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A 26-year-old veterinary technician who became infected with B virus at the site of a needlestick injury is described. After the patient was treated with intravenous acyclovir, all cultures became negative for B virus and have remained so during treatment with oral acyclovir. The literature on infections due to B virus in humans is reviewed, and a detailed discussion of the various aspects of this simian herpesvirus is presented.

A 37-year-old male laboratory technician who sustained a cutaneous penetrating wound from a rhesus monkey developed a progressive ascending encephalomyelitis due to culture-proven herpes B virus (Herpesvirus simiae) infection. He died 6 weeks after his injury despite acyclovir and ganciclovir treatment that was initiated after central nervous system symptoms developed. Histopathological examination of the patient's left eye revealed a multifocal necrotizing retinitis associated with a vitritis, optic neuritis, and prominent panuveitis. Herpes-type virus was identified in the involved retina by electron microscopy. Postmortem vitreous cultures taken from both eyes and retinal cultures taken from the right eye were positive for herpes B virus. Herpes B virus produces infection and destruction of retinal tissues similar to other herpesviruses. To our knowledge, this case represents the first histopathologic demonstration of herpes B virus infection in a human eye.

A number of serologic procedures are available for specifically determining past infection due to H. hominis, or H. simiae (B virus). A herpesvirus isolated from primate tissues, however, does not lend itself to specific identification. Procedures currently in routine use simply do not provide an unequivocal identification of the isolate. We have previously demonstrated that H. simiae contain polypeptide and glycoprotein antigens distinct from those of other herpesviruses. At selected intervals, infected cells and controls were harvested after being both pulsed as well as continuously labelled from 4-24 hours post infection with 3H-glucosamine. 3H-mannose, and 3H-L-amino acid mixture. Between 40-45 infected cell polypeptides were observed by SDS-polyacrylamide gel electrophoresis (SDS-PAGE) with 7-11 glycoproteins noted. Analysis of the bands by electroblot utilizing anti-B virus sera showed the presence of eleven reactive bands within this molecular weight range from preparations in infected Vero and HEp-2 cell lines. Glucosamine labelled major glycoproteins migrated at 130K, 100K, 95K, 65K, 39K; mannose moieties migrated at 95K and 65K. SDS-PAGE profiles of B-virus when reacted with anti-gA/gB from HSV-1 and HSV-2 showed weak reactivities on the 125-130K complex. Anti-VP5 from HSV-1 failed to indicate any reactivity. Three polypeptides were revealed by SDS-hydroxylapatite analysis of the 130K complex with approximate molecular weights of 115K, 123K, and 130K; the 115K and 123K bands reacted with antisera prepared against gA/gB from HSV-1 and HSV-2, but not to anti-IgC or anti-2gC.(ABSTRACT TRUNCATED AT 250 WORDS)

3 different types of observation all demonstrated that B virus (Herpesvirus simiae) infection of monkeys was not confined to the mouth but was also a genital infection. (1) Latent B virus was reactivated in a seropositive female monkey, which was immunosuppressed with antilymphocyte globulin, and infectious virus was excreted in the genital tract. (2) During an epizootic in a breeding colony, B virus was isolated from 4 genital and 3 oral sites as well as from a skin lesion. (3) In cultures of sensory nerve ganglia taken from seropositive monkeys, B virus was recovered more frequently from ganglia subserving the genital region than the oral region.

Studies of B virus (Herpesvirus simiae) antibody in several species of macaque lead to the following generalizations. Newborn monkeys are not infected with B virus, even when born of seropositive mothers. Young monkeys remain uninfected until they become adults. The majority of adults develop B virus antibody unless their physical contact with seropositive adults is restricted. These observations are consistent with sexual transmission of B virus and classification of the disease in monkeys as venereal. However, infection at oral and dermal sites also occurs and may play a part in monkey-to-monkey transmission. Epizootics of B virus occurred during early attempts to start B virus-free breeding colonies. They appeared to originate from reactivated latent B virus in adult monkeys which had only low titres of antibody. The stress produced when groups of adult strangers were assembled to form breeding colonies was the most effective known inducer of latent B virus. Total exclusion of animals with any trace of antibody has enabled the establishment of new breeding colonies which are free from B virus.

A new simian herpes virus with biological properties similar to herpes simplex and to simian "B" virus has been used as a model system for studying virus latency in dorsal root spinal sensory ganglia. Following intradermal injection, virus is present in the skin lesions and corresponding ganglia only, during the acute stage of the disease. By organ-culture techniques, latent virus was rescued from ganglia up to 2 years later. No latent virus was ever found in skin organ cultures of the primary site. Treatment with cortisone up to 18 months later reactivated virus latent in the ganglia, and virus returned to the skin where it produced small but typical herpes lesions which shed virus. Reactivation of Herpesvirus tamarinus was achieved after 28 months. This is believed to be the first report of a model system for the study of herpes latency in which skin lesions are found to recur, and provides an opportunity for more detailed investigations of the mechanisms of virus latency in man. The presumption that reactivation of skin lesions will also be possible in rhesus monkeys seropositive for "B" virus points to a possibly grave and largely unsuspected hazard for those engaged in primate research.

The suspected ability of herpes simiae (B virus) to persist in a latent form has been confirmed in rhesus monkeys. The virus was recovered from primary oral lesions of 2 young monkeys and again, 6 months after disappearance of symptoms, from cultures of Gasserian ganglia taken from the same individuals. B virus was identified by its effects in vivo and in vitro and in cross neutralization tests with antisera to reference B virus and herpes simplex virus. Tests showed that the same virus was present in oral lesions and in ganglia. The one-way immunological relationship between herpes simplex virus and B virus was clearly shown in results of cross neutralization tests.

When small doses of herpes simplex virus (HSV) were given to rabbits a significant degree of protection was afforded against later infection with herpes simiae (B virus). Only 12/47 rabbits died within 3 weeks of receiving B virus dosages that would normally have proved lethal. B virus became latent in survivors and was recovered from brain and spinal cord suspensions from rabbits which died within 6 months and from dorsal root ganglia of rabbits which had survived for more than 2 years without overt signs of infection. A minority of the survivors tested also yielded HSV. Rabbits with latent B virus in the ganglia showed little or no detectable neutralizing antibody to B virus. The possibility is discussed that human populations having a high frequency occurrence of HSV antibody may include carriers of latent B virus.

The methods used at the Clinical Research Centre, Northwick Park Hospital, to treat wounds potentially infected with neurotropic viruses are outlined. Emphasis is laid on first aid and on surgical attention. Patients should remain under medical supervision for at least four weeks after the injury, the need for specific post-exposure treatment depending on the nature of the exposure.

A rhesus monkey housed in the New England Regional Primate Research Center for more than 4 yr died after an illness of 19 da. Clinical signs included central nervous system involvement and ulcers on the labial mucosa. Microscopically, the cause of death was established as multiple cerebral infarction. Lesions characteristic of herpesvirus infections were not present in the brain nor in any other tissue; however, Herpesvirus simiae was isolated from oral and anal swabs as well as from tongue and lung tissue. Inoculation of this agent in H simiae antibody negative rhesus monkeys resulted in infection, as indicated by virus isolation, serologic conversion, conjunctivitis, and development of ulcers at the mucoepithelial border, but fatal infection did not develop.

Twenty isolates, obtained from adult breeding monkeys, were all identified as herpesvirus simiae (B virus) by neutralisation with polyclonal B virus antiserum. Subsequent analysis of restriction enzyme profiles produced by digestion of DNA from the isolates enabled discrimination to be made between them. In particular Cynomolgus monkey isolates could be distinguished from those of Rhesus animals. One isolate (isolate 9) could not be typed either as B virus or as the antigenically related herpesvirus SA8, despite neutralisation by B virus antiserum. Unlike herpes simplex virus, B virus isolates could not be divided into oral and genital types on the basis of restriction enzyme profiles.

Oncogenicity for rabbits of lymphotropic herpesvirus of M. arctoides (HVMA) isolated by us earlier from lymphoid cells of lines MAL-1-3 has been shown in the course of studies. Inoculation of animals both with HVMA-containing cells and cell-free virus caused the development of generalized malignant lymphomas of prolymphocytic-lymphoblastic character leading the animals to death. The molecular hybridization method permitted revealing DNA sequences related to the DNAs of B-lymphotropic herpesviruses of primates in the cells of HVMA-containing cultures, primarily-induced tumours, and in a cell line established from rabbit tumour. This fact is indicative of etiological role of HVMA in the development of malignant lymphomas in rabbits. The question about the origin of the C type particles found in MAL-1-3 and OK-1 cells remains open.