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Published on: March 30, 2018
Primary naive and interleukin-2-activated natural killer cells do not support efficient ectromelia virus replication
April Keim Parker1, Wayne M Yokoyama2, John A Corbett3,1
1Department of Molecular Microbiology and Immunology, Saint Louis University Health Sciences Center, 1402 South Grand Blvd, St Louis, MO 63104, USA.
Ectromelia virus (ECTV) infects natural killer (NK) cells, impairing their function and viability. While the virus replicates within NK cells, it does not produce infectious progeny, suggesting potential immunomodulation.
Area of Science:
- Immunology
- Virology
Background:
- Natural killer (NK) cells are crucial for antiviral defense and tumor surveillance.
- The susceptibility of NK cells to viral infection and the impact on their biology remain poorly understood.
Purpose of the Study:
- To investigate the susceptibility of NK cells to ectromelia virus (ECTV) infection.
- To determine the effects of ECTV infection on NK cell function and viability.
Main Methods:
- In vitro and in vivo infection of NK cells with ECTV.
- Analysis of NK cell proliferation, viability, and cytokine production (IFN-gamma).
- Detection of viral gene expression and particle formation within infected NK cells.
Main Results:
- ECTV successfully infected NK cells, leading to reduced gamma interferon (IFN-gamma) production.
- Infected NK cells exhibited decreased proliferation and viability.
- ECTV exhibited early and late gene expression and formed immature/mature virus particles, but no viable progeny virus was detected.
- Immunomodulatory viral proteins (IFN-gamma-binding protein, EMICE) were secreted, suggesting local environmental modulation.
Conclusions:
- NK cells can be infected by ECTV, resulting in impaired immune function and cell death.
- ECTV infection of NK cells is semi-permissive, allowing viral replication but not the production of infectious virions.
- Secreted viral proteins may modulate the local immune environment despite the lack of productive viral spread from NK cells.
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