West Nile Encephalitis Virus Infection: Viral Pathogenesis and the Host Immune Response

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Several factors are important for promoting chemokine-mediated leukocyte migration. PRR-mediated signaling pathways are also involved in regulating the effector activities of innate immune cells. The RLR and IFN signaling pathways contribute to the regulation of natural killer cell effector activities and the control of pathological inflammation induced in myeloid cells, respectively MAVS expression on hematopoietic cells is critical for regulating the inflammatory response and protecting the host from lethal WNV infection However, a recent study suggests that immature B cells present in B-cell-activating factor receptor-deficient mice also contribute to antiviral immunity and protect the host in passive and active immunizations T cells provide long-lasting protection against WNV.

Graham et al.

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Aging is a known risk factor for WNV-induced encephalitis in mice and humans. Old mice display an enhanced vulnerability to WNV infection, partially due to cell-trafficking defects in the draining lymph nodes, which result in delayed T cell recruitment and antigen recognition and an impaired IgM and IgG response Lastly, although the intrinsic MAVS signaling is dispensable for Treg proliferation and suppressive capacity, the overproduction of proinflammatory cytokines generated in MAVS-deficient mice contributes to a failure of Treg expansion Activated LCs then migrate to local draining lymph nodes from the epidermis, after which viremia begins and WNV disseminates to the kidneys, spleen, and other visceral organs Although how WNV enters the CNS is not clearly understood, both hematogenous and transneural pathways have been proposed 50 , WNV most likely propagates within the CNS transsynaptically by both anterograde and retrograde axonal transport The trafficking of Ly6C hi monocytes into the brain was pathogenic, as blocking these cells using anti-very late antigen 4 integrin antibody at the time of observation of the first weight loss and leukocyte influx resulted in long-term survival in mice with lethal encephalitis In an ex vivo spinal cord slice culture SCSC model, it was shown that CNS-resident cells had the capacity to initiate a robust innate immune response against WNV infection in the absence of infiltrating inflammatory cells and systemic immune responses Furthermore, treatment with minocycline in WNV-infected SCSC induced the expression of genes associated with the anti-inflammatory activation of microglia while inhibiting the expression of genes associated with proinflammatory microglia activation, and this was protective for multiple CNS cell types The enhanced virulence of WNVKOU was associated with its poor viral clearance and the induction of a poor neutralizing antibody response The underlying mechanisms are not clearly understood.

Vasek et al. They demonstrated microglial engulfment of hippocampal CA3 presynaptic terminals via complement during acute WNV infection and after recovery Furthermore, in the same mouse model, Garble et al. Preferential generation of IL-1 in astrocytes impaired the homeostasis of neuronal progenitor cells These results not only suggest a potential mechanism underlying neurocognitive impairment in patients recovering from WNV neuroinvasive disease but also provide potential therapeutic targets.

Increasing evidence suggests that persistent WNV infection also contributes to long-term morbidity. Small animal models have been developed to study persistent WNV infection. We and others have shown that the inbred C57BL6 mice infected with either the wild-type WNV strain or an isolate cultured from the urine of a persistently infected hamster share some similarity and discrepancy in symptoms and tissue tropism compared to the clinical findings in some WNV convalescent patients with long-term morbidity, including chronic kidney diseases and long-term neurological sequelae 62 , More recently, the collaborative cross, a population of recombinant inbred mouse strains with high levels of fixed genetic variation, were used to investigate WNV persistence in the brain.

Results from this model suggest that the Treg response sufficiently restrains the immune response and leads to WNV persistence in the CNS Studies in human cell culture and animal models suggest that both innate and adaptive immune responses are important for protecting the host from WNV infection.

PRR-mediated innate immune responses are critical for the control of WNV dissemination and viral clearance in the CNS, modulation of BBB integrity, and regulation of the effector functions of innate and adaptive immune cells. Adaptive immunity provides long-lasting protection against WNV. Newly developed animal models have provided important insights into the mechanism underlying neurocognitive impairment in patients recovering from WNV neuroinvasive disease and WNV persistence in the CNS.

No competing interests were disclosed. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.


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Home Browse Recent advances in understanding West Nile virus host immunity and ALL Metrics. Get PDF. Get XML. How to cite this article. NOTE: it is important to ensure the information in square brackets after the title is included in all citations of this article. Close Copy Citation Details. Recent advances in understanding West Nile virus host immunity and viral pathogenesis [version 1; peer review: 2 approved]. West Nile virus WNV , a mosquito-borne flavivirus, has been a significant public health concern in the United States for nearly two decades.

The virus has been linked to acute viral encephalitis, neurological sequelae, and chronic kidney diseases. Neither antiviral drugs nor vaccines are currently available for humans. In vitro cell culture and experimental animal models have been used to study WNV infection in humans. In this review, we will focus on recent findings and provide new insights into WNV host immunity and viral pathogenesis.

Recent advances in understanding West Nile virus host immunity and viral pathogenesis

Corresponding Author s. Introduction West Nile virus WNV , a mosquito-borne, single-stranded, positive-sense flavivirus, has been a significant public health concern in the United States for nearly two decades.

Age‐related alterations in immune responses to West Nile virus infection

Conclusions Studies in human cell culture and animal models suggest that both innate and adaptive immune responses are important for protecting the host from WNV infection. Competing interests No competing interests were disclosed. F recommended References 1. Res Vet Sci. If the address matches an existing account you will receive an email with instructions to reset your password Close. Request Username Can't sign in? Forgot your username? Enter your email address below and we will send you your username. Viral Immunology Vol. Bradley S. Schneider Search for more papers by this author.

Lynn Soong Search for more papers by this author. Yvette A. Girard Search for more papers by this author. Gerald Campbell Search for more papers by this author. Peter Mason Search for more papers by this author. Stephen Higgs Search for more papers by this author. Mosquito saliva alone has profound effects on the human immune system. Host inflammatory response to mosquito bites enhances the severity of arbovirus infection.

Infection via mosquito bite alters Zika virus tissue tropism and replication kinetics in rhesus macaques. Innate immunity against Zika virus. Flavivirus Pathogenesis in the Mosquito Transmission Vector. Regulatory considerations in development of vaccines to prevent disease caused by Chikungunya virus. West Nile Virus.

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Victoria Pando-Robles and Cesar V. Mosquito Modulation of Arbovirus—Host Interactions. Mosquito saliva induced cutaneous events augment Chikungunya virus replication and disease progression. Experimental infection of rock pigeons Columba livia with three West Nile virus lineage 1 strains isolated in Italy between and Influences of Arthropod Vectors on Encephalitic Arboviruses.

Dissecting vectorial capacity for mosquito-borne viruses. Vector-transmitted disease vaccines: targeting salivary proteins in transmission SPIT.

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Bunyaviruses: from transmission by arthropods to virus entry into the mammalian host first-target cells. Chikungunya Virus and Its Mosquito Vectors. Role of the Vector in Arbovirus Transmission. The salivary secretome of the biting midge, Culicoides sonorensis. Characterization of chikungunya virus infection of a human keratinocyte cell line: Role of mosquito salivary gland protein in suppressing the host immune response. West Nile Fever. West Nile virus infection and immunity. Mouse models for Chikungunya virus: deciphering immune mechanisms responsible for disease and pathology.

Implication of haematophagous arthropod salivary proteins in host-vector interactions.