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Persistent infection of BSC-1 cells by defective measles virus derived from subacute sclerosing panencephalitis
Abstract:
A line of cells (IP-3), persistently infected with defective measles virus, was developed from co-cultures of subacute sclerosing panencephalitis-derived brain cells with monkey kidney cells (BSC-1). The line, carried for more than 45 serial passages, produced neither infectious virus nor hemagglutinin. Cultures consistently displayed a cycling focal cytopathic pattern of infection characterized by formation of syncytia, necrosis, and plaques followed by healing. Fluorescent measles antigen was present in damaged areas only, especially in syncytia. The development of syncytia was suppressed by measles antibody. Syncytia were lysed by antibody plus rabbit complement. A variant noncytopathic subline (IP-3-Ca) was derived from the 16th passage. Infectious virus was not detected. Cells were minimally positive for hemadsorption. Fluorescent measles antigen was present in all cells. Co-cultures of IP-3-Ca cells with normal BSC-1 cells developed massive syncytia and extensive destruction. The IP-3-Ca cells multiplied in the presence of measles antibodies and were destroyed by antibodies plus complement. The possible relevance of these findings to the pathogenesis of subacute sclerosing panencephalitis is discussed.
Insights
Researchers developed a cell line persistently infected with measles virus, revealing insights into subacute sclerosing panencephalitis pathogenesis. This study characterized viral behavior and host cell interactions in a novel cell model.
Area of Science:
- Virology
- Cell Biology
- Neuroscience
Background:
- Subacute sclerosing panencephalitis (SSPE) is a severe neurological complication of measles virus infection.
- Understanding the persistent and defective measles virus interactions with host cells is crucial for elucidating SSPE pathogenesis.
- Previous studies lacked a suitable cell model to investigate these complex interactions over extended periods.
Purpose of the Study:
- To establish and characterize a cell line persistently infected with a defective measles virus.
- To investigate the cytopathic effects and antigen expression of the defective measles virus in the established cell line.
- To explore the behavior of a non-cytopathic variant and its interaction with normal cells and measles antibodies.
Main Methods:
- Co-culturing SSPE-derived brain cells with monkey kidney cells (BSC-1) to establish a persistently infected cell line (IP-3).
- Serial passage of the IP-3 cell line for over 45 passages to assess viral production and cytopathic effects.
- Derivation and characterization of a non-cytopathic subline (IP-3-Ca) and co-culturing with normal BSC-1 cells.
- Analysis of infectious virus production, hemagglutinin, hemadsorption, and fluorescent measles antigen expression.
- Assessment of syncytia formation, cell lysis, and multiplication in the presence of measles antibodies and complement.
Main Results:
- The IP-3 cell line, persistently infected with defective measles virus, did not produce infectious virus or hemagglutinin but showed cycling cytopathic effects including syncytia, necrosis, and plaques.
- Fluorescent measles antigen was localized to damaged areas, particularly syncytia, which were suppressed by measles antibody and lysed by antibody plus complement.
- The IP-3-Ca subline exhibited minimal hemadsorption but widespread fluorescent measles antigen; co-cultures with normal BSC-1 cells led to massive syncytia and cell destruction, with IP-3-Ca cells multiplying in measles antibodies and being destroyed by antibody plus complement.
Conclusions:
- A novel cell line (IP-3) persistently infected with defective measles virus was successfully established, mimicking aspects of SSPE.
- The study demonstrated the complex interplay between defective measles virus, host cells, and immune components, highlighting the role of syncytia formation and lysis.
- Findings provide a valuable model for further research into the pathogenesis of subacute sclerosing panencephalitis and potential therapeutic strategies.