Background:  Transmission of drug-resistant HIV-1 strains has been reported before. Because the presence of drug resistance at baseline might hamper not only the success of first-line therapy, but also of successive therapy lines, intensive research is performed to estimate the prevalence of HIV-1 drug resistance. Additionally, many studies have investigated the persistence of resistant HIV-1 strains in absence of therapy because long-term persistence could result in further transmission. Here, we report a consecutive transmission chain of resistant HIV-1 in 2 untreated individuals.

Methods:  A baseline resistance test is performed for all patients who are diagnosed with HIV-1 and who are attending our hospital. Plasma samples are extracted and genotyped with Viroseq v2.0. Subsequently, sequences are subtyped with the Rega HIV-1 subtyping tool (v1.0) and are interpreted according to the drug resistance interpretation algorithm that is implemented at that time (currently Rega 6.4.0).

Results:  At the end of 2001, patient 1 was diagnosed with HIV-1 and the subtype B HIV-1 strain displayed RT mutations 210W and 215Y; and PR mutations 20R, 36I, 54V, 71V, 88D, and 90M. At the beginning of 2005, the partner of patient 1 was diagnosed with HIV-1 and this strain displayed RT mutations 210W and 215S; and PR mutations 10I, 20R, 36I, 54V, 71V, and 88D. Retrospectively, the HIV-1 sequences from patient 1 at the estimated time point of the transmission event (mid 2004) and at the beginning of 2005 were determined. In mid-2004, the strain displayed RT mutations 210W and 215S; and PR mutations 10IL, 20R, 36I, 54V, 71V, 88D, and 90M. Beginning of 2005, the strain displayed RT mutations 210W and 215S; and PR mutations 10IL, 20R, 36I, 54V, 71V, 88D, and 90ML.

Conclusions:  This is the first report on a consecutive transmission of dual-class resistant HIV-1 in untreated patients. It confirms the long-term persistence of transmitted dual-class resistant HIV-1 and the establishment of revertant mutations at RT position 215. Additionally, it shows that in absence of therapy a secondary PR mutation can further develop followed by loss of a major PR mutation.