Herpes B

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Herpes B

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Herpes B virus is an alpha herpesvirus that is particularly enzootic (endemic in animals) in the rhesus (Macaca mulatta) and cynomolgus (Macaca fascicularis) members of the macaque genus, Macaca (as seen in the image below). Among the nonhuman-primate herpesviruses, only herpes B virus is clearly able to cause disease in humans. The disease, usually a devastating infection of the central nervous system, occurs in humans and some primates that are not common hosts for this virus.

The pathogen is an enveloped herpesvirus, approximately 160-180 nm in size, that is quite similar to the human herpes simplex virus (HSV). Herpes B contains double-stranded linear DNA and has a molecular weight of approximately 110 megadaltons (approximately 162 kilobase pairs). Analysis of the envelope glycoproteins suggests cross-reactivity of glycoproteins B and D between herpes B and HSV types 1 and 2. Herpes B virus demonstrates a broad host range in tissue culture, producing a lytic infection in cells of humans, nonhuman primates, small mammals, and many birds. [1, 2]

In 1934, the term herpes B was derived from the initials of the first human case, which was described in detail by Sabin and Wright. The case was that of a 29-year-old laboratory worker (“W.B.”) who developed fatal meningoencephalitis and transverse myelitis following a bite on the hand from a seemingly healthy rhesus monkey.

Herpes B virus infects a broad range of mammalian and avian species, including New World monkeys, Old World monkeys, and humans. Most infected macaques are asymptomatic. When symptoms do occur, they are very similar to those caused by HSV. The most obvious manifestation of herpes B virus infection is fluid-filled vesicles on the back of the tongue, lips, and elsewhere in the mouth; occasionally, the vesicles appear on the skin. When the vesicles rupture, they often give rise to ulcers and fibronecrotic scabs, which may lead to secondary bacterial and fungal infections. Scabs typically heal within 7-14 days. Conjunctivitis of varying severity is another common symptom. In rare instances, systemic illness is associated with herpes B virus in macaques, including the occurrence of ulcerative lesions in the mouth, esophagus, and stomach and necrosis of the liver, spleen, and adrenal glands.

Members of the genus Macaca (>16 species) are natural hosts of herpes B virus, and almost all of these hosts naturally exist in Asia. Both wild and captive macaque populations generally exhibit high rates of herpes B virus infection, but most individuals exhibit few or no symptoms of infection. The strongest evidence for this pattern of high prevalence and mild infection comes from the rhesus, Japanese, and long-tailed (or cynomolgus) macaques, all of which are very closely related phylogenetically.

In captive populations of Japanese long-tailed and rhesus macaques, the prevalence of herpes B virus–induced antibodies is quite variable but may reach 100%. In wild and semi–free-ranging populations of long-tailed and rhesus macaques, seroprevalence rates (or prevalence of serum-detected herpes B virus–induced antibodies) typically exceed 70%.

Reports show that no herpes B virus exists in a population of long-tailed macaques introduced 400 years ago on the island of Mauritius. In all populations studied, the likelihood of infection increases dramatically with age. For example, in a study of semi–free-ranging macaques on the island of Cayo Santiago, Puerto Rico, 50% of 1-year-old macaques were infected, compared to 100% of adults. In a study of captive rhesus and Japanese macaques in Japan, the prevalence rates were 20% in 1-year-old monkeys and 60% in adults. Other macaque species readily acquire and transmit the virus, but whether these species serve as natural hosts is unclear.

Cercopithecine herpesvirus 1 (CHV-1), interestingly, is the formal name of the virus, which implies that all members of the primate family Cercopithecidae serve as natural hosts. Nevertheless, little evidence supports this theory for nonmacaque species of this taxon (eg, baboons, mangabeys, guenons, vervet monkeys); thus, CHV-1 may be a misnomer. Part of the difficulty in identifying taxonomic patterns is that many of the nonmacaque Cercopithecine species are natural carriers of closely related viruses (including the baboon herpesvirus SA8), which are serologically difficult to distinguish from herpes B.

After inoculation of herpes B virus in humans, dissemination to the central nervous system appears to occur neurally; however, herpes B virus can produce local infection in the skin at the inoculation site, with concomitant local and regional inflammatory changes. Indeed, lymph nodes draining the entry point can be histopathologically hemorrhagic and focally necrotic.

Introduction of the virus causes necrosis in the spinal cord with ascent to the brain. At least one case in which disease occurred years after exposure has been reported, suggesting that herpes B virus might be able to become latent in humans. Self-limited aseptic meningitis has been reported, but almost all cases produce substantial morbidity and mortality.

United States

No evidence shows that the prevalence of herpes B virus in macaques varies by country; however, the pattern of human infection is remarkable. Of the roughly 45 well-documented cases of herpes B virus infection in humans, two thirds occurred in the United States and the others were reported in Canada and Great Britain. Interestingly, most of the well-documented human cases of herpes B virus infection occurred in the 1950s and 1960s, when large numbers of rhesus macaques were used in the production and testing of poliomyelitis vaccines. In the late 1980s, several cases in Pensacola, Florida and Kalamazoo, Michigan, refocused attention on herpes B virus, and several other cases have since been documented. This increased frequency coincides with an increased use of macaques in retroviral research.

International

The absence of reports of human herpes B virus infection from countries where macaques are prevalent and commonly interact with humans (eg, Japan) is striking. Whether the absence of these reports is due to the limited availability of herpes B virus diagnostic facilities (ie, actual cases not identified) or if some other factors are responsible (eg, different animal-handling procedures) is unclear. Concern exists that pet macaques (in addition to laboratory macaques) can spread the herpes B virus. Children are 3 times more likely to be bitten than adults. Macaques in 7 nonoccupational exposure incidents were found to be seropositive for herpes B virus in two thirds of cases.

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.

The average age of persons who develop herpes B virus infection reflects the demographics of individuals involved with the care of primate hosts in research laboratories.

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.

Fan Q, Amen M, Harden M, Severini A, Griffiths A, Longnecker R. Herpes B virus utilizes human nectin-1 but not HVEM or PILRa for cell-cell fusion and virus entry. J Virol. 2012 Apr. 86(8):4468-76. [Medline]. [Full Text].

Ohsawa K, Black D, Ohsawa M, Eberle R. Genome sequence of a pathogenic isolate of monkey B virus (species Macacine herpesvirus 1). Arch Virol. 2014 Oct. 159(10):2819-21. [Medline]. [Full Text].

Cohen JI, Davenport DS, Stewart JA, et al. Recommendations for Prevention of and Therapy for Exposure to B Virus. Clin Infect Dis. Nov 2002. 35:1191-203. [Medline]. [Full Text].

Du T, Zhou G, Roizman B. Modulation of reactivation of latent herpes simplex virus 1 in ganglionic organ cultures by p300/CBP and STAT3. Proc Natl Acad Sci U S A. 2013 Jul 9. 110(28):E2621-8. [Medline]. [Full Text].

Fujima, A, Ochiai Y, Saito A, et al. Discrimination of Antibody to Herpes B Virus from Antibody to Herpes Simplex Virus Types 1 and 2 in Human and Macaque Sera. J Clin Microbiol. Jan 2008. 46(1):56-61. [Medline]. [Full Text].

Oya C, Ochiai Y, Taniuchi Y, Takano T, Ueda F, Yoshikawa Y, et al. Specific detection and identification of herpes B virus by a PCR-microplate hybridization assay. J Clin Microbiol. 2004 May. 42(5):1869-74. [Medline].

Focher F, Lossani A, Verri A, et al. Sensitivity of Monkey B Virus (Cercopithecine herpesvirus 1) to Antiviral Drugs: Role of Thymidine Kinase in Antiviral Activities of Substrate Analogs and Acyclonucleosides. Antimicrob. Agents Chemother. Jun 2007. 51(6):2028-2024. [Medline]. [Full Text].

Bennett AM, Slomka MJ, Brown DW, et al. Protection against herpes B virus infection in rabbits with a recombinant vaccinia virus expressing glycoprotein D. J Med Virol. 1999 Jan. 57(1):47-56. [Medline].

Bryan BL, Espana CD, Emmons RW, et al. Recovery from encephalomyelitis caused by Herpesvirus simiae. Report of a case. Arch Intern Med. 1975 Jun. 135(6):868-70. [Medline].

Chellman GJ, Lukas VS, Eugui EM, et al. Activation of B virus (Herpesvirus simiae) in chronically immunosuppressed cynomolgus monkeys. Lab Anim Sci. 1992 Apr. 42(2):146-51. [Medline].

Davenport DS, Johnson DR, Holmes GP, et al. Diagnosis and management of human B virus (Herpesvirus simiae) infections in Michigan. Clin Infect Dis. 1994 Jul. 19(1):33-41. [Medline].

Fierer J, Bazely P, Braude AI. Herpes B virus encephalomyelitis presenting as ophthalmic zoster. A possible latent infection reactivated. Ann Intern Med. 1973 Aug. 79(2):225-8. [Medline].

Freifeld AG, Hilliard J, Southers J, et al. A controlled seroprevalence survey of primate handlers for evidence of asymptomatic herpes B virus infection. J Infect Dis. 1995 Apr. 171(4):1031-4. [Medline].

Hilliard JK, Weigler BJ. The existence of differing monkey B virus genotypes with possible implications for degree of virulence in humans. Lab Anim Sci. 1999 Feb. 49(1):10-1. [Medline].

Holmes GP, Chapman LE, Stewart JA, et al. Guidelines for the prevention and treatment of B-virus infections in exposed persons. The B virus Working Group. Clin Infect Dis. 1995 Feb. 20(2):421-39. [Medline].

Holmes GP, Hilliard JK, Klontz KC, et al. B virus (Herpesvirus simiae) infection in humans: epidemiologic investigation of a cluster. Ann Intern Med. 1990 Jun 1. 112(11):833-9. [Medline].

Jainkittivong A, Langlais RP. Herpes B virus infection. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1998 Apr. 85(4):399-403. [Medline].

Kessler MJ, Hilliard JK. Seroprevalence of B virus (Herpesvirus simiae) antibodies in a naturally formed group of rhesus macaques. J Med Primatol. 1990. 19(2):155-60. [Medline].

Ostrowski SR, Leslie MJ, Parrott T, Abelt S, Piercy PE. B-virus from pet macaque monkeys: an emerging threat in the United States?. Emerg Infect Dis. 1998 Jan-Mar. 4(1):117-21. [Medline].

Palmer AE. B virus, Herpesvirus simiae: historical perspective. J Med Primatol. 1987. 16(2):99-130. [Medline].

Perelygina L, Patrusheva I, Hombaiah S, Zurkuhlen H, Wildes MJ, Patrushev N, et al. Production of herpes B virus recombinant glycoproteins and evaluation of their diagnostic potential. J Clin Microbiol. 2005 Feb. 43(2):620-8. [Medline].

Scinicariello F, Eberle R, Hilliard JK. Rapid detection of B virus (herpesvirus simiae) DNA by polymerase chain reaction. J Infect Dis. 1993 Sep. 168(3):747-50. [Medline].

Weigler BJ. Biology of B virus in macaque and human hosts: a review. Clin Infect Dis. 1992 Feb. 14(2):555-67. [Medline].

Weigler BJ, Scinicariello F, Hilliard JK. Risk of venereal B virus (cercopithecine herpesvirus 1) transmission in rhesus monkeys using molecular epidemiology. J Infect Dis. 1995 May. 171(5):1139-43. [Medline].

Jin Z, Sun T, Xia X, Wei Q, Song Y, Han Q, et al. Optimized Expression, Purification of Herpes B Virus gD Protein in Escherichia coli, and Production of Its Monoclonal Antibodies. Jundishapur J Microbiol. 2016 Mar. 9 (3):e32183. [Medline].

Hotop SK, Abd El Wahed A, Beutling U, Jentsch D, Motzkus D, Frank R, et al. Multiple antibody targets on herpes B glycoproteins B and D identified by screening sera of infected rhesus macaques with peptide microarrays. PLoS One. 2014. 9 (1):e86857. [Medline].

Sowmya Nanjappa, MD Assistant Member, Department of Internal Medicine, Moffitt Cancer Center; Assistant Professor of Medicine, Department of Internal Medicine and Department of Oncologic Sciences (Joint Appointment), University of South Florida Morsani College of Medicine

Sowmya Nanjappa, MD is a member of the following medical societies: American Association of Physicians of Indian Origin, American College of Physicians, American Medical Association, Infectious Diseases Society of America, Society of Hospital Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Charles V Sanders, MD Edgar Hull Professor and Chairman, Department of Internal Medicine, Professor of Microbiology, Immunology and Parasitology, Louisiana State University School of Medicine at New Orleans; Medical Director, Medicine Hospital Center, Charity Hospital and Medical Center of Louisiana at New Orleans; Consulting Staff, Ochsner Medical Center

Charles V Sanders, MD is a member of the following medical societies: American College of Physicians, Alliance for the Prudent Use of Antibiotics, The Foundation for AIDS Research, Southern Society for Clinical Investigation, Southwestern Association of Clinical Microbiology, Association of Professors of Medicine, Association for Professionals in Infection Control and Epidemiology, American Clinical and Climatological Association, Infectious Disease Society for Obstetrics and Gynecology, Orleans Parish Medical Society, Southeastern Clinical Club, American Association for the Advancement of Science, Alpha Omega Alpha, American Association of University Professors, American Association for Physician Leadership, American Federation for Medical Research, American Geriatrics Society, American Lung Association, American Medical Association, American Society for Microbiology, American Thoracic Society, American Venereal Disease Association, Association of American Medical Colleges, Association of American Physicians, Infectious Diseases Society of America, Louisiana State Medical Society, Royal Society of Medicine, Sigma Xi, Society of General Internal Medicine, Southern Medical Association

Disclosure: Received royalty from Baxter International for other.

Pranatharthi Haran Chandrasekar, MBBS, MD Professor, Chief of Infectious Disease, Department of Internal Medicine, Wayne State University School of Medicine

Pranatharthi Haran Chandrasekar, MBBS, MD is a member of the following medical societies: American College of Physicians, American Society for Microbiology, International Immunocompromised Host Society, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Larry I Lutwick, MD, FACP Editor-in-Chief, ID Cases; Moderator, Program for Monitoring Emerging Diseases; Adjunct Professor of Medicine, State University of New York Downstate College of Medicine

Larry I Lutwick, MD, FACP is a member of the following medical societies: American Association for the Advancement of Science, American Association for the Study of Liver Diseases, American College of Physicians, American Federation for Clinical Research, American Society for Microbiology, Infectious Diseases Society of America, Infectious Diseases Society of New York, International Society for Infectious Diseases, New York Academy of Sciences, Veterans Affairs Society of Practitioners in Infectious Diseases

Disclosure: Nothing to disclose.

Thomas J Marrie, MD Dean of Faculty of Medicine, Dalhousie University Faculty of Medicine, Canada

Thomas J Marrie, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society for Microbiology, Association of Medical Microbiology and Infectious Disease Canada, Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Brian Hogan, MD, MPH&TM Fellow in Infectious Diseases, Brooke Army Medical Center, San Antonio Uniformed Services Health Education Consortium

Disclosure: Nothing to disclose.

Robert O Deaner, PhD Assistant Professor, Department of Psychology, Grand Valley State University

Disclosure: Nothing to disclose.

Jason F Okulicz, MD Assistant Professor of Medicine, Uniformed Services University of the Health Sciences; Staff, Infectious Disease Service, Brooke Army Medical Center

Jason F Okulicz, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

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