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Review
. 2011 Nov;92(2):125-38.
doi: 10.1016/j.antiviral.2011.07.015. Epub 2011 Jul 27.

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

Juan C Zapata  1 , C David Pauza, Mahmoud M Djavani, Juan D Rodas, Dmitry Moshkoff, Joseph Bryant, Eugene Ateh, Cybele Garcia, Igor S Lukashevich, Maria S Salvato
Affiliations
Review

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

Juan C Zapata et al. Antiviral Res. 2011 Nov.

Abstract

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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Figures

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Arenaviruses used for macaque studies. Old world arenaviruses Lassa virus-Josiah strain (LASV-Jos), Mopeia virus (MOPV), the Mopeia/Lassa reassortant (ML29), and the LCMV strains WE and Armstrong (LCMV-WE, LCMV-Arm) have been studied in rhesus macaques (Fisher Hoch et al., 1987; Jahrling et al., 1980; Lukashevich et al., 2002, 2003, 2004, 2005; Rodas et al., 2004). They are mentioned in this review by way of comparison to the LCMV macaque model for Lassa fever.
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Arenavirus reassortment. The two RNA segments of the arenavirus genome can be derived from two parental virus strains that co-infected the same host cell. The ML29 Lassa vaccine candidate was obtained by reassortment between LASV and MOPV parental strains (Lukashevich et al., 1992), and the LCMV-WE/Arm and Arm/WE strains were obtained by reassortment of WE and Arm strains of LCMV (Riviere et al., 1986).
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Arenavirus plaque morphologies. A couple of examples of different plaque morphologies for the LCMV-Arm and Mopeia (strains AN21366 and AN20410) are shown. The blue stain with crystal violet and formalin fixation is more distinct than the red stain with neutral red without fixation, but the latter enables the isolation of infectious plaques. Arenaviruses tend to bud rather than lyse the host cell, so a plaque is due to poor cell growth and adherence rather than to cell lysis (as it is for vesicular stomatitis or polio viruses).
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Healthy and diseased (LCMV-WE-infected) macaque liver and lung tissue (A). A timeline of disease progression for a typical LCMV-WE infected rhesus macaque with viral hemorrhagic fever (B).
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