TRIMs in the placental tissue of HIV-1 infection

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. Overall design: Pregnant women living with HIV-1, as well as placentas from control pregnant women, were submitted to the same for histopathological analysis, total RNA sequencing, real-time PCR and immunohistochemistry.