In humans, the hemochorial placenta is a unique temporary organ that forms during pregnancy to support fetal development, gaseous exchange, delivery of nutrition, removal of waste products and provides immune protection, while maintaining tolerance to the HLA-haploidentical fetus. In this issue, we ask for articles addressing immunity during maternal viral infection with HIV-1, cytomegalovirus (CMV), SARS-CoV-2, and Zika virus, and interactions with decidual and stromal placental macrophages (Hofbauer cells), cytotrophoblasts including extravillous trophoblasts, T cells, and decidual natural killer (dNK) cells. Although these clinically significant viruses elicit both innate and adaptive responses, they also evade immune detection to initiate placental inflammation associated with transmission to the developing fetus. Aside from congenital or perinatal infection, other adverse pregnancy outcomes include preterm labor and spontaneous abortion. We hope the published manuscripts will prompt further (much-needed) research that improves clinical outcomes in the mother-infant dyad during viral infection.
It is important to elucidate mechanisms that HIV-1, HCMV, SARS-CoV-2, and ZIKV utilize to gain access to the fetal side, characterize their intracellular effects, and identify correlates of protection. Although some progress has been made in understanding the determinants of clinical outcomes of perinatal infections, our knowledge remains limited. We will focus on current knowledge on individual host cell-viral interactions within immune cell populations in the decidua and placenta. The significance of characterizing placental immune cell-viral interactions is underscored by the fact that infectious complications that directly impact the placenta lead to adverse outcomes in both mother and fetus/newborn, contributing significantly to perinatal morbidity and mortality. At the same time, identifying immune correlates of protection may prompt development of prophylactic and therapeutic interventions. Novel research addressing mechanisms of pathogenesis, protection, and transmission at the maternal-fetal interface to HIV-1, CMV, SARS-CoV-2, and ZIKV are therefore encouraged including but not limited to high-throughput gene expression, proteomic, and/or genomic data. At the end of each article, knowledge gaps that may prompt future research directions should be included.
This Research Topic accepts original research including in-depth studies supported by longitudinal and/or multi-omics data. Review will also be considered. Data reuse should consist of meta-analyses, incorporating multiple independent public datasets or re-use of public datasets as a reference for the analysis of an original dataset. Submissions should not be limited to the re-analysis of a single public dataset. We welcome manuscripts focusing on, but not limited to, the following sub-topics: • Characterizing immunity at the maternal-fetal interface during maternal infection with CMV • Characterizing immunity at the maternal-fetal interface during maternal infection with HIV • Characterizing immunity at the maternal-fetal interface during maternal CO-infection with HIV and CMV • Characterizing immunity at the maternal-fetal interface during maternal infection with SARS-CoV-2 • Characterizing immunity at the maternal-fetal interface during maternal infection with Zika virus.
The topic editors declare no conflicts of interest in relation to the editorship of this collection.
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This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:
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Classification
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Hypothesis and Theory
Methods
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Article types
This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:
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