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Glycolytic shift during West Nile virus infection provides new therapeutic opportunities

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE233218 | GEO | 2023/09/27

REPOSITORIES: GEO

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Glycolytic shift during West Nile virus infection provides new therapeutic opportunities [Cerebellum]

Project description:To investigate the in vivo metabolic changes during WNV infection in a mouse model, we infected mice with WNV NY99 to compare to uninfected (mock) mice. We also use two compounds targeting energetic metabolism to analysed their effects on WNV infection We then performed gene expression profiling analysis using data obtained from RNA-seq from infected vs uninfected mice and treated mice.

2023-09-27 | GSE233217 | GEO

Glycolytic shift during West Nile virus infection provides new therapeutic opportunities [Brain]

2023-09-27 | GSE233216 | GEO

Glycolytic shift during West Nile virus infection provides new therapeutic opportunities [2DG and DGA compounds]

Project description:To investigate the in vivo metabolic changes during WNV infection in a mouse model, we infected mice with WNV NY99 to compare to uninfected (mock) mice. We also use two compounds targeting energetic metabolism to analyze their effects on WNV infection We then performed gene expression profiling analysis using data obtained from RNA-seq from infected vs uninfected mice and treated mice.

2023-09-27 | GSE233215 | GEO

Glycolytic shift during West Nile virus infection provides new therapeutic opportunities

Project description:Glycolytic shift during West Nile virus infection provides new therapeutic opportunities

| PRJNA975479 | ENA

Glycolytic shift during West Nile virus infection provides new therapeutic opportunities [Cerebellum]

Project description:Glycolytic shift during West Nile virus infection provides new therapeutic opportunities [Cerebellum]

| PRJNA975484 | ENA

Glycolytic shift during West Nile virus infection provides new therapeutic opportunities [Brain]

Project description:Glycolytic shift during West Nile virus infection provides new therapeutic opportunities [Brain]

| PRJNA975481 | ENA

Glycolytic shift during West Nile virus infection provides new therapeutic opportunities [2DG and DGA compounds]

Project description:Glycolytic shift during West Nile virus infection provides new therapeutic opportunities [2DG and DGA compounds]

| PRJNA975482 | ENA

A therapeutic antibody against west nile virus neutralizes infection by blocking fusion within endosomes.

Project description:Defining the precise cellular mechanisms of neutralization by potently inhibitory antibodies is important for understanding how the immune system successfully limits viral infections. We recently described a potently inhibitory monoclonal antibody (MAb E16) against the envelope (E) protein of West Nile virus (WNV) that neutralizes infection even after virus has spread to the central nervous system. Herein, we define its mechanism of inhibition. E16 blocks infection primarily at a post-attachment step as antibody-opsonized WNV enters permissive cells but cannot escape from endocytic compartments. These cellular experiments suggest that E16 blocks the acid-catalyzed fusion step that is required for nucleocapsid entry into the cytoplasm. Indeed, E16 directly inhibits fusion of WNV with liposomes. Additionally, low-pH exposure of E16-WNV complexes in the absence of target membranes did not fully inactivate infectious virus, further suggesting that E16 prevents a structural transition required for fusion. Thus, a strongly neutralizing anti-WNV MAb with therapeutic potential is potently inhibitory because it blocks viral fusion and thereby promotes clearance by delivering virus to the lysosome for destruction.

| S-EPMC2679195 | biostudies-other

New insights into innate immune restriction of West Nile virus infection.

Project description:West Nile virus (WNV) is an encephalitic flavivirus that has provided a valuable experimental system for studying viral pathogenesis and immunity. Although in vitro approaches and mouse models of infection have identified pattern recognition receptor and interferon pathways that control WNV infection, our appreciation of specific antiviral effectors has been more limited. In this review, we highlight recent advances in our understanding of the host factors that restrict WNV infection in mammals and insects, especially those resulting from large-scale screening approaches.

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West Nile virus infection in American Robins: new insights on dose response.

Project description:West Nile virus (WNV) is a vector-borne pathogen that was first detected in the United States in 1999. The natural transmission cycle of WNV involves mosquito vectors and avian hosts, which vary in their competency to transmit the virus. American robins are an abundant backyard species in the United States and appear to have an important role in the amplification and dissemination of WNV. In this study we examine the response of American robins to infection with various WNV doses within the range of those administered by some natural mosquito vectors. Thirty American robins were assigned a WNV dosage treatment and needle inoculated with 10(0.95) PFU, 10(1.26) PFU, 10(2.15) PFU, or 10(3.15) PFU. Serum samples were tested for the presence of infectious WNV and/or antibodies, while oral swabs were tested for the presence of WNV RNA. Five of the 30 (17%) robins had neutralizing antibodies to WNV prior to the experiment and none developed viremia or shed WNV RNA. The proportion of WNV-seronegative birds that became viremic after WNV inoculation increased in a dose dependent manner. At the lowest dose, only 40% (2/5) of the inoculated birds developed productive infections while at the highest dose, 100% (7/7) of the birds became viremic. Oral shedding of WNV RNA followed a similar trend where robins inoculated with the lower two doses were less likely to shed viral RNA (25%) than robins inoculated with one of the higher doses (92%). Viremia titers and morbidity did not increase in a dose dependent manner; only two birds succumbed to infection and, interestingly, both were inoculated with the lowest dose of WNV. It is clear that the disease ecology of WNV is a complex interplay of hosts, vectors, and viral dose delivered.

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