• long-acting progestogens
• intrauterine devices
• human immunodeficiency virus

We thank Quispe Calla and colleagues for their insightful comments1 on our article.2 We agree that basic science evidence showing that various progestogens increase HIV susceptibility is compelling. We also agree that randomised clinical trials (RCTs) are informative regarding the relative risks of HIV between contraceptive alternatives, but not the absolute risks compared with no contraception. However, it is likely that all non-barrier contraceptives increase absolute HIV risk because women wishing to avoid pregnancy are more likely to engage in unprotected sexual intercourse when the fear of pregnancy is reduced. Therefore, for women who desire contraception, it is the relative risk between the available options that is important. As Calla and colleagues point out, the relative effect of other non-barrier contraceptives including levonorgestrel-releasing intrauterine systems on susceptibility to HIV is unexplored.

The reason that clinical trials are needed to complement the basic science data is that human HIV risk is a composite of biological, physiological and behavioural effects. While the data presented by Calla and colleagues1 suggest that progestogen contraception increases biological risk, we have previously suggested that physiological and behavioural effects may reduce risk.3 4 These include reduced risk of viral exposure during menstruation (unpublished data from our study showed that 75% of women experienced amenorrhoea with injectable progestogens) and reduced unprotected sexual exposure due to reduced libido.5 6 Therefore we maintain that relative net biological, physiological and behavioural effects between contraceptive alternatives can only be determined by RCTs.