A Deletion in the Chemokine Receptor 5<i>(CCR5)</i>Gene Is Associated with Tickborne Encephalitis

Kindberg, Elin; Mickienė, Auksė; Ax, Cecilia; Åkerlind, Britt; Vene, Sirkka; Lindquist, Lars; Lundkvist, Åke; Svensson, Lennart

doi:10.1086/524709

Cited by 200 publications

(144 citation statements)

References 14 publications

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“…Those individuals who were CCR5Δ32 homozygous had a higher frequency of multisystemic symptoms such as lymphadenopathy, neurological deficits and gastrointestinal complications. Similar results were obtained for TBEV in which individuals possessing the CCR5Δ32 allele were found to have a statistically higher frequency of symptomatic TBEV infection than subjects who were homozygous for WT CCR5 [68].…”

Section: Host Determinants Of Flavivirus Encephalitissupporting

confidence: 77%

The contribution of rodent models to the pathological assessment of flaviviral infections of the central nervous system

2012

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Members of the genus Flavivirus are responsible for a spectrum of important neurological syndromes in humans and animals. Rodent models have been used extensively to model flavivirus neurological disease, to discover host-pathogen interactions that influence disease outcome, and as surrogates to determine the efficacy and safety of vaccines and therapeutics. In this review, we discuss the current understanding of flavivirus neuroinvasive disease and outline the host, viral and experimental factors that influence the outcome and reliability of virus infection of smallanimal models.

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Section: Host Determinants Of Flavivirus Encephalitissupporting

confidence: 77%

The contribution of rodent models to the pathological assessment of flaviviral infections of the central nervous system

2012

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“…Results from previous cohort studies revealed a direct correlation between CCR5 Δ32 homozygosity and symptomatic disease during infections with WNV and TBEV [257,258]. However, the results from recent follow-up studies using larger cohorts failed to show any association between CCR5 deficiency and symptomatic infection with WNV or TBEV [259].…”

Section: Susceptibility Factors For Arboviral Encephalitis: Lessons Fmentioning

confidence: 88%

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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“…Given the similarities in the pathogenesis of WNV and TBEV, Kindberg et al [105] evaluated the role of CCR5 in the context of TBEV infection in humans. Their study evaluated a cohort of Lithuanian patients infected with TBEV and demonstrated an increase in CCR5D32 allele frequency as well as homozygous frequency among TBEV patients with encephalitis compared with TBEV-negative meningoencephalitis cases or healthy age-, ethnicity-and geographically matched controls.…”

Section: Ccr5mentioning

confidence: 99%

The role of chemokines in the pathogenesis of neurotropic flaviviruses

Bardina

Lim

2012

Immunol Res

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Neurotropic flaviviruses are important emerging and reemerging arthropod-borne pathogens that cause significant morbidity and mortality in humans and other vertebrates worldwide. Upon entry and infection of the CNS, these viruses can induce a rapid inflammatory response characterized by the infiltration of leukocytes into the brain parenchyma. Chemokines and their receptors are involved in coordinating complex leukocyte trafficking patterns that regulate viral pathogenesis in vivo. In this review, we will summarize the current literature on the role of chemokines in regulating the pathogenesis of West Nile, Japanese encephalitis, and tick-borne encephalitis virus infections in mouse models and humans. Understanding how viral infections trigger chemokines, the key cellular events that occur during the infection process, as well as the immunopathogenic role of these cells, are critical areas of research that may ultimately guide a much needed effort toward developing specific immunomodulators and/or antiviral therapeutics.

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A Deletion in the Chemokine Receptor 5(CCR5)Gene Is Associated with Tickborne Encephalitis

Cited by 200 publications

References 14 publications

The contribution of rodent models to the pathological assessment of flaviviral infections of the central nervous system

The contribution of rodent models to the pathological assessment of flaviviral infections of the central nervous system

Encephalitic Arboviruses: Emergence, Clinical Presentation, and Neuropathogenesis

The role of chemokines in the pathogenesis of neurotropic flaviviruses

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