Herpes B virus
المؤلف:
Stefan Riedel, Jeffery A. Hobden, Steve Miller, Stephen A. Morse, Timothy A. Mietzner, Barbara Detrick, Thomas G. Mitchell, Judy A. Sakanari, Peter Hotez, Rojelio Mejia
المصدر:
Jawetz, Melnick, & Adelberg’s Medical Microbiology
الجزء والصفحة:
28e , p494-495
2025-11-26
110
Herpes B virus of Old World monkeys is highly pathogenic for humans. Transmissibility of virus to humans is limited, but infections that do occur are associated with a high mortality rate (∼60%). Herpes B virus disease of humans is an acute ascending myelitis and encephalomyelitis.
Properties of the Virus
Herpes B virus is a typical herpesvirus that is indigenous in macaques, Old World monkeys in Asia. Herpes B virus is enzootic in rhesus, cynomolgus, and other macaque monkeys (genus Macaca). It is designated Macacine herpesvirus or herpesvirus simiae, replacing the older name of Cercopithecine herpesvirus 1. Its genome organization is similar to that of HSV, with many genes arranged colinearly. Its genome is 75% G + C, the highest among herpesviruses. As with all herpesviruses, herpes B virus establishes latent infections in infected hosts. The virus grows well in cultures of monkey kidney, rabbit kidney, and human cells with a short growth cycle. Cytopathic effects are similar to those of HSV.
Pathogenesis and Pathology
Herpes B virus infections seldom cause disease in rhesus monkeys. Vesicular lesions of the oropharynx may occur and resemble those induced in humans by HSV. Genital lesions also occur. Many rhesus monkeys carry latent herpes B virus infections that may be reactivated by conditions of stress.
The virus is transmissible to other monkeys, rabbits, guinea pigs, rats, and mice. Rabbits routinely develop fatal infections after herpes B virus inoculation.
Herpes B virus infections in humans usually result from a monkey bite, although infection by the respiratory route or ocular splash exposure is possible. The striking feature of herpes B virus infections in humans is the very strong propensity to cause neurologic disease. Many survivors are left with neurologic impairment.
Epidemiology and Clinical Findings
Herpes B virus is transmitted by direct contact with virus or virus-containing material. Transmission occurs among Macaca monkeys, between monkeys and humans, and rarely from human to human. Virus may be present in saliva, conjunctival and vesicular fluids, genital areas, and feces of monkeys. Respiratory transmission can occur. Other sources of infection include direct contact with animal cages and with infected monkey cell cultures.
Infection in the natural host is rarely associated with obvious disease. Infections with herpes B virus are very common in colonies of rhesus monkeys. Seroprevalence in adult animals is 70% or higher. Because latent infections may be reactivated, seropositive animals are reservoirs for transmission of herpes B virus infections. The frequency of excretion of herpes B virus by monkeys is probably no more than 3%.
Animal workers and persons handling macaque monkeys, including medical researchers, veterinarians, pet owners, and zoo workers, are at risk of acquiring B virus infection. Individuals having intimate contact with animal workers exposed to the monkeys are also at some risk.
Treatment and Control
There is no specific treatment after the clinical disease is manifest. However, treatment with acyclovir is recommended immediately after exposure. Testing of exposed individuals and monkey tissues by PCR and serology is available through the National B virus Resource Center. γ-Globulin has not proved to be effective treatment for human B virus infections. No vaccine is available.
The risk of B virus infections can be reduced by proper procedures in the laboratory and in the handling and management of macaque monkeys. This risk makes macaques unsuitable as pets.
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