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.

Patients with African origins, advanced HIV infection, or a strong response to cART are at greater risk of unmasking TB-IRIS.

We conducted a descriptive study in 9 cases of acute hepatitis A diagnosed in patients with human immunodeficiency virus (HIV). Despite the small number of cases studied, the results indicate that moderate HIV infection does not impair the natural history of acute hepatitis A.

The key determinant of antibody response was the HIV replication status at immunization. No association was found between antibody response and CD4 T-cell count.