SUMMARY
We examined if Fc receptor‐mediated antibody‐dependent enhancement (FcR‐ADE) or complement‐mediated antibody‐dependent enhancement (C′‐ADE) of virus infection can contribute to increasing replication of HIV‐1 in human syncytiotrophoblast (ST) cells. Here we report that both FcR‐ADE and C′‐ADE may result in enhanced virus release from HIV‐1‐infected ST cells. We show that FcR‐ADF of HIV‐1 infection in ST cells is mediated by FcRIII and other FcR(s) belonging to undetermined Fc classes and does not require CD4 receptors, whereas C'‐ADE uses both CD4 and CR2‐like receptors. FcR‐ADE: seems to be more efficient in enhancing HIV‐I replication than C′‐ADE. While FcR‐ADE leads to increased internalization of HIV‐1. C′‐ADE does not result in enhanced endocytosis of the virus. In addition, antibodies mediating FcR‐ADE arc reactive with the gp120 viral envelope antigen, whereas antibodies involved in C′‐ADE react with the viral transmembrane glycoprotein gp41. Data suggest that both FcR‐ADH and C′‐ADE may contribute lo the spread of HIV‐1 from mother to the fetus.
Human cytomegalovirus (HCMV) and human immunodeficiency virus type 1 (HIV-1) may interact in the pathogenesis of AIDS. The placental syncytiotrophoblast layer serves as the first line of defense of the fetus against viruses. We analyzed the patterns of replication of HIV-1 and HCMV in singly an dually infected human term syncytiotrophoblast cells cultured in vitro. Syncytiotrophoblast cells exhibited restricted permissiveness for HIV-1, while HCMV replication was restricted at the level of immediate-early and early gene products in the singly infected cells. We found that the syncytiotrophoblasts as an overlapping cell population could be coinfected with HIV-1 and HCMV. HIV-1 replication was markedly upregulated by previous or simultaneous infection of the cells with HCMV, whereas prior HIV-1 infection of the cells converted HCMV infection from a nonpermissive to a permissive one. No simultaneous enhancement of HCMV and HIV-1 expression was observed in the dually infected cell cultures. Major immediate-early proteins of HCMV were necessary for enhancement of HIV-1 replication, and interleukin-6 production induced by HCMV and further increased by replicating HIV-1 synergized with these proteins to produce this effect. Permissive replication cycle of HCMV was induced by the HIV-1 tat gene product. We were unable to detect HIV-1 (HCMV) or HCMV (HIV-1) pseudotypes in supernatant fluids from dually infected cell cultures. Our results suggest that interactions between HIV-1 and HCMV in coinfected syncytiotrophoblast cells may contribute to the transplacental transmission of both viruses.
Although syncytiotrophoblast (ST) cells can be infected by human cytomegalovirus (HCMV), in vitro studies have indicated that ST cells do not support the complete viral reproductive cycle, or HCMV replication may occur in less than 3% of ST cells. The present study tested the possibility that placental macrophages might enhance activation of HCMV carried in ST cells and, further, that infected ST cells would be capable of transmitting virus to neighboring macrophages. For this purpose, we studied HCMV replication in ST cells grown alone or cocultured with uninfected placental macrophages. Our results demonstrated that HCMV gene expression in ST cells was markedly upregulated by coculture with macrophages, resulting in release of substantial amounts of infectious virus from HCMV-infected ST cells. After having become permissive for viral replication, ST cells delivered HCMV to the cocultured macrophages, as evidenced by detection of virus-specific antigens in these cells. The stimulatory effect of coculture on HCMV gene expression in ST cells was mediated by marked interleukin-8 (IL-8) and transforming growth factor-beta1 (TGF-beta1) release from macrophages, an effect caused by contact between the different placental cells. Our findings indicate an interactive role for the ST layer and placental macrophages in the dissemination of HCMV among placental tissue. Eventually, these interactions may contribute to the transmission of HCMV from mother to the fetus.
Summary
The significance of fetal arrhythmia presenting during pregnancy and labour has been examined in 68 patients. The different types of rhythm disorders diagnosed included 61 extrasystoles, 6 atrioventricular blocks and 1 auricular fibrillation. Extrasystoles were not associated with acidosis or organic cardiac disease. Atrioventricular block, though not associated with fetal hypoxia, was occasionally associated with congenital cardiac failure.
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