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Session 60 Poster Presentations
Primary HIV/SIV Infection
Session Day and Time: Tuesday 1:30 - 3:30 pm
Room: Hall A


502
Antiretroviral Resistance Among Patients with Primary HIV Infection in the Southeastern U.S.-Impact on Treatment Outcome
C. Hicks*1, J. Eron2, J. Lennox3, C. Pilcher2, S. Fiscus2, A. Weintrob1, J. Giner1, P. Menezes2, E. Patrick3, T. Alcorn4
1Duke Univ Med Ctr, Durham, NC; 2Univ of North Carolina, Chapel Hill; 3Emory Univ, Atlanta, GA; and 4LabCorp, Inc, Research Triangle Park, NC

Background: The frequency of transmission of antiretroviral resistance in primary HIV infection (PHI) patients (pts) varies among different geographic regions. The clinical significance of such resistance is also incompletely defined. We assessed baseline (BL) genotypic and phenotypic resistance and its consequences in a PHI cohort diagnosed and treated in the Southeastern U.S. (North Carolina and Georgia).

Methods: Thirty-one (31) pts with PHI (27 males, 4 females) diagnosed in the Southeastern U.S. during 1998–2002 underwent genotypic (n = 31) (TruGene or VircoGEN) and phenotypic (n = 27) (Antivirogram) resistance testing at time of diagnosis. Thirty (30) pts were treated with d4T + ddI + nevirapine (NVP) ± hydroxyurea (HU) prior to availability of resistance test results. Resistance was defined by the Stanford database website (genotype) or by the following—fold change in susceptibility as recommended by Virco (phenotype): ddI 3.5, d4T 3.0, ZDV 4.5, 3TC 3.5, ddC 3.0, ABC 3.0; NVP 8.0, EFV 6.0, DLV 10.0; RTV 3.5, IDV 3.0, NFV 4.0, SAQ 2.5, APV 2.5, LPV 2.5.

Results: Median time from PHI symptom onset to resistance testing was 26 days [range 8–169 days]; geometric mean HIV RNA at time of testing was 5.54 log10 [range 3.65–7.13 log10]. All cases were sexually acquired. Resistance was present as follows:

Drug Class

Genotypic Resistance

Phenotypic Resistance

NRTI

2/31 (6.5%)

2/27 (7.4%)

NNRTI

1/31 (3.2%)

3/27 (11.1%)

PI

0/31 (0%)

2/27 (7.4%)

 

Only 1 pt had > 10-fold reduced susceptibility to any drug (16.7-fold to DLV) and only 1 pt had both genotypic and phenotypic resistance. A total of 6 pts had BL genotypic and/or phenotypic resistance to ≥1 drug in the initial treatment regimen. Five (5) of 6 were successfully treated and reached VL < 50 c/mL before wk 16 of treatment. One (1) patient with phenotypic resistance to ddI + d4T (BL: ddI = 4.5-fold, d4T = 4.2-fold) but not NVP (BL: NVP = 3.1-fold) achieved > 3 log10 reduction in VL, but had persistently detectable RNA < 1000 c/mL from wk 12 on. Repeat testing at wk 24 revealed loss of the initial NRTI resistance but presence of significant new genotypic and phenotypic NNRTI resistance (genotype 101E, 190A; phenotype NVP > 108.6-fold).

Conclusions: These data suggest that transmitted resistance among pts with PHI in the Southeastern U.S. is relatively infrequent and imperfectly predicts treatment response.