Lymphocytic Choriomeningitis Virus in Man

Deibel, Rudolf; Woodall, John; Decher, W; Schryver, George D.

doi:10.1001/jama.1975.03250050023010

Cited by 69 publications

(6 citation statements)

References 13 publications

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“…Conversely, all facility C employees appeared to have asymptomatic infections, except for 1 with nonspecific illness. Previous LCMV outbreak investigations have found various rates of clinical illness ( 9 , 10 , 13 ), with asymptomatic infections of 25%–55%. Because employee age and sex did not differ among facilities, the reason for the difference in disease manifestation remains unclear.…”

Section: Discussionmentioning

confidence: 99%

Lymphocytic Choriomeningitis Virus in Employees and Mice at Multipremises Feeder-Rodent Operation, United States, 2012

Knust¹,

Ströher²,

Edison³

et al. 2014

Emerg. Infect. Dis.

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Section: Discussionmentioning

confidence: 99%

Lymphocytic Choriomeningitis Virus in Employees and Mice at Multipremises Feeder-Rodent Operation, United States, 2012

Knust¹,

Ströher²,

Edison³

et al. 2014

Emerg. Infect. Dis.

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“…Consequently, numerous outbreaks of aseptic meningitis in laboratory workers or animal handlers have been traced to LCMV infection (Bowen, 1975; Deibel et al, 1975; Hinman et al, 1975; Smith et al, 1984; Emonet et al, 2007). …”

Section: Spectrum Of Lcmv Infection Of Humansmentioning

confidence: 99%

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

et al. 2011

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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.

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“…The prototypic arenavirus, lymphocytic choriomeningitis virus (LCMV), is an agent of acute central nervous system disease as well as a cause of congenital malformations [13], [14], and has been associated on several occasions with fatal outcome in organ-transplanted recipients [15], [16], [17] and immune compromised patients [18], [19]. The high degree of genetic variation among geographic and temporal isolates of the same arenavirus species supports the concept of continued emergence of new pathogens [20], as recently proven by the identification two novel arenaviruses: Lujo and Dandenong; isolated respectively from a fatal outbreak [3], [21] and from fatal organ transplants [22].…”

Section: Introductionmentioning

confidence: 99%

LCMV Glycosylation Modulates Viral Fitness and Cell Tropism

Knopp

Bederka

et al. 2013

PLoS ONE

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The glycoprotein (GP) of arenaviruses is glycosylated at 11 conserved N-glycosylation sites. We constructed recombinant lymphocytic choriomeningitis virus (rLCMV) featuring either additions or deletions of these N-glycans to investigate their role in the viral life cycle. N-glycosylation at two sites, T87 and S97, were found to be necessary to rescue rLCMV. Three of nine successfully rescued mutants, S116A, T234A, and S373A, under selective pressures in either epithelial, neuronal, or macrophage cells reverted to WT sequence. Of the seven stable N-glycan deletion mutants, five of these led to altered viral fitness and cell tropism, assessed as growth in either mouse primary cortical neurons or bone marrow derived macrophages. These results demonstrate that the deletion of N-glycans in LCMV GP may confer an advantage to the virus for infection of neurons but a disadvantage in macrophages.

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Lymphocytic Choriomeningitis Virus in Man

Cited by 69 publications

References 13 publications

Lymphocytic Choriomeningitis Virus in Employees and Mice at Multipremises Feeder-Rodent Operation, United States, 2012

Lymphocytic Choriomeningitis Virus in Employees and Mice at Multipremises Feeder-Rodent Operation, United States, 2012

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

LCMV Glycosylation Modulates Viral Fitness and Cell Tropism

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