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Simple Summary: Considering that the bovine uterine infections caused by bacteria make the host more susceptible to secondary infections, we investigated the role of BoGHV4 and bacterial LPS in cell death in an experimental model of endometrial cells. Various techniques, including staining and molecular analysis, were used. The results showed that the level of cell death following BoGHV4 infection is linked to the timing of viral infection and the presence of LPS. Apoptosis was most prominent in cells infected with BoGHV4 and BoGHV4 + LPS, which correlated with the occurrence of cytopathic effects and high viral titers. Morphological, biochemical, and molecular changes were observed during both the early and late stages of apoptosis. These discoveries offer valuable insights into the factors influencing BoGHV4 pathogenesis and provide an understanding of the mechanisms underlying viral infection. The prevalent pathogens associated with bovine uterine infections are bacteria that appear to increase the host's susceptibility to secondary infections with other bacteria or viruses, among which BoGHV4 is the most frequently found. In this work, the study of the pathways of apoptosis induction was carried out on an experimental model of primary culture of endometrial cells, in order to know the implication of BoGHV4 and the presence of bacterial LPS in the pathogenesis of the bovine reproductive tract. For this, different staining techniques and molecular analysis by RT-PCR were used. The results obtained allowed us to conclude that the level of cell death observed in the proposed primary culture is directly related to the time of viral infection and the presence of LPS in BoGHV4 infection. The apoptosis indices in cells infected with BoGHV4 and BoGHV4 + LPS revealed a maximum that correlated with the appearance of cytopathic effects and the maximum viral titers in the model studied. However, morphological, biochemical, and molecular changes were evident during both early and late stages of apoptosis. These findings provide information on the factors that may influence the pathogenesis of BoGHV4 and help to better understand the mechanisms involved in virus infection. [ABSTRACT FROM AUTHOR]