Herpes B Follow-up
- Author: Sowmya Nanjappa, MD; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD more...
Developing herpes B virus–free colonies
The endeavor to develop virus-free colonies has found some success, especially in the United States, where the National Center for Research Resources took a leading role in the 1990s by promoting experimental strategies in husbandry and management.
Achieving completely herpes B virus–free colonies has proven difficult because some macaques may show no antibodies but may retain latent herpes B virus particles. Furthermore, the B virus may become reactivated and shed without any visible symptoms.
Because of the relative ease of monkey-to-monkey transmission, even a single animal infected with herpes B virus may compromise the virus-free status of an entire facility.
Current research focuses on the development of techniques (eg, PCR) to reduce false-negative results and the implementation of regular screening protocols that quickly identify infected monkeys.
Accepting moderate to high infection rates in macaques but minimizing human exposure to herpes B virus
Minimizing social, nutritional, pharmacological, and psychological stress (especially overcrowding and shipping) can reduce viral shedding by monkeys. Promoting good veterinary care and immunocompetence also can reduce shedding.
Eliminating transmission pathways can prevent human exposure. Some means of prevention include the use of protective suits, gloves, eye shields, and similar devices. Given the difficulties and costs of achieving herpes B virus–free colonies, these methods may remain the reality at most facilities, at least for the near future.
Nonmacaque species are highly susceptible to herpes B virus infection. The risk of infection in these animals can be easily minimized by housing macaques in separate nonadjacent cages. A failure to follow this precaution has sometimes led to cross-species infection and fatalities.
Immunoprevention has been attempted in animal studies using several different vaccines. Most recently, a recombinant vaccinia virus that expresses herpes B glycoprotein D appears promising in preventing infection and/or latency.
Aseptic meningitis results in a moderate lymphocyte pleocytosis and erythrocytes, moderately elevated cerebrospinal fluid (CSF) protein level, and normal CSF glucose. In humans, herpes B virus can be grown from CSF, skin lesions, and urine.
Nonfatal cases of human herpes B virus infection may result in complete recovery, but residua are common and include the following:
Extremity paresis or plegia
Because of prolonged or long-term use of antiviral therapy in surviving patients, the frequency of asymptomatic or symptomatic reactivation and/or viral shedding occur is unclear.
Historically, human herpes B virus infection carries a case-fatality rate of approximately 70%, a rate similar to that of untreated HSV encephalitis.
As with HSV encephalitis, many survivors of herpes B virus infection have substantial residua.
Reported cases seem to have a lower case-fatality rate, possibly because of earlier diagnosis, earlier treatment, and/or better supportive care.
Until a vaccination is available or certified, herpes B virus–free colonies are the rule; educating primate workers on the avoidance of high-risk exposures is mandatory.
All workers should be aware of prevention and treatment protocols.
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