Armelle Le Campion; Ariane Larouche; Sébastien Fauteux-Daniel; Hugo Soudeyns

“ Infection of the placenta and of the foetus depends on the relative permissiveness of these cells to different pathogens. Placental cells produce multiple cytokines, chemokines and hormones. For instance, the production of IFN-β and secretory leukocyte protease inhibitor (SLPI) by trophoblasts following TLR-3 stimulation in response to a viral infection is thought to interfere with MTCT [21] . Transmission of HBV from mother to child can occur early in pregnancy via viral transcytosis across the undifferentiated trophoblasts layer [101] . This was also shown for HIV-1 [102] . Babik et al. ”

“ This has interesting implications regarding the timing and actual mechanisms that are involved in mother-to-child HCV transmission, which might take place earlier during gestation as compared with HIV-1 transmission. Indeed, the detection of HCV viral RNA in some infants in the first 3 days of life suggests that early in utero infection is possible [65] , [84] . ”

“ The characterization of the precise nature of these mechanisms should be the focus of further research, as they hold the keys to a novel understanding of host-pathogen interactions, and, potentially, to the development of new antiviral approaches. ”

“ While results from other groups support these observations [131] , other studies reported a gradual diversification of HCV quasispecies independent of serum ALT levels [115] . Protracted evolution of the variant profile was also observed in children who acquired both HCV and HIV-1 via MTCT [132] , [133] , in HCV-infected children suffering from X-linked agammaglobulinemia [134] , and in an anecdotal case of persistently seronegative, perinatally-acquired HCV infection [135] . In adults, chronic HCV infection may lead to cirrhosis and hepatocellular carcinoma in 10 to 20% of patients [136] . ”

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“ J. Viral Hepat. 2009;16:332–339.10.1111/j.1365-2893.2009.01071.x19228286↑ Guilbert C., Troesch M., Samson J., Lemay M., Pelletier V.A., Bernard-Bonnin A.C., Kozielski R., Lapointe N., Martin S.R., Soudeyns H. Differing patterns of liver disease progression and hepatitis C virus (HCV) quasispecies evolution in children vertically coinfected with HCV and human immunodeficiency virus type 1. ”

“ Trends Microbiol. 2005;13:164–174.10.1016/j.tim.2005.02.00915817386↑ Bhat P., Anderson D.A. Hepatitis B virus translocates across a trophoblastic barrier. J. Virol. 2007;81:7200–7207.10.1128/JVI.02371-0617442714↑ Lagaye S., Derrien M., Menu E., Coïto C., Tresoldi E., Mauclère P., Scarlatti G., Chaouat G., Barré-Sinoussi F., Bomsel M. European Network for the Study of In Utero Transmission of HIV-1. Cell-to-cell contact results in a selective translocation of maternal human immunodeficiency virus type 1 quasispecies across a trophoblastic barrier by both transcytosis and infection. ”

“ Hepatol. 2000;15:175–181.10.1046/j.1440-1746.2000.02060.x10735542↑ Romero-Gómez M., Suárez-García E., Casanovas J., Nogales M.C., Vargas J., Otero M.A., Castro Fernández M. Influencia del embarazo en la infección crónica por el virus C de la hepatitis [Influence of pregnancy in chronic hepatitis C virus infection] Med. Clin. (Barc) . 1998;111:641–644.9881344↑ Billingham R.E., Brent L., Medawar P.B. Actively acquired tolerance of foreign cells. Nature. 1953;172:603–606.10.1038/172603a013099277↑ Munoz-Suano A., Hamilton A.B., Betz A.G. Gimme shelter: the immune system during pregnancy. Immunol. ”

“ T lymphocyte response to viral infection during fetal life. J. Clin. Invest. 2003;111:1747–1755.127826771 2 3 Babik J.M., Cohan D., Monto A., Hartigan-O'Connor D.J., McCune J.M. The human fetal immune response to hepatitis C virus exposure in utero. J. Infect. Dis. 2011;203:196–206.10.1093/infdis/jiq04421288819↑ Burns D.N., Nourjah P., Wright D.J., Minkoff H., Landesman S., Rubinstein A., Goedert J.J., Nugent R.P. Changes in immune activation markers during pregnancy and postpartum. ”