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      Cellular and molecular mechanisms of viral infection in the human placenta

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          Abstract

          The placenta is a highly specialized organ that is formed during human gestation for conferring protection and generating an optimal microenvironment to maintain the equilibrium between immunological and biochemical factors for fetal development. Diverse pathogens, including viruses, can infect several cellular components of the placenta, such as trophoblasts, syncytiotrophoblasts and other hematopoietic cells. Viral infections during pregnancy have been associated with fetal malformation and pregnancy complications such as preterm labor. In this minireview, we describe the most recent findings regarding virus–host interactions at the placental interface and investigate the mechanisms through which viruses may access trophoblasts and the pathogenic processes involved in viral dissemination at the maternal–fetal interface.

          Abstract

          One current overview about viral entry and dissemination mechanism at the maternal–fetal interface.

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          Human antibody responses after dengue virus infection are highly cross-reactive to Zika virus.

          Lalita Priyamvada, Kendra Quicke, William Hudson … (2016)
          Zika virus (ZIKV) is an emerging mosquito-borne flavivirus of significant public health concern. ZIKV shares a high degree of sequence and structural homology compared with other flaviviruses, including dengue virus (DENV), resulting in immunological cross-reactivity. Improving our current understanding of the extent and characteristics of this immunological cross-reactivity is important, as ZIKV is presently circulating in areas that are highly endemic for dengue. To assess the magnitude and functional quality of cross-reactive immune responses between these closely related viruses, we tested acute and convalescent sera from nine Thai patients with PCR-confirmed DENV infection against ZIKV. All of the sera tested were cross-reactive with ZIKV, both in binding and in neutralization. To deconstruct the observed serum cross-reactivity in depth, we also characterized a panel of DENV-specific plasmablast-derived monoclonal antibodies (mAbs) for activity against ZIKV. Nearly half of the 47 DENV-reactive mAbs studied bound to both whole ZIKV virion and ZIKV lysate, of which a subset also neutralized ZIKV. In addition, both sera and mAbs from the dengue-infected patients enhanced ZIKV infection of Fc gamma receptor (FcγR)-bearing cells in vitro. Taken together, these findings suggest that preexisting immunity to DENV may impact protective immune responses against ZIKV. In addition, the extensive cross-reactivity may have implications for ZIKV virulence and disease severity in DENV-experienced populations.
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            Human placental trophoblasts confer viral resistance to recipient cells.

            E. Delorme-Axford, R Donker, J-F Mouillet … (2013)
            Placental trophoblasts form the interface between the fetal and maternal environments and serve to limit the maternal-fetal spread of viruses. Here we show that cultured primary human placental trophoblasts are highly resistant to infection by a number of viruses and, importantly, confer this resistance to nonplacental recipient cells by exosome-mediated delivery of specific microRNAs (miRNAs). We show that miRNA members of the chromosome 19 miRNA cluster, which are almost exclusively expressed in the human placenta, are packaged within trophoblast-derived exosomes and attenuate viral replication in recipient cells by the induction of autophagy. Together, our findings identify an unprecedented paracrine and/or systemic function of placental trophoblasts that uses exosome-mediated transfer of a unique set of placental-specific effector miRNAs to directly communicate with placental or maternal target cells and regulate their immunity to viral infections.
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              CNS Delivery Via Adsorptive Transcytosis

              Françoise Hervé, Nicolae Ghinea, Jean-Michel Scherrmann (2008)
              Adsorptive-mediated transcytosis (AMT) provides a means for brain delivery of medicines across the blood-brain barrier (BBB). The BBB is readily equipped for the AMT process: it provides both the potential for binding and uptake of cationic molecules to the luminal surface of endothelial cells, and then for exocytosis at the abluminal surface. The transcytotic pathways present at the BBB and its morphological and enzymatic properties provide the means for movement of the molecules through the endothelial cytoplasm. AMT-based drug delivery to the brain was performed using cationic proteins and cell-penetrating peptides (CPPs). Protein cationization using either synthetic or natural polyamines is discussed and some examples of diamine/polyamine modified proteins that cross BBB are described. Two main families of CPPs belonging to the Tat-derived peptides and Syn-B vectors have been extensively used in CPP vector-mediated strategies allowing delivery of a large variety of small molecules as well as proteins across cell membranes in vitro and the BBB in vivo. CPP strategy suffers from several limitations such as toxicity and immunogenicity—like the cationization strategy—as well as the instability of peptide vectors in biological media. The review concludes by stressing the need to improve the understanding of AMT mechanisms at BBB and the effectiveness of cationized proteins and CPP-vectorized proteins as neurotherapeutics.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Pathog Dis
                Journal ID (iso-abbrev): Pathog Dis
                Journal ID (publisher-id): femspd
                Title: Pathogens and Disease
                Publisher: Oxford University Press
                ISSN (Electronic): 2049-632X
                Publication date (Electronic): 29 July 2017
                Publication date Collection: October 2017
                Volume: 75
                Issue: 7
                Electronic Location Identifier: ftx093
                Affiliations
                [1 ]Departamento de Inmunobioquímica, Instituto Nacional de Perinatología “Isidro Espinosa de los Reyes”, Montes Urales 800, Col. Lomas Virreyes, CP 11000, Ciudad de México, México
                [2 ]Departamento de Biomedicina Molecular, Centro de Investigación y de Estudios Avanzados del I.P.N. Av. I.P.N 2508 Col. San Pedro Zacatenco, CP 07360 Ciudad de México, México
                [3 ]Departamento de Infectología e Inmunología Instituto Nacional de Perinatología “Isidro Espinosa de los Reyes”, Montes Urales #800, Col. Lomas Virreyes, CP 11000. Ciudad de México, México
                [4 ]Unidad de Investigación en Reproducción Humana, Instituto Nacional de Perinatología-Facultad de Química UNAM, Ciudad de México, México
                [5 ]Coordinación de Endocrinología, Instituto Nacional de Perinatología “Isidro Espinosa de los Reyes”, Montes Urales #800, Col. Lomas Virreyes, CP 11000. Ciudad de México. México
                Author notes
                [* ] Corresponding author: Departamento de Inmunobioquímica, Instituto Nacional de Perinatología “Isidro Espinosa de los Reyes”, Montes Urales #800, Col. Lomas Virreyes,CP 11000. Ciudad de México, México. Tel: +0155 55209900; E-mail: moisesleoninper@ 123456gmail.com
                Article
                Publisher ID: ftx093
                DOI: 10.1093/femspd/ftx093
                PMC ID: 7108519
                PubMed ID: 28903546
                SO-VID: d5c1de57-5e3a-4595-bbaa-6e9e6f2bb2c2
                Copyright © © FEMS 2017. All rights reserved. For permissions, please e-mail: journals.permissions@ 123456oup.com
                License:

                This article is made available via the PMC Open Access Subset for unrestricted re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the COVID-19 pandemic or until permissions are revoked in writing. Upon expiration of these permissions, PMC is granted a perpetual license to make this article available via PMC and Europe PMC, consistent with existing copyright protections.

                History
                Date accepted : 27 July 2017
                Date received : 02 May 2017
                Page count
                Pages: 15
                Funding
                Funded by: National Council for Science and Technology 10.13039/501100003141
                Award ID: CB-2015-01-255007
                Funded by: Instituto Nacional de Perinatología 10.13039/501100007686
                Award ID: 212250-3210-21007-03-15
                Categories
                Subject: Minireview

                Keywords: viruses,maternal–fetal interface,viral entry,trophoblasts,viral pathogenesis,vertical infection
                Data availability:
                Keywords: viruses, maternal–fetal interface, viral entry, trophoblasts, viral pathogenesis, vertical infection

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