Parasitic worm infections increase risk of mother-to-child HIV spread

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Treating helminth (parasitic worm) infections in pregnant women with HIV might reduce the rate of mother-to-child HIV transmission, researchers from Kenya and the United States suggest in a report published in the November 4th edition of the journal AIDS.

Helminth infections are widespread in resource-limited settings, and are known to increase susceptibility of cells to HIV infection. Some have even suggested that regular treatment of helminth infections in HIV-positive people may delay HIV disease progression, by lessening harmful activation of the immune system caused by helminths.

Researchers investigated the prevalence of parasitic infections in mother and infant pairs in the Coast province of Kenya between 1996 and 2002. The study enrolled 936 pregnant women, of whom 83 were found to be HIV-positive.

Glossary

lymphatic system

The lymphatic system is made up of lymphoid tissues (lymph nodes, spleen, tonsils, adenoids, gut-associated lymphoid tissue (GALT), Peyer’s patches, and local immune cells in many other tissues) and lymphatic vessels, leading from lymphatic tissues toward the heart. The lymphatic system is essential to fighting infections. 

mother-to-child transmission (MTCT)

Transmission of HIV from a mother to her unborn child in the womb or during birth, or to infants via breast milk. Also known as vertical transmission.

loss to follow up

In a research study, participants who drop out before the end of the study. In routine clinical care, patients who do not attend medical appointments and who cannot be contacted.

immune system

The body's mechanisms for fighting infections and eradicating dysfunctional cells.

disease progression

The worsening of a disease.

HIV-positive women were matched with two HIV-negative controls (n=166) and examined for parasitic infection prior to delivery. Wherever possible, the infant follow-up twelve months after delivery included HIV testing, but 40 of the HIV-positive mothers were lost to follow-up.

The researchers found that women with HIV were twice as likely to be infected with malaria and with lymphatic filariasis, but did not have a greater likelihood of internal hookworm infection nor of schistosomiasis.

Women who transmitted HIV to their infants were significantly more likely to have some form of helminth infection, with lymphatic filariasis most strongly associated with mother-to-child HIV transmission.

Eleven of 23 coinfected women transmitted HIV to their infants, compared with two of 20 women without coinfection (48% vs 10% transmission rate, p

The authors suggest that lymphatic filariasis increases a woman’s risk of HIV infection if exposed, probably because in common with other helminth infections it causes chronic activation of the cells that are targets for HIV infection and because it increases the number of receptors on the surface of cells that can be used by HIV to gain entry to cells.

They point out that another study has demonstrated that lymphocytes from people infected with lymphatic filariasis are more susceptible to HIV infection prior to anti-filarial treatment.

Infants exposed to helminths in the womb respond with an immune activation pattern (a Th-2-type cytokine response), and when the researchers examined cord blood samples from infants of HIV-positive mothers in the Kenyan study, they found that those infants that responded most strongly to helminths with a Th-2-type response were also most likely to have HIV infection.

The authors do not think that helminths increase the risk of mother-to-child transmission by increasing levels of viral load, but were unable to measure viral load in this study.

They suggest that mass treatment programmes for lymphatic filariasis and intestinal helminths in Kenya should be used to determine whether rates of mother-to-child HIV transmission and sexual HIV transmission are reduced by helminth treatment.

References

Gallagher M et al. The effects of maternal helminth and malaria infections on mother-to-child HIV transmission. AIDS 19: 1849-1855, 2005.