Several adverse intrauterine conditions during pregnancy may increase the risk of neurodevelopmental disorders, including Autism Spectrum Disorder (ASD). Endogenous retroviruses (ERVs) have been proposed as co-factors in the pathogenesis of ASD, also potentially useful as early biomarkers of derailed neurodevelopment. Two preclinical models of ASD, the inbred BTBR T+tf/J (BTBR) mice, and mice prenatally exposed to valproic acid, showed an altered expression of several ERVs and cytokines, in embryos, blood and brain samples at different post-natal ages. The present study aimed to characterize the transcriptional profile of selected ERVs and inflammatory mediators at the maternal-fetal interface and in dissected embryos from BTBR and C57BL6/J (C57) mice, used as control. For this purpose, whole embryos were explanted at 10.5 gestational day, separated from maternal tissues, and dissected to obtain: cephalic and non-cephalic embryonic tissues, maternal decidua and extra-embryonic tissues. The expression of several ERVs and inflammatory mediators was assessed by Real-Time PCR. Our results showed a global deregulation of ERVs and selected inflammatory mediators in maternal decidua and extra-embryonic tissues, respectively maternal and fetal compartments of the neo-forming placenta, and cephalic and non-cephalic embryonic tissues obtained from BTBR mice compared to C57. Several correlations among all ERV expression levels emerged in different tissues obtained from C57 mice, particularly in cephalic and non-cephalic ones, while in BTBR mice, most of the correlations were lost. Our study provides new insights into the transcriptional landscape of ERVs and inflammatory mediators in intra-uterine life supporting the involvement of ERVs in neurodevelopmental derailment related to ASD.