HHV-6B causes 97 – 100% of primary HHV-6 infections in the USA and Japan and is responsible for a 97% of reactivation in transplant patients. HHV-6B primary infections can cause febrile seizures, and a large NIH funded study found HHV-6B to be responsible for over a third of status epilepticus cases in infants (Epstein 2011). Recently several studies have tied HHV-6B to a subset of patients with mesial temporal lobe epilepsy.
HHV-6A has been found more frequently in patients with neuroinflammatory diseases such as multiple sclerosis (MS) and rhomboencephalitis (Alvarez Lafuente 2006, Crawford 2007). It has also been suggested as co-factor in the progression of HIV to AIDS (Lusso 2007). HHV-6A is acquired later in life, usually without clinical symptoms, except in Africa where HHV-6A is more prevalent than HHV-6B in children (Kasolo 2009). HHV-6B antibodies are presumed to offer partial protection against HHV-6A and vice versa.
It is only possible to differentiate HHV-6A from HHV-6B using a PCR DNA test, and due to the extremely low levels of latent virus in the blood, typing is difficult except when the virus is actively replicating during an acute illness.
To make matters more complicated, the percentage of HHV-6A and HHV-6B DNA can vary dramatically depending on whether serum, saliva or the white blood cells are used in the testing procedure. HHV-6B is more likely to be found in the white blood cells and in the saliva, while HHV-6A is more likely to be found in the spinal fluid or serum (Nitsche 2001). HHV-6A can’t be found in the saliva (Aberle 1996).