Analyses of retrospective data in the TAHOD suggest that the overall response to HAART in Asian populations is similar to that seen in Western countries.

In predominantly lipoatrophic patients, switching from HIV protease inhibitor therapy lead to improved lipids and less intra-abdominal fat, but also to less peripheral fat, and had minimal effect on insulin resistance. Virological control in these heavily pretreated patients was unaffected, despite frequent switch drug cessations.

NRTIs and, specifically tenofovir at therapeutic concentrations, inhibit telomerase activity leading to accelerated shortening of TL in activated PBMCs. The relationship between NRTI, reduced telomerase activity, and accelerated aging requires further investigation in HIV-infected individuals on cART.

PLA did not increase FSTV, although tissue thickness in injection planes increased modestly, an improvement observed by patients. PLA was safe and well tolerated. Facial lipoatrophy severity and some quality-of-life domains improved.

Background Random effects models were used to explore how the shape of CD4 cell count responses after commencing combination antiretroviral therapy (cART) develop over time, and in particular the role of baseline and follow-up covariates. Methods Patients in APHOD who first commenced cART after January 1, 1997, and who had a baseline CD4 cell count and viral load measure and at least one follow-up measure between 6 and 24 months, were included. CD4 cell counts were determined at every 6-month period following the commencement of cART for up to 6 years. Results 1638 patients fulfilled the inclusion criteria with a median follow up time of 58 months. Lower post-cART mean CD4 cell counts were found to be associated with increasing age (p<0.001), pre-cART hepatitis C co-infection (p=0.038), prior AIDS (p=0.019), baseline viral load ≤ 100,000 copies/ml (p<0.001), and the Asia-Pacific region compared with Australia (p=0.005). A highly significant 3-way interaction between the effects of time, baseline CD4 cell count and post-cART viral burden (p<0.0001) was demonstrated. Higher long-term mean CD4 cell counts were associated with lower baseline CD4 cell count and consistently undetectable viral loads. Among patients with consistently detectable viral load CD4 cell counts appeared to converge for all baseline CD4 levels. Conclusion Our analyses suggest that the long-term shape of post-cART CD4 cell count changes depends only on a 3-way interaction between baseline CD4 cell count, viral load response and time.