World AIDS Day is held on December 1 every year to show support for those living with HIV, commemorate the estimated 35 million who have died from HIV or AIDS and unite in the global fight against the disease. Though much progress has been made in raising awareness about HIV, few know about a major risk factor for the disease among girls and women living in Sub-Saharan Africa: female genital schistosomiasis.

Female genital schistosomiasis, or FGS, is found in approximately 50 percent of girls and women infected with the parasitic worm Schistosoma haemotobium – an estimated 20 to 150 million women and girls in Sub-Saharan Africa. This parasite causes the neglected tropical disease urinary tract schistosomiasis, which is responsible for severe kidney and bladder damage, bloody urine and increased risk of bladder cancer in infected patients.

In women and girls with FGS, the worm’s eggs block the blood vessels in their uterus, cervix and lower reproductive tracts, causing painful lesions known as “sandy patches.” These sandy patches have been associated with pain, bleeding, social stigma and depression. If that’s not worrying enough, it’s been known for over two decades that FGS leaves women more susceptible to both contracting and spreading HIV infection, and is believed to significantly accelerate disease progression. One study in the journal PLOS Neglected Tropical Diseases estimated FGS puts its sufferers at three-fold higher risk of contracting HIV – a number the paper’s authors admit is likely very conservative.

How does a worm infection acquired from wading in contaminated water affect infection with a sexually-transmitted virus? The answer, as far as we understand it, is three-fold. The first reason is fairly straightforward – FGS disrupts tissue in the genital tract, providing an easy way for HIV to enter the body during sexual intercourse. The last two explanations are, perhaps counterintuitively, a result of the way the immune system tries to fight these infections.

When a woman contracts FGS, the immune system responds to the challenge posed by the worm eggs by drawing activated immune cells to the site of infection (i.e. the genital tract). Unfortunately, these immune cells are the same ones that HIV infects and destroys, leading to the immunodeficiency characteristic of AIDS. To make a bad situation worse, the fact that these cells are activated means that they bear a protein on their surface that makes it even easier for HIV to enter them. To put it simply, FGS draws the cells that are prime targets for HIV infection directly to the site where the virus is entering the body and serves them up on a silver platter.

This makes these women susceptible to developing a systemic HIV infection more rapidly than women without FGS; in fact, in one study, the risk was even higher than if HIV entered directly into the bloodstream, indicating that the recruitment of activated immune cells to the site of infection was very important in accelerating disease progression. For similar reasons, FGS and HIV co-infected women also release more virus in the genital tract than women with HIV infection alone, making it much more likely that they will transfer HIV to a sexual partner.

Lastly, having a chronic, long-lasting FGS infection makes it difficult for the immune system to control an HIV infection. FGS orients the immune system toward an immune response that is typically seen during worm infections. However, to adequately resist HIV infection, the immune system needs to mount a different, in some ways opposite, type of immune response that is more common of a viral infection. Since it is hard for the immune system to shift gears once it is biased one way or the other, the immune system is less able to resist HIV, and the virus is able to propagate more easily.

As a disease that affects as many as 150 million women and girls in Sub-Saharan Africa, FGS is likely a major cofactor for the transmission of HIV in the region. Fortunately, this disease is something we know how to fight. The drug used to kill the schistosome worms that cause FGS is relatively inexpensive and effective – US $0.32 treats one woman. Research to find vaccines that protect against these worms is also underway, including one in development at Sabin’s research labs in Houston. With a continued global commitment to fighting FGS and other neglected tropical diseases by agencies like the World Health Organization and the Schistosomiasis Control Initiative, we have an opportunity to improve the lives of millions of African women and make real progress towards curbing the AIDS epidemic.