Human T cell leukemia virus type 1 and Zika virus: tale of two reemerging viruses with neuropathological sequelae of public health concern

Chigbu, DeGaulle I.; Jain, Pooja; Crumley, Brenndan L.; Patel, Dip; Khan, Zafar K.

doi:10.1007/s13365-019-00720-7

Cited by 2 publications

(3 citation statements)

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“…Astrocytes, dendritic cells, dermal fibroblasts, endothelial cells, monocytes, macrophages, microglia, neural stem cells, mesenchymal stem cells, neural crest cells, neurons, epiderma keratinocytes, and trophoblasts are cells that support the infection and replication of ZIKV, as well as the subsequent dissemination of the virus to other permissive cells and tissues [28][29][30]. When an Aedes mosquito takes a blood meal from an infected individual it becomes infected and capable of transmitting ZIKV to uninfected humans during future blood meals.…”

Section: Host-virus Interactionmentioning

confidence: 99%

“…Dendritic cell-specific intercellular adhesion molecule-3 grabbing nonintegrin (DC-SIGN) or CD209 are expressed on dendritic cells and macrophages [96,97]. TIM-1 (T-cell immunoglobulin and mucin domain 1) is an attachment molecule for ZIKV [28,29], whereas TAM (TYRO3, AXL and MER) is a receptor tyrosine kinase that serves as a cellular receptor for the ZIKV family of receptors [28,29,98]. AXL and TYRO3 are expressed on retinal pericytes, retinal microvascular endothelial cells [24], and neural progenitor cells (NPCs) [99].…”

Section: Pathological Mechanismsmentioning

confidence: 99%

“…AXL and TYRO3 are expressed on retinal pericytes, retinal microvascular endothelial cells [24], and neural progenitor cells (NPCs) [99]. Furthermore, TYRO3, AXL, and TIM-1 are expressed on human placenta cells, endothelial cells, trophoblast cells, fibroblasts, trophoblast progenitor cells, macrophages [27,29], epidermal keratinocytes, and dermal fibroblasts [96]. Additionally, AXL and TYRO3 facilitate the ZIKV infection of astrocytes and microglia cells [95] whereas AXL facilitates the infection of neural stem cells [99], neural crest cells [100], and mesenchymal stem cells [101].…”

Section: Pathological Mechanismsmentioning

confidence: 99%

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Pathogenesis and Manifestations of Zika Virus-Associated Ocular Diseases

Labib

Chigbu

2022

TropicalMed

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Zika virus (ZIKV) is mosquito-borne flavivirus that caused a significant public health concern in French Polynesia and South America. The two major complications that gained the most media attention during the ZIKV outbreak were Guillain–Barré syndrome (GBS) and microcephaly in newborn infants. The two modes of ZIKV transmission are the vector-borne and non-vector borne modes of transmission. Aedes aegypti and Aedes albopictus are the most important vectors of ZIKV. ZIKV binds to surface receptors on permissive cells that support infection and replication, such as neural progenitor cells, dendritic cells, dermal fibroblasts, retinal pigment epithelial cells, endothelial cells, macrophages, epidermal keratinocytes, and trophoblasts to cause infection. The innate immune response to ZIKV infection is mediated by interferons and natural killer cells, whereas the adaptive immune response is mediated by CD8+T cells, Th1 cells, and neutralizing antibodies. The non-structural proteins of ZIKV, such as non-structural protein 5, are involved in the evasion of the host’s immune defense mechanisms. Ocular manifestations of ZIKV arise from the virus’ ability to cross both the blood–brain barrier and blood-retinal barrier, as well as the blood-aqueous barrier. Most notably, this results in the development of GBS, a rare neurological complication in acute ZIKV infection. This can yield ocular symptoms and signs. Additionally, infants to whom ZIKV is transmitted congenitally develop congenital Zika syndrome (CZS). The ocular manifestations are widely variable, and include nonpurulent conjunctivitis, anterior uveitis, keratitis, trabeculitis, congenital glaucoma, microphthalmia, hypoplastic optic disc, and optic nerve pallor. There are currently no FDA approved therapeutic agents for treating ZIKV infections and, as such, a meticulous ocular examination is an important aspect of the diagnosis. This review utilized several published articles regarding the ocular findings of ZIKV, antiviral immune responses to ZIKV infection, and the pathogenesis of ocular manifestations in individuals with ZIKV infection. This review summarizes the current knowledge on the viral immunology of ZIKV, interactions between ZIKV and the host’s immune defense mechanism, pathological mechanisms, as well as anterior and posterior segment findings associated with ZIKV infection.

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Section: Host-virus Interactionmentioning

confidence: 99%