ICAM-1 Participates in the Entry of West Nile Virus into the Central Nervous System

Dai, Jianfeng; Wang, Penghua; Bai, Fengwei; Town, Terrence; Fikrig, Erol

doi:10.1128/jvi.02621-07

Cited by 75 publications

(81 citation statements)

References 32 publications

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“…Consistent with this notion, increased expression of ICAM-1 has been shown to precede CNS invasion of mice infected with WNV [165]. Additionally, mice deficient in ICAM-1 displayed decreased CNS viral loads, diminished neuronal damage, and reduced BBB permeability following infection with WNV [166]. The Trojan horse model has also been suggested for JEV [167,168].…”

Section: Entry Of Arboviruses Into the Cnssupporting

confidence: 49%

Encephalitic Arboviruses: Emergence, Clinical Presentation, and Neuropathogenesis

2016

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Arboviruses are arthropod-borne viruses that exhibit worldwide distribution, contributing to systemic and neurologic infections in a variety of geographical locations. Arboviruses are transmitted to vertebral hosts during blood feedings by mosquitoes, ticks, biting flies, mites, and nits. While the majority of arboviral infections do not lead to neuroinvasive forms of disease, they are among the most severe infectious risks to the health of the human central nervous system. The neurologic diseases caused by arboviruses include meningitis, encephalitis, myelitis, encephalomyelitis, neuritis, and myositis in which virus-and immune-mediated injury may lead to severe, persisting neurologic deficits or death. Here we will review the major families of emerging arboviruses that cause neurologic infections, their neuropathogenesis and host neuroimmunologic responses, and current strategies for treatment and prevention of neurologic infections they cause.

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Section: Entry Of Arboviruses Into the Cnssupporting

confidence: 49%

Encephalitic Arboviruses: Emergence, Clinical Presentation, and Neuropathogenesis

2016

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“…A murine model characterized the kinetics of WNV, a neurotrophic virus that replicates in peripheral organs, crosses the blood-brain barrier (BBB), and infects the CNS, leading to death (3)(4)(5)(6). Studies using genetically modified mice that lack specific immune molecules provided insight into the immunopathogenesis of WNV (7)(8)(9)(10)(11)(12)(13). However, studies that characterize molecules involved in cross-talk between the nervous and immune system upon WNV infection are lacking.…”

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confidence: 99%

Semaphorin 7A Contributes to West Nile Virus Pathogenesis through TGF-β1/Smad6 Signaling

Sultana

Neelakanta

Foellmer

et al. 2012

The Journal of Immunology

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Semaphorin 7A (Sema7A) is a membrane-associated/secreted protein that plays an essential role in connecting the vertebrate neuronal and immune systems. However, the role of Sema7A has not been elucidated in viral pathogenesis. In this study, we show that abrogation of Sema7A protects mice from lethal West Nile virus (WNV) infection. Mice lacking Sema7A showed increased survival, reduced viral burden, and less blood–brain barrier permeability upon WNV infection. Increased Sema7A levels were evident in murine tissues, as well as in murine cortical neurons and primary human macrophages upon WNV infection. Treatment with Sema7A Ab blocked WNV infection in both of these cell types. Furthermore, Sema7A positively regulates the production of TGF-β1 and Smad6 to facilitate WNV pathogenesis in mice. Collectively, these data elucidate the role of Sema7A in shared signaling pathways used by the immune and nervous systems during viral pathogenesis that may lead to the development of Sema7A-blocking therapies for WNV and possibly other flaviviral infections.

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“…Early ring-stage parasites were incubated with M5 protein (15 mM) and allowed to grow through different developmental stages. For microscopic analysis, smears were made from each well at different time points (10,20,24,30,36, 48 and 52 hpi), fixed and subsequently stained with Giemsa, and the number of parasites at different developmental stages counted.…”

Section: Methodsmentioning

confidence: 99%

“…The progression of West Nile virus across the blood brain barrier has also been attributed to an increased expression of ICAM-1 (ref. 24). Ever since, the role of ICAM-1 in the context of host-pathogen interactions continues to be an area of active research.…”

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confidence: 99%

Host ICAMs play a role in cell invasion by Mycobacterium tuberculosis and Plasmodium falciparum

et al. 2015

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Intercellular adhesion molecules (ICAMs) belong to the immunoglobulin superfamily and participate in diverse cellular processes including host-pathogen interactions. ICAM-1 is expressed on various cell types including macrophages, whereas ICAM-4 is restricted to red blood cells. Here we report the identification of an 11-kDa synthetic protein, M5, that binds to human ICAM-1 and ICAM-4, as shown by in vitro interaction studies, surface plasmon resonance and immunolocalization. M5 greatly inhibits the invasion of macrophages and erythrocytes by Mycobacterium tuberculosis and Plasmodium falciparum, respectively. Pharmacological and siRNA-mediated inhibition of ICAM-1 expression also results in reduced M. tuberculosis invasion of macrophages. ICAM-4 binds to P. falciparum merozoites, and the addition of recombinant ICAM-4 to parasite cultures blocks invasion of erythrocytes by newly released merozoites. Our results indicate that ICAM-1 and ICAM-4 play roles in host cell invasion by M. tuberculosis and P. falciparum, respectively, either as receptors or as crucial accessory molecules.

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ICAM-1 Participates in the Entry of West Nile Virus into the Central Nervous System

Cited by 75 publications

References 32 publications

Encephalitic Arboviruses: Emergence, Clinical Presentation, and Neuropathogenesis

Encephalitic Arboviruses: Emergence, Clinical Presentation, and Neuropathogenesis

Semaphorin 7A Contributes to West Nile Virus Pathogenesis through TGF-β1/Smad6 Signaling

Host ICAMs play a role in cell invasion by Mycobacterium tuberculosis and Plasmodium falciparum

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