Microcephaly caused by Zika virus and viral detection in maternal urine

Joob, Beuy; Wiwanitkit, Viroj

doi:10.1590/1806-9282.64.12.1060

Cited by 1 publication

(1 citation statement)

References 3 publications

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“…Apart from its primary mode of transmission via mosquito bites, ZIKV can be transmitted via sexual activities, passed from mother to fetus during pregnancy, and via blood transfusions in humans [2][3][4]. Although ZIKV infection is generally known to cause mild clinical symptoms in adults, recent outbreaks of ZIKV were linked to an increase in the birth of microcephalic babies from infected mothers [5][6][7][8][9][10][11][12]. Both, clinical studies in humans and animal models have reported that ZIKV primarily targets neuronal cells [13,14], and cells of the reproductive tract including Sertoli and Leydig cells, spermatogonia, and vaginal epithelium [15,16] [17].…”

Section: Introductionmentioning

confidence: 99%

Interferon-stimulated gene 15 (ISG15) restricts Zika virus replication in primary human corneal epithelial cells

Singh

Farr

et al. 2019

The Ocular Surface

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Purpose: Zika virus (ZIKV) has emerged as an important human pathogen causing ocular complications. There have been reports of the shedding of ZIKV in human as well as animal tears. In this study, we investigated the infectivity of ZIKV in corneal epithelial cells and their antiviral immune response. Methods: Primary human corneal epithelial cells (Pr. HCECs) and an immortalized cell line (HUCL) were infected with two different strains of ZIKV (PRVABC59 & BeH823339) or dengue virus (DENV, serotypes 1-4). Viral infectivity was assessed by immunostaining of viral antigen and plaque assay. qRT-PCR and immunoblot analyses were used to assess the expression of innate inflammatory and antiviral genes. Supplementation of recombinant ISG15 (rISG15) and gene silencing approaches were used to elucidate the role of ISG15 in corneal antiviral defense. Results: Pr. HCECs, but not the HUCL cells, were permissive to both ZIKV strains and specifically to DENV3 infection. ZIKV induced the expression of viral recognition receptors (TLR3, RIG-I, & MDA5), and genes involved in inflammatory (CXCL10& CCL5) and antiviral (IFNs, MX1, OAS2, ISG15) responses in Pr. HCECs. Furthermore, ZIKV infection caused Pr. HCECs cell death, as evidenced by TUNEL staining. Silencing of ISG15 increased ZIKV infectivity while supplementation with rISG15 reduced ZIKV infection by direct inactivation of ZIKV and inhibiting its entry. Conclusions: Our study demonstrates for the first time, that ZIKV virus can readily infect and replicate in Pr. HCECs. Therefore, ZIKV may persist in the cornea and pose the potential risk of transmission via corneal transplantation.

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