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Table 1 Baseline demographic and clinical characteristics by arm

From: Outcomes of switching from protease inhibitor-based antiretroviral therapy to bictegravir/emtricitabine/tenofovir alafenamide (B/F/TAF) in virologically suppressed adults with nucleos(t)ide analogue resistance– a phase IV randomised, open-label study (PIBIK study)

 

Immediate switch arm

N = 33

Delayed switch arm

N = 39

Age, mean years (SD)

53 (8)

56 (7)

Self-reported male sex, n (%)

29 (88.0)

35 (90.0)

White race, n (%)

23 (69.7)

30 (76.9)

CD4 T count, median cells/mm3 (IQR)a

560 (457–800)a

632 (453–854)

ART duration, median years (IQR)

30; 17.1 (8.7–21.3)b

39; 17.6 (10.9–23.8)

bPI at randomisation, n (%)

Darunavir

28 (84.8)

30 (76.9)

 

Atazanavir

5 (15.2)

9 (23.1)

NRTI backbone, n (%)

TDF-based

17 (51.5)

20 (51.3)

 

TAF-based

6 (18.2)

7 (17.9)

 

Non TDF/TAF-based

4 (12.1)

8 (20.5)

 

3TC or FTC

22 (66.7)

31 (79.5)

On lipid lowering drugs, n (%)

11 (33.3)

14 (35.9)

NRTI RAMs in historical genotypec, n (%)

   M184V/I alone

12 (36.4)

9 (23.1)

   1 TAM

6 (18.2)

10 (25.6)

   1 TAM + M184V/I

4 (12.1)

7 (18.0)

   2 TAMs

1 (3.0)

3 (7.7)

   2 TAMs + M184V/I

2 (6.1)

5 (12.8)

   1 NAM + M184V/I

3 (9.1)

2 (5.1)

   1 TAM + M184V/I + 1 NAM

1 (3.0)

2 (5.1)

   2 TAMs + M184V/I + 1 NAM

3 (9.1)

1 (2.6)

   1 TAM + 1 NAM

1 (3.0)

0 (0.0)

NRTI RAMs in baseline genotyped

   Any

13 (39.4)

20 (51.3)

   None

19 (57.6)

16 (41.0)

   Not available

1 (3.0)

3 (7.7)

  1. an= 32; bn= 30; cCumulative of all available historical plasma genotypes. dTested retrospectively using HIV-1 DNA from peripheral blood mononuclear cells collected at study entry. ART = Antiretroviral therapy; PI/b = Boosted protease inhibitor; NRTI = Nucleos(t)ide reverse transcriptase inhibitor; TDF = Tenofovir disoproxil fumarate; TAF = Tenofovir alafenamide; 3TC = Lamivudine; FTC = Emtricitabine; RAMs = Resistance-associated mutations; TAMs = Thymidine analogue mutations; NAM = NRTI RAM other than M184V/I or TAMs