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Interferon production and response to exogenous interferon in two cell lines of mouse brain origin persistently
Abstract:
Two persistently infected cell lines established from C3H mouse brain cells infected in vivo with Sendai virus were shown to differ with respect to interferon (IF) production and response to exogenous IF. MB/Sen carrier cells contained 1-5 per cent antigen positive cells when examined by immunofluorescence, and virus was occasionally recovered from the culture medium. MB/SenAS carrier cells were maintained with 0.16 per cent Sendai antiserum in the supernatant medium. All MB/SenAS cells contained viral antigen and infectious virus was present in the culture medium. MB/Sen released IF spontaneously into the culture medium. Further IF production could be stimulated in MB/Sen by superinfection with Newcastle disease virus (NDV) or vesicular stomatitis virus (VSV). Exogenous IF provided good protection against VSV challenge. In contrast, MB/SenAS produced no IF spontaneously but could be stimulated by NDV and VSV to produce IF. Exogenous IF failed to reduce the amount of VSV released into the supernatant fluid. Replication of VSV was restricted in MB/SenAS as shown by a 2.3 log10 lower virus yield compared to MB/Sen.
Insights
Sendai virus infection in mouse brain cells created two cell lines with differing interferon production and responses. One cell line produced interferon spontaneously, while the other required stimulation, impacting their defense against viral challenges.
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Persistent viral infections can alter host cell responses.
- Sendai virus is known to induce interferon production.
- Cellular models are crucial for studying virus-host interactions.
Purpose of the Study:
- To characterize interferon (IF) production and response in two distinct Sendai virus-infected mouse brain cell lines.
- To investigate the impact of persistent Sendai virus infection on cellular antiviral mechanisms.
- To compare the efficacy of exogenous interferon in protecting against viral challenge in different cell lines.
Main Methods:
- Establishment of persistently infected C3H mouse brain cell lines (MB/Sen and MB/SenAS).
- Immunofluorescence assays to detect viral antigen.
- Virus recovery from culture medium.
- Interferon induction assays using Newcastle disease virus (NDV) and vesicular stomatitis virus (VSV).
- Assessment of exogenous interferon protection against VSV challenge.
- Quantification of VSV yield in infected cell lines.
Main Results:
- MB/Sen cells spontaneously produced interferon and were protected by exogenous interferon against VSV challenge.
- MB/SenAS cells, maintained with antiserum, produced no spontaneous interferon but could be stimulated. Exogenous interferon failed to protect MB/SenAS cells.
- VSV replication was significantly restricted in MB/SenAS cells compared to MB/Sen cells, showing a 2.3 log10 lower virus yield.
Conclusions:
- Persistent Sendai virus infection leads to distinct cellular phenotypes regarding interferon production and response.
- The presence of antiserum in MB/SenAS cells influences interferon production and exogenous interferon efficacy.
- Cellular interferon production and response are critical determinants of viral replication control in persistently infected cells.