The NF-κB/leukemia inhibitory factor/STAT3 signaling pathway in antibody-mediated suppression of Sindbis virus replication in neurons

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Abstract
Significance: Mature neurons are postmitotic cells with limited regenerative capacity, so damage following infection may result in permanent neurologic deficits. Successful recovery from viral infection of neurons requires immune mechanisms that preserve neuron viability and functionality. Sindbis virus (SINV) infects neurons and causes viral encephalomyelitis from which mice recover. Bivalent antibody to the SINV E2 glycoprotein provides noncytolytic control of neuronal infection in vivo and in vitro, but the mechanism is unknown. We used a high-throughput protein microarray and neuronal cultures to identify the NF-κB/leukemia inhibitory factor/STAT3 signaling cascade as important for antibody-mediated inhibition of viral replication. These studies offer insights into the mechanism of antibody-mediated noncytolytic virus clearance from neurons.
Funding Information
  • HHS | National Institutes of Health (R01 NS087539)
  • HHS | National Institutes of Health (R01 NS038932)
  • HHS | National Institutes of Health (T32 AI007247)
  • HHS | National Institutes of Health (T32 AI 007417)
  • HHS | National Institutes of Health (F31 NS 101824)
  • Mason | College of Science, George Mason University (1000)

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