Abstract
HIV drug resistance has been described in all antiretroviral drug classes and threatens the long-term success of HIV treatment. Here, we describe the first reported case of acquired resistance to the integrase strand transfer inhibitors in South Africa. This case illustrates the dilemma of treatment in the context of inadequate adherence and poor psychosocial support and highlights the potential risk of transmission of multidrug-resistant virus. Keywords: HIV drug resistance; third line
Highlights
The development of drug resistance is one of the biggest concerns in the long-term management of HIV-infected patients
The patient tested HIV-positive in 2006 at the age of 8 years. Her exposure to perinatal antiretroviral treatment (ART) is unknown. She started her first ART regimen consisting of stavudine, lamivudine and efavirenz in the private sector in 2006 after completing a course of treatment for pulmonary tuberculosis
In 2007, she was transferred to the state sector. She was changed to the standard second-line regimen in use at the time – zidovudine (AZT), didanosine and ritonavir-boosted lopinavir – because of virological treatment failure in October 2008. But her viral load became detectable again in September 2009 and she was referred to an academic ART clinic in March 2010 because of virological failure
Summary
The development of drug resistance is one of the biggest concerns in the long-term management of HIV-infected patients. In 2007, she was transferred to the state sector She was changed to the standard second-line regimen in use at the time – zidovudine (AZT), didanosine and ritonavir-boosted lopinavir – because of virological treatment failure in October 2008. She initially responded well, but her viral load became detectable again in September 2009 and she was referred to an academic ART clinic in March 2010 because of virological failure. She reported poor adherence with her ART treatment because it was unpalatable She had three genotypic drug resistance tests (DRTs) over the 2 years and the mutations evolved from low-level resistance to ritonavir-boosted lopinavir to extensive three-class resistance during this time (Table 1). A tropism assay predicted that CCR5-antagonists are likely to be effective
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