Simian B virus is the most potentially dangerous zoonotic virus carried by non-human primates, which can cause severe infectious diseases shared by humans and monkeys. Simian B virus is also known as simian herpesvirus type 1. It belongs to the Herpesviridae family, the Alphaherpesvirus subfamily, and is a member of the genus Herpes Simplex Virus along with human herpes simplex virus type 1 and human herpes simplex virus type 2.
When simian B virus infects its natural host, rhesus monkeys, it is benign and does not cause obvious clinical symptoms. Its clinical manifestations are similar to HSV-1 infection in humans. Its characteristic symptoms are the appearance of small herpes on the back of the tongue, the lips at the junction of the oral mucosa and the skin, and other parts of the oral cavity, followed by the rupture of the herpes, the formation of ulcers, fibrinous exudation on the surface, and the formation of crusts, usually within 7 to 14 days. Self-healing without scarring. B virus can be latent in the ganglia and tissues and organs near the upper respiratory tract or urogenital organs for a long time, and is intermittently excreted through saliva, urine and genital secretions. The mechanism is similar to that of HSV. The initial viral replication occurs at the site of mucosal infection, which is then taken up by sensory and motor nerve endings, transported to sensory neurons through axons, and latent in sensory ganglia. During the incubation period, the virus no longer replicates. . B virus can be activated from a latent state, propagated through neuronal axons to mucosal epithelial cells for re-replication, recurrent infection can lead to intermittent release of virus, social stress, transport, immunosuppression, or a new rearing environment can increase viral reactivation and possibility of release. Only one case of human-to-human transmission of B virus is reported, mainly through mating, bites or scratches, and poisonous saliva. The typical clinical course of B virus infection in humans occurs 1 to 3 days after exposure, with cold-like symptoms, blisters on the exposed site, and symptoms of fever, muscle pain, fatigue, and headache. Other symptoms include lymphangitis. , nausea, vomiting, and abdominal pain. As the virus spreads, symptoms of infection in the central or peripheral nervous system also develop, including ataxia, hyperthermia, paralysis, and agitation. Untreated infections have a mortality rate of up to 80%, and survivors also experience neurological sequelae and further neurological deterioration.
Monkey B virus and HSV are two homologous viruses. Humans and rhesus monkeys originated from a common ancestor of apes. With the process of biological evolution, the two viruses co-evolved with their respective hosts. Humans and rhesus monkeys are in different ecological niches, and there is a natural environmental barrier between them. Under the action of some natural and human factors, it may cause the intersection of ecological niches and lead to the risk of monkey B virus exposure. The simian B virus can cause human infection only by crossing the environmental barrier, and the clinical symptoms and outcome after infection depend on the virulence of the virus and the interaction between the host and the virus.