Improved virological outcome in White patients infected with HIV-1 non-B subtypes compared to subtype B

Publication

Improved virological outcome in White patients infected with HIV-1 non-B subtypes compared to subtype B

Journal Paper/Review - Oct 13, 2011

Scherrer Alexandra U, Günthard Huldrych F, Held Leonhard, Bernasconi Enos, Vernazza Pietro, Elzi Luigia, Cavassini Matthias, Hirschel Bernard, Rauch Andri, Bürgisser Philippe, Klimkait Thomas, Yerly Sabine, Böni Jürg, von Wyl Viktor, Ledergerber Bruno, Swiss HIV Cohort Study

Citation

Scherrer A, Günthard H, Held L, Bernasconi E, Vernazza P, Elzi L, Cavassini M, Hirschel B, Rauch A, Bürgisser P, Klimkait T, Yerly S, Böni J, von Wyl V, Ledergerber B, Swiss HIV Cohort Study. Improved virological outcome in White patients infected with HIV-1 non-B subtypes compared to subtype B. Clin Infect Dis 2011; 53:1143-52.

Type

Journal Paper/Review (English)

Journal

Clin Infect Dis 2011; 53

Publication Date

Oct 13, 2011

Issn Electronic

1537-6591

Pages

1143-52

Brief description/objective

BACKGROUND
Antiretroviral compounds have been predominantly studied in human immunodeficiency virus type 1 (HIV-1) subtype B, but only ~10% of infections worldwide are caused by this subtype. The analysis of the impact of different HIV subtypes on treatment outcome is important.

METHODS
The effect of HIV-1 subtype B and non-B on the time to virological failure while taking combination antiretroviral therapy (cART) was analyzed. Other studies that have addressed this question were limited by the strong correlation between subtype and ethnicity. Our analysis was restricted to white patients from the Swiss HIV Cohort Study who started cART between 1996 and 2009. Cox regression models were performed; adjusted for age, sex, transmission category, first cART, baseline CD4 cell counts, and HIV RNA levels; and stratified for previous mono/dual nucleoside reverse-transcriptase inhibitor treatment.

RESULTS
Included in our study were 4729 patients infected with subtype B and 539 with non-B subtypes. The most prevalent non-B subtypes were CRF02_AG (23.8%), A (23.4%), C (12.8%), and CRF01_AE (12.6%). The incidence of virological failure was higher in patients with subtype B (4.3 failures/100 person-years; 95% confidence interval [CI], 4.0-4.5]) compared with non-B (1.8 failures/100 person-years; 95% CI, 1.4-2.4). Cox regression models confirmed that patients infected with non-B subtypes had a lower risk of virological failure than those infected with subtype B (univariable hazard ratio [HR], 0.39 [95% CI, .30-.52; P < .001]; multivariable HR, 0.68 [95% CI, .51-.91; P = .009]). In particular, subtypes A and CRF02_AG revealed improved outcomes (multivariable HR, 0.54 [95% CI, .29-.98] and 0.39 [95% CI, .19-.79], respectively).

CONCLUSIONS
Improved virological outcomes among patients infected with non-B subtypes invalidate concerns that these individuals are at a disadvantage because drugs have been designed primarily for subtype B infections.