Professor Emerita Janet Hapgood
Affiliations
- Full Member, Institute of Infectious Disease and Molecular Medicine
Key Expertise
HIV, contraceptives, endocrinology, steroid receptors, gene regulation
Main Research Focus
Professor Hapgood's field is broadly in intracellular molecular mechanisms of action of steroid receptors, in particular the glucocorticoid receptor (GR). Research is focussed on ligand-selectivity, regulation of gene expression as well as cross talk between steroid receptors and other signalling pathways, which allows functional integration between stress, reproduction and immune function. This research is conducted in the broad context of reproduction, inflammation, contraception and infectious disease, in particular HIV-1. Different progestins are used in contraception. MPA, widely used as an injectable contraceptive in Sub-Saharan Africa, has been reported in observational clinical studies to increase HIV-1 acquisition, unlike another injectable contraceptive NET-EN. The Hapgood lab is investigating the molecular basis for this difference. Broadly, the lab is investigating the mechanisms and effects on immune function and HIV-1 pathogenesis of different progestin contraceptives via the GR, as well as cross talk between the GR and other receptors, and the role of the unliganded GR. The effects of different progestins via different steroid receptors, as well as their metabolism, are also being investigated. Reciprocal modulation of progestins and ARVs is another area of interest, with a view to choice of combination therapies to inhibit both HIV-1 acquisition and pregnancy. The work on HIV and contraceptives is highly relevant to women’s choice of contraception in areas of high risk of HIV-1 infection in Sub-Saharan Africa and South Africa in particular.
Most Significant Paper Authored in 2025
Avenant C, Bick AJ, Moliki JM, Dlamini S, Tomasicchio M, Hofmeyr GJ, Morrison C, Chen PL, Hapgood JP. (2025)
Systemically, DMPA-IM and NET-EN similarly reduced the frequency and number of some CD4+ cells and expression of some CD4+ cell surface markers. In contrast, female genital tract (FGT) results showed significantly different cell numbers between contraceptives for most cell populations; DMPA-IM tended to increase, but NET-EN tended to decrease cell numbers. Excluding for non-study progestin use revealed significant increases in frequency and/or number of several FGT cell populations from baseline to 25 weeks, within the DMPA-IM arm. Both contraceptives exert minimal effects on systemic CD4+ cells but have differential effects in the FGT. The changes in frequency and numbers of HIV-1 target cells investigated, particularly after exclusion for non-study progestin use, suggest that DMPA-IM use may increase HIV-1 acquisition in the FGT compared to NET-EN use.