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Published on: January 18, 2019
Efficient Human Cytomegalovirus Replication in Primary Endothelial Cells Is SOCS3 Dependent
Olmo Sonzogni1, Anne-Laure Millard2, Aline Taveira2
1Division of Hematology/Oncology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, USA, olmo.lab@gmail.com.
Insights
Human cytomegalovirus (HCMV) exploits SOCS3 protein for replication in endothelial cells. Silencing SOCS3 inhibits HCMV replication and enhances anti-viral STAT1/STAT2 signaling, revealing a key viral immune evasion mechanism.
Area of Science:
- Virology
- Immunology
- Cell Biology
Background:
- Human cytomegalovirus (HCMV) infection poses significant risks to immunocompromised individuals.
- Suppressor of cytokine signaling (SOCS) proteins negatively regulate JAK/STAT pathways.
- HCMV may leverage SOCS1 and SOCS3 to facilitate its replication.
Purpose of the Study:
- To investigate the role of SOCS1 and SOCS3 in HCMV replication.
- To determine if HCMV exploits SOCS proteins for its advantage.
Main Methods:
- Experiments utilized primary human lung-derived microvascular endothelial cells (HMVEC).
- SOCS1 and SOCS3 were silenced using small interfering RNA (siRNA).
- Viral replication was assessed via real-time PCR, Western blot, and viral titration.
Main Results:
- HCMV replication in HMVEC is dependent on SOCS3 protein.
- Silencing SOCS3 significantly inhibited viral antigen production and viral titers.
- SOCS3 silencing led to increased STAT1 and STAT2 phosphorylation, indicating enhanced anti-viral signaling.
Conclusions:
- SOCS3 plays a crucial role in HCMV replication.
- HCMV appears to utilize SOCS3 to suppress cellular anti-viral immune responses.
Background:
In immunocompromised patients, human cytomegalovirus (HCMV) infection is a major cause of morbidity and mortality. Suppressor of cytokine signaling (SOCS) proteins are very potent negative regulators of the janus kinase/signal transducer and activator of transcription (JAK/STAT) pathways. We hypothesized that HCMV exploits SOCS1 and/or SOCS3 to its advantage.
Methods:
All experiments were carried out with primary human lung-derived microvascular endothelial cells (HMVEC). SOCS1 and SOCS3 were silenced by transfecting the cells with siRNA. HCMV was propagated and titered on human lung-derived fibroblasts MRC5. Real-time PCR and Western blot were used to detect mRNA and protein levels, respectively.
Results:
The data presented show that an efficient replication of HCMV in HMVEC is dependent on SOCS3 protein. Time course analysis revealed an increase in SOCS3 protein levels in infected cells. Silencing of SOCS3 (siSOCS3) resulted in inhibition of viral immediate early, early, and late antigen production. Consistently, HCMV titers produced by siSOCS3 cultures were significantly decreased when compared to control transfected cultures (siCNTRs). STAT1 and STAT2 phosphorylation was increased in siSOCS3-infected cells when compared to siCNTR-treated cells.
Conclusion:
These findings indicate the implication of SOCS3 in the mechanism of HCMV-mediated control of cellular immune responses.
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