A recent study in PLoS One found that DC-SIGNR, a protein found on the surface of immune cells, plays an important role in preventing mother-to-child transmission of HIV-1 and that impaired DC-SIGNR expression in the placenta may increase risk of transmission.

DC-SIGNR is a type of sugar-binding protein found on two types of immune cells in the body: dendritic cells and macrophages. The proteins can bind to various microorganisms by recognizing sugar molecules on their surfaces.

Some studies have suggested that they can act as receptors for viruses such as HIV and hepatitis C, thereby helping viruses attack the healthy T cells of the body. Other studies have found that DC-SIGNR might have a protective effect.

This newest study was conducted in Harare, Zimbabwe, on 197 HIV-infected mothers and their infants.

After adjusting for a number of maternal factors, it was found that infants with two copies of particular variants of DC-SIGNR, known as H1 and H3 haplotypes, had a 3.6-fold increased risk of contracting HIV infection in the uterus.

They also had a 5.7-fold increased risk of contracting HIV infection during childbirth.

Results showed that DC-SIGNR may play a role in protecting infants from HIV by binding to the virus before it is able to invade the infant’s cells. The researchers found that these particular variants, however, are present in lower amounts in the placenta compared to normal DC-SIGNR, which could lead to less protection for a fetus from HIV during pregnancy.

The study’s results imply that DC-SIGNR may play a pivotal role in preventing mother-to-child transmission, which is currently the main cause of HIV-1 infection in children worldwide. The protein may be involved in transmission of HIV-2, hepatitis C, and dengue viruses as well.

For more information, please see the original study in PLoS One.