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TRIMs in the placental tissue of HIV-1 infection

ABSTRACT: Innate immunity is a crucial mechanism for protecting the maternal-fetal interface, whereas little is known about the placenta in chronic HIV-1 infection in mothers treated with antiretroviral therapy (ART). The maternal-fetal interface, we previously observed an enrichment of antiviral factors and inflammatory components in HIV-1 infection. TRIM family proteins are potent antagonists of viral replication; however, others can promote viral replication by ubiquitinating and degrading specific innate immune signalling proteins. We verified the expression of genes involved in innate immunity focusing on the TRIM gene profile in placental tissue (villus and decidua) from HIV-1-infected mothers. We conducted RNA sequencing of placental tissue (villus and decidua) from HIV-1 infected and control mothers. DEGs validation performed by the RT-qPCR method confirms the upregulation of TRIM21 and TRIM39 in both the decidua and the villus of HIV-1-infected samples.

ORGANISM(S): Homo sapiens

PROVIDER: GSE319583 | GEO | 2026/03/01

REPOSITORIES: GEO

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Project description:The transplacental transfer of maternal IgG to the developing fetus is critical for infant protection against infectious pathogens in the first year of life. However, factors that modulate the transplacental transfer efficiency of maternal IgG that could be harnessed for maternal vaccine design remain largely undefined. HIV-infected women have impaired placental IgG transfer, yet the mechanism underlying this impaired transfer is unknown, presenting an opportunity to explore factors that contribute to the efficiency of placental IgG transfer. We measured the transplacental transfer efficiency of maternal HIV and other pathogen-specific IgG in historical U.S. (n=120) and Malawian (n=47) cohorts of HIV-infected mothers and their HIV58 exposed uninfected and HIV-infected infants. We then examined the role of maternal HIV disease progression, infant factors, placental Fc receptor expression, and IgG Fc region subclass and glycan signatures and their association with transplacental transfer efficiency of maternal antigen-specific IgG. We established 3 distinct phenotypes of placental IgG transfer efficiency in HIV-infected women, including: 1) efficient transfer of the majority of antigen-specific IgG populations; 2) generally poor IgG transfer phenotype that was strongly associated with maternal CD4+ T cell counts, hypergammaglobulinemia, and frequently yielded non-protective levels of vaccine-specific IgG; and 3) variable transfer of IgG across distinct antigen specificities. Interestingly, maternal IgG characteristics, such as binding to placentally expressed Fc receptors FcgRIIa and FcgRIIIa, IgG subclass frequency, and Fc region glycan profiles were associated with placental IgG transfer efficiency. These maternal IgG transplacental transfer determinants were distinct among different antigen-specific IgG populations. Our findings suggest that in HIV-infected women, both maternal disease progression and Fc region characteristics modulate the selective placental transfer of distinct IgG subpopulations, with implications for both the health of HIV-exposed uninfected infants and maternal vaccine design.

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TRIMs in the placental tissue of HIV-1 infection

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