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Updated: Dec 2, 2025
Evaluation of Zika Virus-specific T-cell Responses in Immunoprivileged Organs of Infected Ifnar1-/- Mice
Published on: October 17, 2018
Impact of Zika virus on the human type I interferon osteoimmune response
Arnaud Drouin1, Nicholas Wallbillich2, Marc Theberge3
1Department of Medicine, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA, 70114, United States; Department of Pathology, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA, 70114, United States.
Background:
The developing field of osteoimmunology supports importance of an interferon (IFN) response pathway in osteoblasts. Clarifying osteoblast-IFN interactions is important because IFN is used as salvage anti-tumor therapy but systemic toxicity is high with variable clinical results. In addition, osteoblast response to systemic bursts and disruptions of IFN pathways induced by viral infection may influence bone remodeling. ZIKA virus (ZIKV) infection impacts bone development in humans and IFN response in vitro. Consistently, initial evidence of permissivity to ZIKV has been reported in human osteoblasts.
Hypothesis:
Osteoblast-like Saos-2 cells are permissive to ZIKV and responsive to IFN.
Methods:
Multiple approaches were used to assess whether Saos-2 cells are permissive to ZIKV infection and exhibit IFN-mediated ZIKV suppression. Proteomic methods were used to evaluate impact of ZIKV and IFN on Saos-2 cells.
Results:
Evidence is presented confirming Saos-2 cells are permissive to ZIKV and support IFN-mediated suppression of ZIKV. ZIKV and IFN differentially impact the Saos-2 proteome, exemplified by HELZ2 protein which is upregulated by IFN but non responsive to ZIKV. Both ZIKV and IFN suppress proteins associated with microcephaly/pseudo-TORCH syndrome (BI1, KI20A and UBP18), and ZIKV induces potential entry factor PLVAP.
Conclusions:
Transient ZIKV infection influences osteoimmune state, and IFN and ZIKV activate distinct proteomes in Saos-2 cells, which could inform therapeutic, engineered, disruptions.
Insights
Osteoblast cells can be infected by Zika virus (ZIKV) and respond to interferon (IFN). This study shows ZIKV and IFN trigger different protein changes in osteoblasts, impacting bone health.
Area of Science:
- Osteoimmunology
- Virology
- Cell Biology
Background:
- Osteoimmunology highlights the role of interferon (IFN) pathways in osteoblasts.
- IFN therapy for cancer has limitations; understanding osteoblast-IFN interactions is crucial.
- Viral infections, like ZIKA virus (ZIKV), can disrupt IFN pathways, potentially affecting bone remodeling.
Purpose of the Study:
- To investigate if osteoblast-like Saos-2 cells are susceptible to ZIKV infection.
- To determine if Saos-2 cells exhibit an IFN-mediated suppression of ZIKV.
- To analyze the proteomic impact of ZIKV and IFN on Saos-2 cells.
Main Methods:
- Utilized Saos-2 cells, a human osteoblast-like cell line.
- Assessed ZIKV permissivity and IFN-mediated ZIKV suppression.
- Employed proteomic analysis to evaluate cellular responses to ZIKV and IFN.
Main Results:
- Confirmed Saos-2 cells are permissive to ZIKV and support IFN-mediated ZIKV suppression.
- Demonstrated differential proteomic changes induced by ZIKV and IFN.
- Identified specific protein alterations, including upregulation of HELZ2 by IFN and induction of PLVAP by ZIKV.
Conclusions:
- Transient ZIKV infection influences the osteoimmune state in Saos-2 cells.
- IFN and ZIKV activate distinct proteomes, offering insights for therapeutic strategies.
- Findings may inform engineered interventions targeting ZIKV-induced bone alterations.
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