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Serum predictors of susceptibility to infection with West Nile virus

ABSTRACT: West Nile virus (WNV) is a mosquito-borne RNA flavivirus which has caused more than 31,000 cases in the USA from 1999-2011 including 1,262 fatalities. WNV infections are typically asymptomatic, but some patients, especially the elderly and immunocompromised, may experience severe neurological disease and even death. Control of WNV infection by the immune system is multifactorial. We profiled antibody and cytokine responses from a stratified cohort of WNV subjects to define immune responses that contribute to disease severity. While antibody levels were not significantly different between asymptomatic and severely ill subjects in our cohort, subjects with severe infections had lower levels of serum IL-4. Further, we detected 158 genes that were differentially expressed by asymptomatic and severely infected cohorts and using cluster analysis correlated WNV susceptibility with IL-4 related gene expression pathways. Our results suggest an important contribution for IL4 in more severe responses to WNV.

ORGANISM(S): Homo sapiens

PROVIDER: GSE43190 | GEO | 2012/12/29

SECONDARY ACCESSION(S): PRJNA184867

REPOSITORIES: GEO

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Serum predictors of susceptibility to infection with West Nile virus

Project description:West Nile virus (WNV) is a mosquito-borne RNA flavivirus and the cause of more than 31,000 cases in the USA from 1999-2011 including 1, 262 fatalities. WNV infections are typically asymptomatic, but some patients, especially the elderly and immunocompromised, may experience severe neurological disease and even death. Control of WNV infection by the immune system is multifactorial. We profiled antibody, cytokine responses and gene expression from a stratified cohort of WNV subjects to define immune responses that contribute to disease severity and outcome. Differential gene expression by human PBMCs from asymptomatic and severe patients with WNV infection were generated by microarray.

2012-12-29 | E-GEOD-43190 | biostudies-arrayexpress

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Project description:West Nile virus (WNV) is a neurotropic flavivirus and the leading cause of mosquito-borne encephalitis in the United States. Recent studies in humans have found that dysfunctional T cell responses strongly correlate with development of severe WNV neuroinvasive disease. However, the contributions of human dendritic cells (DCs) in priming WNV-specific T cell immunity remains poorly understood. Here, we demonstrate that human monocyte derived DCs (moDCs) support productive viral replication following infection with a pathogenic strain of WNV. Antiviral effector gene transcription was strongly induced during the log-phase viral growth, while secretion of type I interferons (IFN) occurred with delayed kinetics. Activation of RIG-I like receptor (RLR) or type I IFN signaling prior to log-phase viral growth significantly diminished viral replication, suggesting that early activation of antiviral programs can block WNV infection. In contrast to the induction of antiviral responses, WNV infection did not promote transcription or secretion of pro-inflammatory (IL-6, GM-CSF, CCL3, CCL5, CXCL9) or T cell modulatory cytokines (IL-4, IL-12, IL-15). There was also minimal induction of molecules associated with antigen presentation and T cell priming, including the co-stimulatory molecules CD80, CD86, and CD40. Functionally, WNV-infected moDCs dampened allogenic CD4 and CD8 T cell activation and proliferation. Combined, we propose a model where WNV subverts human DC activation to compromise priming of WNV-specific T cell immunity.

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