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Replication of lactate dehydrogenase-elevating virus in cells infected with murine leukaemia viruses in vitro
1Central Virus Diagnostic Laboratory, National Institute of Health, Tokyo, Japan.
Abstract:
Although the majority of mouse strains infected with lactate dehydrogenase-elevating virus (LDV) do not show any particular symptoms, the virus is able to induce acute poliomyelitis in C58 or AKR mice. Murine leukaemia virus (MuLV) has been detected at a high titre in the spinal cord of affected mice. In this study, we have analysed the possible role of MuLV in the induction of neurological disease by LDV. Immunofluorescent staining, autoradiography and an infectivity assay of virus yield have shown that LDV replicated in continuous mouse and rat cell lines that had been infected with an ecotropic MuLV isolated from C58 mice, but did not replicate in cells not infected with MuLV. No significant differences in infection were observed among the various ecotropic MuLVs employed, except for Friend leukaemia virus which rendered the cells susceptible to LDV least efficiently. The infectivity of the neurovirulent strain, LDV-C, to MuLV-infected cells was 50- to 100-fold greater than that of the avirulent strains (LDV-N, -Nu, -R and -P). The infectivity to macrophages was almost the same for virulent and avirulent strains. Adsorption studies using a radiolabelled virus revealed that LDV-C was adsorbed to MuLV-infected cells more efficiently than the avirulent strain, LDV-N. The difference in infectivity to these cells, therefore, may be due in part to the difference in adsorption rate. This may suggest differences in the interaction of the viral proteins with MuLV-infected cells from those with macrophages at the initiation of virus infection. These results may be relevant to the mechanisms of paralytic disease caused by LDV infection in C58 mice.
Insights
Murine leukaemia virus (MuLV) facilitates lactate dehydrogenase-elevating virus (LDV) replication in specific mouse cells, contributing to LDV-induced neurological disease. This interaction, particularly with neurovirulent LDV strains, highlights MuLV
Area of Science:
- Virology
- Neuroimmunology
- Molecular Biology
Background:
- Lactate dehydrogenase-elevating virus (LDV) typically causes asymptomatic infections in most mouse strains.
- However, LDV can induce acute poliomyelitis in specific strains like C58 or AKR mice.
- Murine leukaemia virus (MuLV) is found at high levels in the spinal cords of affected mice.
Purpose of the Study:
- To investigate the potential role of MuLV in LDV-induced neurological disease.
- To determine if MuLV infection influences LDV replication and neurovirulence.
Main Methods:
- Utilized immunofluorescent staining, autoradiography, and virus yield infectivity assays.
- Compared LDV replication in MuLV-infected and uninfected mouse and rat cell lines.
- Assessed the infectivity of different LDV strains (virulent LDV-C vs. avirulent strains) to MuLV-infected cells and macrophages.
- Conducted adsorption studies with radiolabeled LDV to analyze viral binding efficiency.
Main Results:
- LDV replicated efficiently in mouse and rat cell lines infected with ecotropic MuLV, but not in uninfected cells.
- The neurovirulent LDV-C strain showed 50- to 100-fold greater infectivity to MuLV-infected cells compared to avirulent strains.
- LDV-C adsorption to MuLV-infected cells was more efficient than that of avirulent LDV strains, suggesting a role for adsorption rate in differential infectivity.
- Infectivity to macrophages was similar for both virulent and avirulent LDV strains.
Conclusions:
- MuLV infection is crucial for LDV replication in certain cell types, potentially explaining LDV's ability to cause neurological disease in susceptible mouse strains.
- Differences in viral adsorption rates to MuLV-infected cells may contribute to the differential neurovirulence observed between LDV strains.
- These findings suggest distinct interactions between viral proteins, MuLV-infected cells, and macrophages during the initiation of LDV infection.