Many events determine the severity, duration, and predisposition to recurrent herpes simplex virus (HSV) disease. Unlike human T-cell lines derived from tumours or those transformed by human T-lymphotropic virus 1, herpesvirus saimiri-immortalized T-cells (HVS T-cells) retain many functions of primary activated T-lymphocytes. MD immunity, either natural or vaccinal, is directed against both the viral and the tumor-specific antigens and is mediated by the cellular immune mechanisms. Most of the 74 predicted protein sequences are conserved; only eleven are less than 98% conserved. During the active stage of the disease, herpes virus replication within cells causes development of tissue lesions in the affected area. Many strains of the herpes virus produce external blisters and sores on the skin and these are highly contagious and can be transmittable between species. Some species of herpes virus can be transmitted between humans and animals but transmission from animals to humans is rare.
Rabbits can acquire a handful of different herpes viruses, but for pet rabbits, the most common infections are caused by Herpes simplex virus 1 (HSV-1), Herpes cuniculi (LHV-4), Herpes cuniculi (LHV-2) and Herpes sylvilagus (LHV-1/LHV-3). These results suggest that the activation of CD4+ T lymphocytes with mitogens such as PHA or IL-2 and the expression of some cellular gene or the HTLV-I gene might be essential for efficient propagation of HHV-6B. However, group Ia MAbs blocked HveC but not HveA binding, and conversely, group VII MAbs blocked HveA but not HveC binding. Signs of this condition can include watery eyes, squinting, conjunctivitis, ulceration of the cornea and blindness. It is a condition that can come and go as the virus re-emerges after periods of dormancy. Exposure of the HSV-1 strain to pet rabbits has also rarely resulted in brain lesions.