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C terminal CYS-RICH region of mumps virus structural V protein correlates with block of interferon alpha and gamma
T Kubota1, N Yokosawa, S Yokota
1Department of Microbiology, Sapporo Medical University School of Medicine, South 1, West 16, Chou-ku, Sapporo, Hokkaido, 060-8556, Japan.
Abstract:
It has been reported that interferon (IFN)-alpha/gamma signal transduction pathway is blocked in several cell lines persistently infected with mumps virus (MV) through decrease of STAT-1alpha. Expression of the MV structural V protein (MV-V) or C terminal CYS-RICH region of the V protein (MV-Vsp) inhibited the establishment of the antivirus state induced by IFN, but not by expression of the MV-P protein. Suppression of IFN-induced STAT-1alpha, STAT-2, and IRF-9 (p48) induction was also recognized in the cells transfected with expression vector of the MV-V (pTM-V) or MV-Vsp (pTM-Vsp) protein, even though it was in the absence of the other virus protein. It is supposed that the cysteine-rich domain of V protein (Vsp) is involved in the suppression of the IFN signal transduction pathway.
Insights
Mumps virus (MV) infection blocks interferon (IFN) signaling by decreasing STAT-1alpha. The MV V protein, specifically its cysteine-rich Vsp domain, inhibits IFN-induced antiviral states and STAT protein induction.
Area of Science:
- Virology
- Immunology
- Molecular Biology
Background:
- Interferon (IFN) signaling is crucial for antiviral responses.
- Persistent mumps virus (MV) infection is associated with blocked IFN-alpha/gamma signal transduction.
- Decreased STAT-1alpha levels have been observed in MV-infected cells.
Purpose of the Study:
- To investigate the mechanism by which mumps virus interferes with IFN signaling.
- To identify the specific viral component responsible for blocking the IFN pathway.
- To elucidate the role of STAT proteins in MV-induced immune evasion.
Main Methods:
- Expression of mumps virus proteins (MV-V, MV-Vsp, MV-P) in cell lines.
- Analysis of IFN-alpha/gamma signal transduction pathway components (STAT-1alpha, STAT-2, IRF-9).
- Transfection with expression vectors (pTM-V, pTM-Vsp) to study protein function independently.
Main Results:
- Expression of MV-V or its C-terminal cysteine-rich region (MV-Vsp) inhibited IFN-induced antiviral states.
- MV-P protein expression did not inhibit the antiviral state.
- Suppression of IFN-induced STAT-1alpha, STAT-2, and IRF-9 (p48) was observed in cells expressing MV-V or MV-Vsp.
Conclusions:
- The mumps virus V protein, particularly its cysteine-rich domain (Vsp), plays a key role in suppressing the IFN signal transduction pathway.
- MV-V inhibits the induction of essential STAT proteins required for IFN signaling.
- This viral mechanism contributes to immune evasion during persistent mumps virus infections.