Mechanisms of human immunodeficiency virus vertical transmission
In the absence of interventions, 30-45% of exposed infants acquire human immunodeficiency virus type 1 (HIV-1) through mother-to-child transmission. It remains unclear why some infants become infected while others do not, despite significant exposure to HIV-1 in utero, during delivery and while breastfeeding. Ths paper discusses the correlates of vertical transmission with an emphasis on factors that increase maternal HIV-1 levels, either systemically or locally in genital secretions and breast milk. Immune responses may influence maternal viral load, and data suggest that maternal neutralising antibodies reduce infection rates. In addition, infants may be capable of mounting HIV-specific cellular immune responses. The authors propose that both humoral and cellular responses are necessary to reduce infection because cell-free as well as cell-associated virus appears to play a role in vertical transmission. These distinct forms of the virus may be targeted most effectively by different components of the immune system. They also discuss the use of antiretrovirals to reduce transmission, focusing on the mechanisms of action of regimens currently used in developing country settings. Their conclusion is that that prevention relies not only on reducing maternal HIV-1 levels within blood, genital tract and breast milk, but also on pre- and/or post-exposure prophylaxis to the infant. However, HIV-1 has the capacity to mutate under drug pressure and rapidly acquires mutations conferring antiretroviral resistance. This review concludes with data on persistence of low-level resistance after delivery as well as recent guidelines for maternal and infant regimens designed to limit resistance.
Related:
- Cytopathic mechanisms of HIV-1 – is the envelope glycoprotein a viroporin?
- Variation in two key genes can predict the course of progression to AIDS
- HIV vaccines – bad news, good news
Tags: Biology, Health, HIV/AIDS, Medicine, Microbiology, Science, Virology



In addition to CD4 receptors on the T cell membranes, HIV needs additional co-receptors CXCR4 and CCR5 as well. absence of CCR5 has been shown to confer ‘immunity’ from HIV infection.
However, in this case, this could not be the sole cause, as the CCR5 mutation is rare. The extent of the viral load (of the mother), in terms of RNA copies, in addition to the cellular and humoral immunity of the infants, are the probable reasons here.