| Herpes simian B Virus | |
|---|---|
| Virus classification | |
| Group: | Group I (dsDNA) |
| Family: | Herpesviridae |
| Subfamily: | Alphaherpesvirinae |
| Genus: | Simplexvirus |
Herpes simian B virus (Macacine herpesvirus 1 (formerly Cercopithecine herpesvirus 1, CHV-1 [1]) , Herpesvirus simiae, B virus) is the endemic simplexvirus of macaque monkeys. B virus is an alphaherpesvirus, which consists of a subset of herpes viruses that travel within hosts using the peripheral nerves. As such, this neurotropic virus is not found in the blood.
In the natural host, the virus exhibits pathogenesis similar to that of herpes simplex virus (HSV) in humans. Conversely, when humans are zoonotically infected with B virus, patients can present with severe central nervous system disease, resulting in permanent neurological dysfunction or death. Severity of the disease increases for untreated patients, with a mortality rate of approximately 80%. Early diagnosis and subsequent treatment are the linchpins of surviving the infection.
Linked with more than two dozen deaths since its discovery, B virus is the only identified nonhuman primate herpesvirus that displays severe pathogenicity in humans. The last identified case of human B virus infection occurred in 2008, with the last known fatality occurring when a worker at the Yerkes National Primate Research Center was infected in 1997 after an eye splash occurred. Proper personal protective equipment is essential when working with macaques, especially those who have tested positive for the virus. Bites, scratches and exposures to mucous membranes, including the eye, must be cleaned immediately. Samples from both the macaque and human should be sent for B virus diagnostic testing as recommended by the B Virus Working Group here: BVIRUS.pdf
As of 2002, there were 26 documented cases of human B virus infection, 16 of which led to death. At least 20 of the patients developed some degree of encephalitis.[2][3]
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Herpes B virus was first identified in 1932 following the death of Dr. William Brebner, a young physician who was bitten by a monkey while researching the virus that causes poliomyelitis. Soon after, Brebner developed localized erythema, followed by lymphangitis, lymphadenitis and, ultimately, transverse myelitis. Neurologic tissues obtained during Dr. Brebner’s autopsy revealed the presence of an ultrafilterable agent that appeared similar to HSV.[4] This isolate was originally termed “W virus.”
Within a year of Brebner’s death, Dr. Albert Sabin identified an unfilterable agent from the same tissue,[5] which he later named B virus. Sabin further described the lethality of B virus by showing that infectivity was independent of the route of inoculation.[5] Additionally, it was observed that B virus induced immunologic responses similar to HSV-1,[6] as well as shared similarities to HVP-2 and Langur herpesvirus, two other nonhuman primate alphaherpesviruses.[6][7][8][9][10][11]
By 1959, B virus was identified as the causative agent in 17 human cases, 12 of which resulted in death.[12][13][14] Approximately 50 cases had been identified by 2002, although only 26 were well documented. The latest identified case of B virus occurred in 2008, per the National B Virus Resource Center in Atlanta, GA.
The B virus genome was fully sequenced in 2003 from an isolate found in a rhesus macaque.[15] Like all herpesviruses, the B virus genome contains double-stranded DNA and is approximately 157 kbp in length. Two unique regions (UL and US) are flanked by a pair of inverted repeats, two of which are found at the termini, with the other two internally located. This arrangement, which is identical in nature to HSV, results in four sequence-oriented isomers. Cytosine and guanine nucleotides represent 75% of the sequence.
Sequence analyses suggest that B virus and HSV types 1 and 2 most likely diverged from a common ancestor during the evolution of these pathogens. Each gene-encoded glycoprotein, including gB, gC, gD, gE and gG, has approximately 50% homology with HSV, with a slightly higher predilection towards HSV-2 over HSV-1.[15] Additionally, glycoprotein sequences have demonstrated that all cysteine residues are conserved, as are most glycosylation sites.
Acyclovir has prevented progression of the disease in some patients and may be life saving. Prompt treatment is essential to prevent permanent neurological impairment.[16]
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