Herpes B Virus

John E. Bennett MD , in Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases , 2020

Prevention

Prevention of herpes B virus requires strict precautions when working with nonhuman primates. In view of a fatal instance of herpes B virus occurring in a adult female who received a splash to her eyes, primate workers exposed to macaques should article of clothing goggles or glasses with side shields and a mask or a mentum-length face shield and a mask to prevent infection of the eyes and oral mucosa. 4 Although only a unmarried case of person-to-person transmission of herpes B virus has been reported, 10 individuals infected with the virus can shed infectious virus for more 1 week fifty-fifty while receiving intravenous acyclovir iv ; therefore body fluids should be considered potentially infectious. Oral and genital secretions from individuals who have been exposed to canker B virus, when information technology is non withal known whether they are infected, should exist considered potentially infectious to others. If the incubation period for canker B virus (by and large 5 weeks in untreated individuals) has passed and the person is asymptomatic or serologies are persistently negative (at least 12 weeks after exposure in patients given antiviral prophylaxis), the likelihood of infection and virus transmission is exceedingly low.

It is essential that individuals exposed to macaques be educated regarding the importance of outset assistance and the demand for rapid cleansing of wounds or mucosal exposures, the need to see health care personnel regarding evaluation for postexposure prophylaxis, and the signs and symptoms of herpes B virus disease so that early therapy can be initiated. Specific pathogen-free colonies of macaques have reduced the risk of herpesvirus B virus exposure almost twenty-fold. 31

Herpes B Virus

Jeffrey I. Cohen , in Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases (8th Edition), 2015

Epidemiology

Herpes B virus is endemic in Onetime World macaques, and most macaques in captivity (unless separated from their parents at birth and reared autonomously from other animals) should be considered equally possibly infected. About macaques are infected during adolescence, and nearly 100% of adult (≥2.5 years sometime) macaques bred in captivity or in the wild are infected. 5 The virus naturally infects all types of Old World macaques, including rhesus macaques (Macaca mulatta), cynomolgus monkeys (Macaca fascicularis), and pigtailed macaques (Macaca nemestrina). The virus has as well been isolated from bonnet, Japanese, stumptail, and other macaques, but no other Onetime or New Earth monkeys are naturally infected. 6 Herpes B virus has also been detected in gratuitous-ranging monkeys in Bali and other sites in Southeast Asia. 7

Humans are inadvertent hosts. Humans take been infected by bites and scratches from macaques. Other exposures that have transmitted the virus are a needlestick injury from a needle that was exposed to tissue effectually the middle of a macaque or a needle that was thought to be used to inject monkeys, contamination of wounds with macaque saliva, lacerations from bottles containing macaque cell cultures, scratches from cages, exposure to monkey nervous tissue at dissection, and possible aerosol exposures. 3 One case was reported acquired by a splash to the heart from material from a caged macaque. 8 A single example of human-to-human being transmission of canker B virus was reported in a woman who became infected after applying hydrocortisone cream to her contact dermatitis lesions and her husband's herpes B virus skin lesions. nine Herpes B virus was reported in a primate worker who had not cared for primates for more than 10 years. The disease was presumed to be due to reactivation of the virus from latency in the worker 10 ; notwithstanding, this instance is considered controversial, and the patient may take had an unrecognized exposure to herpes B virus more recently. All cases of herpes B virus, except for the patient with mucosal splash, accept been due to percutaneous exposure. Although a large number of animal bites and scratches occur each year, cases of herpes B virus are rare; notwithstanding, the potential for fatalities requires that each of these exposures be evaluated.

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Viral Encephalitis and Meningitis

Joseph Jankovic MD , in Bradley and Daroff'due south Neurology in Clinical Exercise , 2022

Herpes B Virus (Cercopithecine Herpesvirus 1)

Herpes B virus of One-time World monkeys is highly pathogenic to humans, and untreated infection has an estimated seventy% bloodshed. Ocular, oral, and genital secretions of monkeys, as well equally CNS tissues and CSF, are potentially infectious. Illness is transmitted by straight contact with the virus, normally by brute bite or by virus-containing fomites. One reported fatal instance of Herpes B virus infection was due to mucosal splash exposure ( Cohen et al., 2002).

Fever, myalgia, herpetiform rash, meningismus, and early-stage nystagmus or diplopia are followed by an ascending encephalomyelitis causing flaccid paralysis, urinary retention, and signs of CNS involvement including seizures, progressive lethargy, and coma. Diagnosis is made past isolation of virus or viral DNA from wound or contact sites and/or past demonstration of seroconversion between acute and ambulatory sera.

Preventive measures for primate workers include use of protective eyewear including side shields and a mask to protect from mucous membrane exposure. Should exposure occur, the about critical period for prevention of infection is within the starting time few minutes after exposure. Immediate cleansing of the affected peel surface should be undertaken by soaking or scrubbing the contact area with povidone-iodine, chlorhexidine, or detergent soap for 15 minutes. Eyes or mucous membranes should be immediately irrigated with sterile saline solution or water for 15 minutes. Postexposure prophylaxis within v days of exposure is recommended with oral valacyclovir, ane k three× daily for ii weeks; oral ACV, 800 mg 5× daily for 2 weeks; or famciclovir, 500 mg 3× daily for 2 weeks. Symptomatic patients without CNS symptoms should be treated with either Four ACV (xv mg/kg every eight hours) or Four ganciclovir (five mg/kg every 12 hours). When CNS symptoms are present, most experts advise handling with IV ganciclovir in preference to ACV, although comparative trials are lacking. Treatment should be continued until symptoms resolve and the results of two sets of cultures are negative for B Canker virus later on beingness held for 10–14 days. Following 4 therapy, therapy is switched to oral valacyclovir, famciclovir, or ACV in the dosages used for postexposure prophylaxis. Considering of the potential risk of reactivation of latent virus and development of CNS disease, indefinite maintenance of oral suppressive therapy following documented infection may be warranted.

Nonhuman Primate Diseases of Relevance in Drug Development and their Impact on the Interpretation of Study Findings

Chandrassegar Saravanan , ... Keith Thousand. Mansfield , in The Nonhuman Primate in Nonclinical Drug Development and Safety Assessment, 2015

Macacine Herpesvirus-one (Herpes B Virus)

Herpes B virus is a member of the genus Simplexvirus and subfamily Alphaherpesvirinae [67,68]. Herpes B virus is highly endemic as a latent infection in almost populations of macaques [67–69]. Factors contributing to recrudescence of infection are poorly understood, merely stress related to irresolute social dynamics, transportation or relocation, fever, ultraviolet light, tissue or nerve damage, and immunosuppression may play a part. Though information technology rarely causes illness in the natural host, accidental infection in humans and nonmacaque primates take been reported to crusade fatal disseminated infection. Macaques periodically shed the virus via oral, ocular, and genital secretions. While sexual contact is an important means of virus transmission, other routes such as biting, fomites, overcrowding, and unsanitary conditions might as well contribute to viral infection [70,71].

Infections of Asian macaques are usually mild and self-limiting. Vesicles and ulcerations may occur in oral and genital mucosa and may resolve in ten-14 days. Disseminated viral infection is rare in macaques, but if it occurs it is ordinarily fatal. The clinical course of disseminated viral infection can be peracute to slowly progressive, and herpes B virus infection equally an underlying causative amanuensis may non be suspected. In such cases the risk of homo exposure may be increased. Herpes B virus infection of humans is characterized past ascending paralysis and a high mortality rate. Common sites of viral infection include buccal, gingival, conjunctival, anal, and genital mucosa [72]. In these sites, infection tin be accompanied by erythema, vesicles, and ulcerations. Histologically, there is ballooning degeneration of keratinocytes with progression to vesiculations accompanied by inflammatory cells (Figure ten.1). Multinucleated syncytial cells with eosinophilic to basophilic intranuclear viral inclusions may be prominent. Endothelial jail cell necrosis with intranuclear viral inclusions may be seen. In disseminated disease at that place is widespread, multifocal, hemorrhagic necrosis within the liver, lung, encephalon, adrenal gland, and lymphoid organs [67–69]. Canker B viral infection should exist included as a differential diagnosis in primate diseases with multifocal necrotizing hepatitis. Seroconversion occurs soon after the primary infection and is ofttimes associated with the resolution of clinical signs. False-negative results and latent infection may complicate the interpretation of serological assays [73,74]. Because of infrequent viral shedding, PCR-based detection of viral Dna is of limited value for diagnosis. Immunohistochemistry using a commercially available rabbit polyclonal antibiotic against the closely related human herpesvirus-1 can be used to demonstrate viral antigen in equivocal lesions [65,75] (Effigy x.1). Yet, this antibody detects viral glycoproteins shared by all simplex viruses and therefore is not able to definitively ostend herpes B viral infection. Molecular tools or viral isolation are required if definitive identification is desired. The samples tin be submitted to the National B Virus Resource Laboratory (Georgia State University, Atlanta, Georgia) for viral culture and molecular diagnosis.

Figure 10.1. Canker B virus infection. Viral infection causes epithelial cell necrosis inside the oral mucosa, with infiltration of neutrophils. Note the presence of multinucleated syncytial cells with intranuclear inclusions (arrows in (a)). Immunohistochemistry demonstrates the viral antigen within the epithelial cells (b).

Reactivation of herpes B virus with clinical disease or death has been reported in captive macaques with immunosuppression from natural viral infection (e.g., SRV infection) or those administered immunosuppressive therapeutics [76,77]. For example, 3 of 14 cynomolgus macaques given the highest dose of an immunosuppressive drug in a vi-month toxicology study adult herpes B virus oral lesions after iii months of dosing [76]. This resulted in early removal of all high-dose monkeys from the written report because of zoonotic concerns. In another study [77] ii adult cynomolgus monkeys that were housed together died from fatal disseminated herpes B virus infection due to immunosuppression caused by SRV infection. In addition to a propensity to cause fatal disease in immunosuppressed macaques, there is high zoonotic risk associated with herpes B virus. Therefore every endeavor should be fabricated to employ SPF animals in models that are probable to result in immunosuppression. Decision of canker B virus status in an individual animal can be difficult because both serological assays and viral isolation accept limitations. Thus SPF status can be ascertained only by knowing the virologic history of the animal under consideration and the history of all its contacts. For these reasons, treating all macaque species as if they are potentially infected with herpes B virus and taking appropriate precautions is advisable.

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Maternal and Perinatal Infection in Pregnancy : Viral

Mark B. Landon MD , in Gabbe's Obstetrics: Normal and Problem Pregnancies , 2021

Man Immunodeficiency Virus/Hepatitis B Virus Coinfection

Women testing positive for HBsAg are coinfected with HIV/HBV and additional cess should include liver transaminases, prothrombin time, HB due east-antigen, HB e-antibody, and HBV Deoxyribonucleic acid. A positive test for anti-HBc alone tin be a imitation-positive; alternatively, information technology may signify remote exposure with subsequent loss of anti-HBs antibiotic or longstanding chronic HBV infection with loss of surface antigen ("occult" HBV infection, which can be confirmed past HBV Deoxyribonucleic acid assessment). The incidence of HBV viremia in HIV-infected patients with isolated anti-HBc antibody ranges from i% to 36%. Antepartum ART in HIV/HBV-coinfected women should include tenofovir disoproxil fumarate plus lamivudine or emtricitabine to care for their HBV infection. 2 Meaning women with HIV/HBV coinfection receiving ARV drugs should be counseled about signs and symptoms of liver toxicity and liver transaminase levels, and HBV Dna should be assessed one month following initiation of ARV drugs and at least every 3 months thereafter during pregnancy.

If HBV DNA remains detectable on therapy, referral to a provider experienced with HIV/HBV coinfection is recommended. Decisions concerning mode of commitment in HIV/HBV-coinfected pregnant women should be based on standard obstetric and HIV-related indications lone; HBV coinfection does not necessitate cesarean delivery if non otherwise indicated. Inside 12 hours of birth, infants built-in to women with HBV infection should receive hepatitis B immune globulin and the first dose of the HBV vaccine series to prevent perinatal HBV transmission. To prevent horizontal transmission of HIV as well as HBV from HIV/HBV-coinfected women, their sexual contacts should be counseled and tested for HIV, HBV, and HAV. HAV/HBV-susceptible contacts should receive both HAV and HBV vaccines. Women with chronic HBV should be counseled on the importance of continuing anti-HBV medications indefinitely, both during and after pregnancy. If ARV drugs with anti-HBV activity are discontinued in women with HIV/HBV coinfection, frequent monitoring of liver part tests for potential exacerbation of HBV infection is recommended, with prompt reinitiation of treatment if a hepatic flare is suspected.

Viral Diseases of Nonhuman Primates

Lynn Wachtman , Keith Mansfield , in Nonhuman Primates in Biomedical Research (Second Edition), Volume 2, 2012

Etiology

Herpes B virus is a member of the subfamily Alphaherpesvirinae and genus Simplexvirus. The 157-kb-long viral genome encodes approximately seventy proteins. Homologs of all of these genes occur in related viruses of humans, such as Human being herpesvirus i and ii (HHV1 and HHV2; Herpes simplex virus ane and 2), and of primates, such every bit Papiine herpesvirus two (Herpesvirus papio ii) and Cercopithecine herpesvirus two (Ohsawa et al., 2002a, 2003; Perelygina et al., 2003b). Notably, herpes B virus lacks a homolog of the HHV neurovirulence factor γ134.5 suggesting alternate strategies to promote replication of B virus within neurons (Perelygina et al., 2003b). The viral envelope contains at least nine glycoproteins that are targets of the immune response and aid to ascertain cellular tropism. Glycoproteins B and D have 80% and 56% identity with the respective HHV1 glycoproteins, while glycoproteins Chiliad and C demonstrate significant sequence variation (Ohsawa et al., 2002a; Perelygina et al., 2002). Genomic sequencing and brake fragment length polymorphism analysis have demonstrated that distinct genotypes of herpes B virus occur in unlike species of macaques including rhesus, cynomolgus, pig-tailed, lion-tailed, and Japanese macaques (Smith et al., 1998; Thompson et al., 2000; Ohsawa et al., 2002b). The parallel system of phylogenic trees for B virus isolates and mitochondrial Deoxyribonucleic acid sequences from the respective macaque species indicates probable co-speciation. Viral replication occurs rapidly, with enveloped capsids present 8–10   h after infection. In jail cell culture, syncytial cells and Cowdry-blazon A intranuclear inclusions are readily apparent.

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Antivirals against Herpes Viruses

Fred Y. Aoki , in Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases (8th Edition), 2015

Other Viruses

Valacyclovir is recommended in managing herpes B virus (cercopithecine herpesvirus 1) exposures, and high-dose intravenous acyclovir (12.5 to 15 mg/kg/8 hr) or ganciclovir is recommended for treating non-CNS herpes B virus infections; intravenous ganciclovir is advised for CNS infection (run into Chapter 144). 130 High-dose acyclovir has been reported to provide a modest survival benefit in avant-garde HIV infection, although this remains controversial. 131 Loftier-dose valacyclovir, merely not acyclovir, reduces CMV illness hazard in advanced HIV infection simply is less well tolerated and is associated with college bloodshed. 40 Valacyclovir reduced oropharyngeal shedding of HHV-8 in HIV-1 infected individuals, merely not equally markedly equally did antiretroviral drugs. 132

In infectious mononucleosis, acyclovir is associated with transient suppression of salivary EBV excretion but no important effects on affliction parameters. 133 High-dose acyclovir is ineffective in patients with chronic fatigue syndrome. 134 Some cases of mail service-transplantation EBV-related polyclonal lymphoproliferation may respond to acyclovir, 135 and long-term acyclovir or related antivirals mayhap reduce the risk for AIDS-related lymphoma. 136 EBV-related oral hairy leukoplakia ordinarily regresses with oral acyclovir or valacyclovir treatment but recurs. 137 Topical 5% acyclovir with 25% podophyllin resin is effective in resolving the lesions with a reduced recurrence rate compared with podophyllin resin alone in HIV-1 seropositive patients. 138 Neither intravenous nor oral acyclovir enhances the response to IFN in patients with chronic hepatitis B. Long-term acyclovir does not reduce neurologic deterioration in multiple sclerosis. 139

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Neurovirology

John Booss , Alex C. Tselis , in Handbook of Clinical Neurology, 2014

Herpes B virus

Infrequent but highly lethal, herpes B virus infection has a tragic link to studies of poliomyelitis. The virus is a beneficial enzootic infection of its natural host, the Macaque rhesus monkey, but can be mortal on its rare transmission to those working with macaques ( Weigler, 1992). "B" stands for Brebner, the concluding name of the victim from whom the virus was start isolated. Dr. William Brebner was a highly respected young Canadian researcher (Pimentel, 2008). At the time of his expiry he was working equally an assistant professor of bacteriology at NYU in the Bureau of Laboratories of the City of New York on the pathogenesis of infantile paralysis (Cowdry, 1933). He was bitten on fingers of his left mitt while transferring a monkey from a sack in which it was being transported (Sabin and Wright, 1934). Three days afterward hurting, redness, and swelling adult at the site, an ascending myelitis developed, and he passed abroad from respiratory paralysis in the tertiary week after infection. Ironically, Dr. Brebner'due south paper on purification of poliovirus would be published after in that year in the same journal, Archives of Pathology, in which his obituary by Cowdry appeared (Schaeffer and Brebner, 1933).

Sabin and Wright (1934) were able to demonstrate that an isolate from the case was different from all viruses known at the time. Albert Sabin would continue to a career as one of America's about distinguished virologists, producing, amidst other accomplishments, the oral form of the polio vaccine. He and Wright commented in their report that ascending myelitis was not a unmarried disease and that the most common class was secondary or postinfectious. The feature pathology of postinfectious myelitis, perivascular demyelination, was missing from this case. They noted that chief infectious myelitis was "almost unknown," including cases of the spinal form of encephalitis lethargica, inductive poliomyelitis which involved the residue of the spinal string, and rabies virus. Thus they had established a new viral cause of ascending myelitis.

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Virology Research

Barry Peter , ... Miller Christopher J. , in The Laboratory Primate, 2005

Cercopithecine herpesvirus 1 (Herpes B virus)

Cercopithecine herpesvirus 1, by and large referred to as herpes B virus (BV), is an alphaherpesvirus of the rhesus macaque with strong genetic, virological and immunological relatedness to herpes simplex virus (HSV) of humans. BV infection of the rhesus monkey seems to accurately model HSV infection of humans, merely the deadly zoonotic potential of BV has prevented its use in an animal model. Notwithstanding, it was recently listed as a categorical pathogen by the U.S. Public Health Service and could be an agent of bioterror. Thus a brief discussion of BV is included hither.

BV is endemic in Asian macaque populations (Weigler, 1992), and closely related alphaherpesviral variants are present in African NHP (Eberle and Hilliard, 1995). BV equitably bears the most attention of the NHP alphaherpesviruses because of its pathogenic potential in humans. Zoonotic infection of humans with B virus is virtually invariably fatal (>70%) in the absence of antiviral chemotherapies, and astringent, non-fatal infections can outcome in encephalomyelitis or severe neurological damage (Huff and Barry, 2003). BV is the just simian herpesvirus that is known to cause disease in humans. The most salient characteristic of BV natural history, in terms of its occupational risk, is that an overwhelming majority of macaques shed B virus without overt signs of disease (Huff, J.E. et al., 2003; Weigler et al., 1993; Zwartouw and Boulter, 1984). Thus, every BV-seropositive macaque must be considered as a potential source of infectious BV, whether through its actual fluids or its tissues.

Despite the preceding risk assessment, there take only been approximately twoscore documented cases of human infection since the first reported transmission to humans in 1932 (Huff and Barry, 2003). The disproportionality between the number of zoonotic infections and the high seroprevalence of BV in breeding age animals is a office of the BV life cycle. The biology of BV infection in macaques is characterized by a lifelong persistence with infrequent, and usually subclinical, shedding at mucosal surfaces. Although the natural history of BV has non been described in detail, the replication cycle of HSV serves as a precedent (Roizman and Sears, 1993). Virus is transmitted across a mucosal surface, such as the oral or genital mucosa. Following localized replication in mucosal epithelial cells, the virus is transmitted directly to sensory nerve endings. The prevailing thought is that there is no associated bloodborne stage of infection, except in rare systemic infections (Simon et al., 1993). The virus particle is carried, by axonal transport, to the dorsal root ganglia where the virus establishes a true latent infection in neurons.

Latency is noted for a lack of viral replication and an extremely express blueprint of viral transcription. Periodic reactivation from latency results in the product of progeny virions which send back down the axon to mucosal epithelial cells, where they replicate and the infectious virus is released from the mucosal epithelium. For BV, most episodes of recurrent viral shedding are asymptomatic (Huff et al., 2003; Weigler et al., 1993; Zwartouw and Boulter, 1984), and represent a constant risk of zoonoses. Clinical signs of either chief or recurrent infection (oral herpetic lesions such as gingivostomatitis, oral and lingual ulcers, and conjunctivitis) are the exception (Carlson et al., 1997; Keeble et al., 1958; Weigler, 1992), and usually require firsthand euthanasia of the beast. Virus isolation and molecular detection of BV DNA indicate that the frequency of shedding in a population is low (1–5%), although more studies are needed to establish a true charge per unit. There is bear witness to suggest that shedding frequency may go upwards during convenance flavour (Huff et al., 2003; Weigler et al., 1993).

There is a stiff correlation between the seroconversion to BV and the historic period of the beast. Seroconversion rates increase sharply when monkeys accomplish the age of sexual maturity, with prevalence rates of fourscore–100% in adult populations (Weigler, 1992; Weigler et al., 1993). In that location is no bear witness for vertical transmission of BV.

Human B virus infections take generally involved direct contact with macaques or their tissues or fluids (Huff and Barry, 2003). Methods of contact take included a seize with teeth, scratch, contact of a mucosal surface with a macaque body fluid or tissue, or a contaminated needle puncture or cage scratch (Huff and Barry, 2003). At that place has only been ane documented case of human-to-human transmission, although the potential for secondary transmission is probably low (Holmes et al., 1990). BV disease can begin within a few days to a month, although disease progression is variable in terms of the kinetics and clinical signs. Guidelines for reducing potential exposure and treatment of suspected BV infections in humans take recently been published (Holmes et al., 1995).

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Neurological disease with a viral aetiology

Stephen N.J. Korsman MMed FCPath , ... Wolfgang Preiser MRCPath , in Virology, 2012

Prevention

Vaccination and post-exposure prophylaxis for rabies are discussed in another section. Vaccination for mutual childhood diseases such as measles, rubella and varicella dramatically reduce the risk of the corresponding CNS complications.

Vector command is important in preventing arboviral encephalitis. Vaccines are as well available for Japanese encephalitis and some of the other arboviruses. Beast handlers exposed to canker B virus should immediately utilize acyclovir post-exposure prophylaxis.

Stop/Think

▪

It is summer and the patient is a child with meningitis and clear CSF, normal glucose and normal neutrophils; what would exist the near likely diagnosis?

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Why should empiric aciclovir treatment be started in a asleep patient with focal neurological signs?

Key points

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Enteroviruses are the most common cause of hygienic meningitis in children.

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Herpes simplex virus (HSV) encephalitis commonly involves the one temporal or parietal lobe in allowed competent adults and children.

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Early anti-herpes virus therapy has a dramatic outcome on the outcome of HSV encephalitis and should, therefore, be empirically initiated on suspicion of HSV encephalitis.

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