First‐line antiretroviral treatment outcome in a patient presenting an HIV‐1/2 multiclass drug resistant infection

Abstract

Background

With the expansion of HIV‐2 epidemic beyond African countries, co‐infection with HIV‐1 becomes a global challenge. We have recently identified an HIV‐1/2 dual infection with both viruses bearing multiclass drug resistance in an untreated patient [1]. We now present the patient's combined antiretroviral treatment (cART) outcome after 6 months follow‐up.

Patient and Methods

Clinical samples were obtained upon informed consent from a 23‐year‐old man living in Guinea‐Bissau until March 2011 when he moved to Switzerland. As previously reported [1], HIV‐1/2 co‐infection was confirmed by HIV‐1 PCR (21.000 copies/ml) and total HIV‐1/2 viremia (4.351 nU/ml) by product‐enhanced reverse transcriptase (PERT) assay. The patient denied previous HIV testing or exposure to antiretroviral drugs. Dual infection consisted of HIV‐1 CRF02_AG bearing resistance mutations M184V/V90I and HIV‐2 clade A, harboring K65R/D67N mutations as amplified from proviral‐DNA. Baseline CD4 + T‐cell count was 408 cell/mm³. We initiated cART in accordance to drug resistance mutations (see below). Treatment compliance was assessed with an electronic pillbox device and drug‐plasma concentrations. Clinical and laboratory follow up were done at weeks 2, 4, 9, 12 and 24.

Results

cART was initiated with tenofovir/emtricitabine (TDF/FTC), boosted‐darunavir (DRV/r) and raltegravir(RAL). Treatment compliance was fluctuant during the first 3 months after which it remained stable with an average monthly intake of 92%. Antiretroviral drug‐plasma concentrations were traced at percentile 25th. HIV‐1 viremia became undetectable at week 12. Additionally, HIV‐2 viremia was retrospectively assessed by real‐time RT‐PCR at two independent laboratories showing undetectable values across the study period including baseline. Thus, baseline viremia, as assessed by the PERT test for particle‐associated reverse transcriptase activity was due to HIV‐1 alone. CD4 + T‐cell count was 559 cell/mm³ at week 24. Laboratory assessments showed a neutrophile drop to 0.96 at week 4, fully restored at week 9.

Conclusion

This case of HIV‐1/2 dual infection underscores the importance of assessing genotypic analysis of both viruses ahead to treatment choice. It also highlights viral load platforms constraints when it comes to clinical monitoring of HIV‐1/2 co‐infection in western settings. Overall, first‐line salvage treatment was well tolerated and suppressed HIV‐1 resistant clade allowing recovery of CD4+ T‐cell count.