It was proposed that microbial translocation affects HIV disease progression in part by LPS activation of monocytes, leading to increased production of soluble CD14 (sCD14)[6, 7]. Cassol et al [1] found a significant positive correlation between LPS and sCD14 levels in patients with AIDS who did not have opportunistic infections, but they found a negative correlation between LPS and sCD14 levels in individuals with an opportunistic infection, even though the levels of sCD14 were similar between the 2 groups. It was speculated by the investigators that ‘‘[t] his observation suggests that, in untreated patients, the increase in sCD14 was driven predominantly by microbial translocation’’[1]. However, a recent study by Rempel et al [13] demonstrated that monocytes from HIV-1-infected individuals with high viral loads are not activated by LPS. Moreover, in our longitudinal study we found no association between disease progression rates and sCD14 levels [3]. This suggests that the increased levels of sCD14 seen in late-stage HIV disease are not directly caused by microbial translocation.

The cross-sectional data from Africa [1, 2, 8], as well as North America and Europe [5–7], demonstrate that there is most likely an association between low levels of microbial translocation and advanced HIV disease, and this has led to the inference that ‘‘microbial translocation contributes to immune activation and disease progression during chronic HIV-1 infection’’[1]. However,