The risk of MI was increased by cumulative exposure to all the studied PIs except saquinavir and particularly to amprenavir/fosamprenavir with or without ritonavir and lopinavir with ritonavir, whereas the association with abacavir cannot be considered causal.

The incidence of myocardial infarction (MI) is lower in France than in English-speaking and northern European countries. We estimated the incidence of MI in the HIV-infected population in France, on the basis of the data from the FHDH-ANRS CO4 cohort, by comparison with the general population. The sex- and age-standardized morbidity ratio was estimated as 1.5 [95% confidence interval (CI) 1.3-1.7] overall, 1.4 (95% CI 1.3-1.6) in men and 2.7 (95% CI 1.8-3.9) in women.

Our observations of discrepant immunological and virological responses to treatment raise the issue of the significance of persistent elevated levels of plasma HIV RNA and of the relevance of measurements of plasma viral load for assessing the efficacy of antiretroviral therapy in patients whose CD4 cell counts increase despite the absence of significant decrease in plasma HIV viral load.

Independently of cardiovascular risk factors and antiretroviral therapy, HIV replication, a low CD4 T-cell nadir and a high current CD8 T-cell count are associated with an increased risk of MI in HIV-infected individuals. This suggests new paths for interventions to diminish the risk of MI in HIV-infected patients.

We discovered a highly virulent variant of subtype-B HIV-1 in the Netherlands. One hundred nine individuals with this variant had a 0.54 to 0.74 log 10 increase (i.e., a ~3.5-fold to 5.5-fold increase) in viral load compared with, and exhibited CD4 cell decline twice as fast as, 6604 individuals with other subtype-B strains. Without treatment, advanced HIV—CD4 cell counts below 350 cells per cubic millimeter, with long-term clinical consequences—is expected to be reached, on average, 9 months after diagnosis for individuals in their thirties with this variant. Age, sex, suspected mode of transmission, and place of birth for the aforementioned 109 individuals were typical for HIV-positive people in the Netherlands, which suggests that the increased virulence is attributable to the viral strain. Genetic sequence analysis suggests that this variant arose in the 1990s from de novo mutation, not recombination, with increased transmissibility and an unfamiliar molecular mechanism of virulence.