Stable virulence levels in the HIV epidemic of Switzerland over two decades

Publication

Stable virulence levels in the HIV epidemic of Switzerland over two decades

Journal Paper/Review - Apr 4, 2006

Müller Viktor, Bonhoeffer Sebastian, Günthard Huldrych F, Vernazza Pietro, Bernasconi Enos, Telenti Amalio, Furrer Hansjakob, Klimkait Thomas, Perrin Luc, Ledergerber Bruno, Swiss HIV Cohort Study

Citation

Müller V, Bonhoeffer S, Günthard H, Vernazza P, Bernasconi E, Telenti A, Furrer H, Klimkait T, Perrin L, Ledergerber B, Swiss HIV Cohort Study. Stable virulence levels in the HIV epidemic of Switzerland over two decades. AIDS (London, England) 2006; 20:889-94.

Type

Journal Paper/Review (English)

Journal

AIDS (London, England) 2006; 20

Publication Date

Apr 4, 2006

Issn Print

0269-9370

Pages

889-94

Brief description/objective

OBJECTIVE: To determine whether the virulence of HIV-1 has been changing since its introduction into Switzerland. DESIGN: A prospective cohort study of HIV-1 infected individuals with well-characterized pre-therapy disease history. METHODS: To minimize the effect of recently imported viruses and ethnicity-associated host factors, the analysis was restricted to the white, north-west-European majority population of the cohort. Virulence was characterized by the decline slope of the CD4 cell count (n = 817 patients), the decline slope of the CD4:CD8 ratio (n = 815 patients) and the viral setpoint (n = 549 patients) in untreated patients with sufficient data points. Linear regression models were used to detect correlations between the date of diagnosis (ranging between 1984 and 2003) and the virulence markers, controlling for gender, exposure category, age and CD4 cell count at entry. RESULTS: We found no correlation between any of the virulence markers and the date of diagnosis. Inspection of short-term trends confirmed that virulence has fluctuated around a stable level over time. CONCLUSIONS: The lack of long-term time trends in the virulence markers indicates that HIV-1 is not evolving towards increasing or decreasing virulence at a perceptible rate. Both highly virulent and attenuated strains have apparently been unable to spread at the population level. This result suggests that either the evolution of virulence may be slow or inhibited due to evolutionary constraints, or HIV-1 may have already evolved to optimal virulence in the human host.