHF, but it is similar in cases where vascular leakage leads to lethal systemic failure. The LCMV-infected macaque has been valuable for describing the course of disease with differing viral strains, doses and routes of infection. By monitoring system-wide changes in physiology and gene expression in a controlled experimental setting, it is possible to identify events that are pathognomonic for developing VHF and potential treatment targets.
AbstractList Arenaviruses such as Lassa fever virus (LASV) and lymphocytic choriomeningitis virus (LCMV) are benign in their natural reservoir hosts, and can occasionally cause severe viral hemorrhagic fever (VHF) in non-human primates and in human beings. LCMV is considerably more benign for human beings than Lassa virus, however certain strains, like the LCMV-WE strain, can cause severe disease when the virus is delivered as a high-dose inoculum. Here we describe a rhesus macaque model for Lassa fever that employs a virulent strain of LCMV. Since LASV must be studied within Biosafety Level-4 (BSL-4) facilities, the LCMV-infected macaque model has the advantage that it can be used at BSL-3. LCMV-induced disease is rarely as severe as other VHF, but it is similar in cases where vascular leakage leads to lethal systemic failure. The LCMV-infected macaque has been valuable for describing the course of disease with differing viral strains, doses and routes of infection. By monitoring system-wide changes in physiology and gene expression in a controlled experimental setting, it is possible to identify events that are pathognomonic for developing VHF and potential treatment targets.
Arenaviruses such as Lassa fever virus (LASV) and lymphocytic choriomeningitis virus (LCMV) are benign in their natural reservoir hosts, and can occasionally cause severe viral hemorrhagic fever (VHF) in non-human primates and in human beings. LCMV is considerably more benign for human beings than Lassa virus, however certain strains, like the LCMV-WE strain, can cause severe disease when the virus is delivered as a high-dose inoculum. Here we describe a rhesus macaque model for Lassa fever that employs a virulent strain of LCMV. Since LASV must be studied within Biosafety Level-4 (BSL-4) facilities, the LCMV-infected macaque model has the advantage that it can be used at BSL-3. LCMV-induced disease is rarely as severe as other VHF, but it is similar in cases where vascular leakage leads to lethal systemic failure. The LCMV-infected macaque has been valuable for describing the course of disease with differing viral strains, doses and routes of infection. By monitoring system-wide changes in physiology and gene expression in a controlled experimental setting, it is possible to identify events that are pathognomonic for developing VHF and potential treatment targets.Arenaviruses such as Lassa fever virus (LASV) and lymphocytic choriomeningitis virus (LCMV) are benign in their natural reservoir hosts, and can occasionally cause severe viral hemorrhagic fever (VHF) in non-human primates and in human beings. LCMV is considerably more benign for human beings than Lassa virus, however certain strains, like the LCMV-WE strain, can cause severe disease when the virus is delivered as a high-dose inoculum. Here we describe a rhesus macaque model for Lassa fever that employs a virulent strain of LCMV. Since LASV must be studied within Biosafety Level-4 (BSL-4) facilities, the LCMV-infected macaque model has the advantage that it can be used at BSL-3. LCMV-induced disease is rarely as severe as other VHF, but it is similar in cases where vascular leakage leads to lethal systemic failure. The LCMV-infected macaque has been valuable for describing the course of disease with differing viral strains, doses and routes of infection. By monitoring system-wide changes in physiology and gene expression in a controlled experimental setting, it is possible to identify events that are pathognomonic for developing VHF and potential treatment targets.
► History of LCMV infections of primates (from mice to monkeys and man). ► Comparison of outcomes in murine and primate infections. ► Description of findings from LCMV-infected rhesus macaques. ► Utility of the model for testing host-response antivirals over virus-specific antivirals. Arenaviruses such as Lassa fever virus (LASV) and lymphocytic choriomeningitis virus (LCMV) are benign in their natural reservoir hosts, and can occasionally cause severe viral hemorrhagic fever (VHF) in non-human primates and in human beings. LCMV is considerably more benign for human beings than Lassa virus, however certain strains, like the LCMV-WE strain, can cause severe disease when the virus is delivered as a high-dose inoculum. Here we describe a rhesus macaque model for Lassa fever that employs a virulent strain of LCMV. Since LASV must be studied within Biosafety Level-4 (BSL-4) facilities, the LCMV-infected macaque model has the advantage that it can be used at BSL-3. LCMV-induced disease is rarely as severe as other VHF, but it is similar in cases where vascular leakage leads to lethal systemic failure. The LCMV-infected macaque has been valuable for describing the course of disease with differing viral strains, doses and routes of infection. By monitoring system-wide changes in physiology and gene expression in a controlled experimental setting, it is possible to identify events that are pathognomonic for developing VHF and potential treatment targets.
Author Zapata, Juan C.
Garcia, Cybele
Pauza, C. David
Ateh, Eugene
Lukashevich, Igor S.
Bryant, Joseph
Moshkoff, Dmitry
Djavani, Mahmoud M.
Rodas, Juan D.
Salvato, Maria S.
AuthorAffiliation 3 Laboratorio de Virología, Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Argentina
2 Grupo de Investigaciones en Ciencias Veterinarias Centauro, Facultad de Ciencias Agrarias, Universidad de Antioquia, Medellín, Colombia
1 Institute of Human Virology, University of Maryland School of Medicine, Baltimore, MD
AuthorAffiliation_xml – name: 1 Institute of Human Virology, University of Maryland School of Medicine, Baltimore, MD
– name: 2 Grupo de Investigaciones en Ciencias Veterinarias Centauro, Facultad de Ciencias Agrarias, Universidad de Antioquia, Medellín, Colombia
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  surname: Salvato
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Sat Nov 29 08:09:16 EST 2025
Fri Feb 23 02:28:26 EST 2024
IsDoiOpenAccess false
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Issue 2
Keywords ML29
LCMV
sIL6R
Lassa fever virus
TACV
LCMV-WE
Rhesus macaques
PICV
Arenaviruses
MOPV
sc
Monkey models
AST/ALT
VHF
LCMV-ARM
ig
sTnfRI
im
Viral hemorrhagic fever
iv
IL-6
PMN
ffu
sTNFRII
LASV
pfu
Hemorrhagic fever
Monkey
Macaca mulatta
Lassa virus
Arenavirus
Virus
Infection
Vertebrata
Lassa fever
Mammalia
Lymphocytic choriomeningitis virus
Viral disease
Animal
Arbovirus disease
Primates
Simioidea
Models
Arenaviridae
Language English
License https://www.elsevier.com/tdm/userlicense/1.0
CC BY 4.0
Copyright © 2011 Elsevier B.V. All rights reserved.
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ObjectType-Article-2
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OpenAccessLink https://www.ncbi.nlm.nih.gov/pmc/articles/3209703
PMID 21820469
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PublicationTitle Antiviral research
PublicationTitleAlternate Antiviral Res
PublicationYear 2011
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Elsevier
Publisher_xml – name: Elsevier B.V
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Snippet ► History of LCMV infections of primates (from mice to monkeys and man). ► Comparison of outcomes in murine and primate infections. ► Description of findings...
Arenaviruses such as Lassa fever virus (LASV) and lymphocytic choriomeningitis virus (LCMV) are benign in their natural reservoir hosts, and can occasionally...
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SubjectTerms Animals
Antibiotics. Antiinfectious agents. Antiparasitic agents
Antiviral agents
Arenaviridae Infections - pathology
Arenaviruses
Biological and medical sciences
Disease Models, Animal
Human viral diseases
Humans
Infectious diseases
Lassa Fever - pathology
Lassa fever and arenovirus diseases
Lassa fever virus
Lassa virus
LCMV
Lymphocytic choriomeningitis virus
Lymphocytic choriomeningitis virus - pathogenicity
Macaca mulatta
Medical sciences
Monkey models
Pharmacology. Drug treatments
Primates
Rhesus macaques
Tropical viral diseases
Viral diseases
Viral hemorrhagic fever
Title Lymphocytic choriomeningitis virus (LCMV) infection of macaques: A model for Lassa fever
URI https://dx.doi.org/10.1016/j.antiviral.2011.07.015
https://www.ncbi.nlm.nih.gov/pubmed/21820469
https://www.proquest.com/docview/900642349
https://www.proquest.com/docview/911151441
https://pubmed.ncbi.nlm.nih.gov/PMC3209703
Volume 92
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