Summary auto-generated
This study established persistent mumps virus infections in two neural cell lines—rat PC-12 pheochromocytoma cells and human TE-671 medulloblastoma cells—to investigate viral effects on cellular electrical properties. PC-12 cells produced significant infectious virus, while TE-671 cells produced minimal virus, likely due to restricted fusion protein expression. The researchers measured stimulus-evoked action potentials (SEAPs) in mock-infected and persistently infected cells. In uninfected cells, most responses were normal, rapidly-rising, all-or-nothing action potentials. In virus-infected cultures, this pattern dramatically shifted: 86.5% of PC-12 infected cells and 88.3% of TE-671 infected cells exhibited abnormal, slowly-rising, graded responses or no electrical response at all. Importantly, resting membrane potentials remained unchanged, suggesting the virus specifically impaired voltage-gated sodium channel function rather than affecting basic ion gradients. These findings suggest that persistent mumps infection alters neural cell excitability through disruption of spike-generation mechanisms, potentially disrupting synaptic transmission and neural integration. This represents a novel mechanism by which persistent paramyxovirus infections might contribute to chronic neurological dysfunction.
Key findings
- Persistent mumps virus infection altered the distribution of cellular electrical responses from predominantly normal action potentials to predominantly abnormal or absent responses in both PC-12 and TE-671 neural cell lines.
- The virus impaired voltage-gated ion channel function without affecting resting membrane potential, suggesting selective interference with spike-generating mechanisms rather than basic ion homeostasis.
- PC-12 cells supported robust viral replication while TE-671 cells showed restricted virus production correlated with reduced expression of the viral fusion glycoprotein.
- Virus-induced alterations in action potential properties could disrupt synaptic transmission and neural integration, proposing a new mechanism linking persistent mumps infection to chronic neurological disease.
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Abstract
Persistent mumps virus infections were established in rat pheochromocytoma (PC-12) and human medulloblastoma (TE-671) continuous cell lines. Significant amounts of infectious virus were produced by the PC-12 cells; infectious virus production by the TE-671 cells was limited. This restricted replication may be due to decreased production of viral envelope glycoproteins by TE-671 cells. The presence of virus changed the distribution of stimulus-evoked electrical responsiveness of both cell lines from responsiveness composed primarily of normal, rapidly rising, all-or-nothing action potentials to one dominated by abnormal, slowly rising, graded responses or by no response at all. Such changes have the potential to disrupt neural integration within the nervous system, and suggest a new mechanism by which persistent virus infections might play a role in chronic neurological and/or mental disease.