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Rescue of Recombinant Newcastle Disease Virus from cDNA
10:55

Rescue of Recombinant Newcastle Disease Virus from cDNA

Published on: October 11, 2013

Incorporation of host complement regulatory proteins into Newcastle disease virus enhances complement evasion

Moanaro Biswas1, John B Johnson, Sandeep R P Kumar

  • 1Department of Biomedical Sciences and Pathobiology, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Blacksburg, Virginia, USA.

Journal of Virology
|September 14, 2012
PubMed

Insights

Newcastle disease virus (NDV) grown in mammalian cells resists complement neutralization. Incorporating regulators of complement activity (RCA) into NDV provides species-specific resistance, impacting its use as an oncolytic virus.

Area of Science:

  • Virology
  • Immunology
  • Oncolytic Virus Therapy

Background:

  • Newcastle disease virus (NDV) is an avian paramyxovirus with inherent tumor selectivity, making it a candidate for oncolytic virotherapy and vaccine vectors.
  • Understanding virus-host interactions, particularly complement system effects, is crucial for optimizing NDV's clinical application.

Purpose of the Study:

  • To investigate the impact of complement activation on NDV neutralization.
  • To determine if NDV grown in different cell types affects its susceptibility to complement-mediated lysis.
  • To explore the role of regulators of complement activity (RCA) in conferring complement resistance to NDV.

Main Methods:

  • NDV was purified from embryonated chicken eggs and grown in mammalian cell lines (CHO, HeLa) engineered to express RCA (CD46, CD55).
  • Neutralization assays were performed using normal human serum (NHS) and chicken sera.
  • Complement component deposition (C3) and activation pathways were analyzed.

Main Results:

  • Fresh NHS effectively neutralized NDV from embryonated eggs via complement activation (C3, C4, C5), independent of antibodies.
  • NDV grown in mammalian cell lines, particularly those expressing RCA (CD46, CD55), exhibited resistance to complement neutralization by NHS.
  • Incorporation of mammalian RCA (CD46, CD55) conferred resistance, but these molecules also induced homologous restriction, allowing chicken sera to neutralize RCA-expressing NDV.
  • Chicken RCA incorporation into NDV produced in eggs also conferred species-specific resistance to chicken sera.

Conclusions:

  • Complement system plays a significant role in neutralizing NDV produced in embryonated eggs.
  • NDV's complement susceptibility is dependent on its production system, with mammalian cell-derived viruses showing resistance due to RCA incorporation.
  • Engineering NDV with specific RCA can modulate its species-specific complement resistance, offering potential strategies for therapeutic applications.

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