evidence: The team’s analyses of the data indicated that individuals with the VB variant had a viral load of between 3.5 times and 5.5 times higher than individuals with a non-VB variant. "When replicating the BEEHIVE test with the ATHENA data, we again observed a large rise in viral load in individuals with this viral variant …" In addition, the rate of CD4 cell decline, which represents a hallmark of immune system damage by HIV, occurred twice as fast in individuals with the VB variant, placing them at risk of developing AIDS much more rapidly. Individuals with the VB variant also showed an increased risk of transmitting the virus to others. [...] The VB variant is characterized by many mutations spread throughout the genome, meaning that a single genetic cause cannot be identified at this stage. By analysing the patterns of genetic variation among the samples, the researchers estimate that the VB variant first arose during the late 1980s and 1990s in the Netherlands. "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." It spread more quickly than other HIV variants during the 2000s, but its spread has been declining since around 2010.