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Nonproductive, cell-associated virus exists before the appearance of antiviral antibodies in experimental measles
Abstract:
The ability of measles virus to induce a cell-associated state of infection in the central nervous system (CNS) plays an important role in the pathogenesis of subacute sclerosing panencephalitis (SSPE), a fatal disease of children and young adults. The mechanism by which such an infection state is established is unknown, but several hypotheses have been proposed. One of these suggests that antiviral antibodies induce the nonproductive infection state by a process termed antigenic modulation. Results presented here demonstrate that antigenic modulation is not involved in the induction of a cell-associated CNS infection in newborn hamsters by the LEC strain of SSPE derived measles virus. This follows from the finding that nonproductive, cell-associated virus can be isolated from infected CNS tissues prior to the appearance of antiviral antibodies.
Insights
Antiviral antibodies do not cause measles virus to establish a persistent, nonproductive infection in the central nervous system (CNS). Measles virus establishes CNS infection before antibodies appear, refuting the antigenic modulation hypothesis for subacute sclerosing panencephalitis.
Area of Science:
- Virology
- Neuroscience
- Immunology
Background:
- Measles virus establishes persistent, cell-associated infections in the central nervous system (CNS).
- This CNS infection is critical for subacute sclerosing panencephalitis (SSPE) pathogenesis.
- The mechanism of establishing this nonproductive infection state remains unclear.
Purpose of the Study:
- To investigate the role of antigenic modulation in measles virus-induced CNS infection.
- To determine if antiviral antibodies contribute to the nonproductive, cell-associated infection state in the CNS.
Main Methods:
- Infection of newborn hamsters with the LEC strain of SSPE-derived measles virus.
- Isolation of nonproductive, cell-associated measles virus from infected CNS tissues.
- Monitoring for the appearance of antiviral antibodies in infected animals.
Main Results:
- Nonproductive, cell-associated measles virus was isolated from CNS tissues of infected hamsters.
- Viral isolation occurred *before* the detection of antiviral antibodies.
- This temporal relationship demonstrates that antibodies are not the initial cause of the nonproductive infection.
Conclusions:
- Antigenic modulation by antiviral antibodies is not involved in establishing cell-associated CNS infection by measles virus.
- Measles virus establishes a nonproductive CNS infection independently of the host's antibody response.
- This finding challenges existing hypotheses on SSPE pathogenesis and measles virus CNS persistence.