Fatal human herpesvirus type 1 infection in a white-handed gibbon (Hylobates lar).

This report documents a case of spontaneous, fatal, and likely recrudescent human herpesvirus type 1 (HHV-1) infection in a captive white-handed gibbon (Hylobates lar) confirmed by polymerase chain reaction (PCR). An approximately 44-year-old, captive, female, white-handed gibbon with a history of recurrent conjunctivitis and occasional seizures became acutely weak, disoriented, and ataxic. A postictal state was suspected by caretakers and veterinary staff, and euthanasia was ultimately elected because of lack of clinical improvement with supportive care. No significant abnormalities were detected at necropsy. Histologically, sections of cerebrum and midbrain contained minimal to mild, multifocal lymphoplasmacytic meningoencephalitis with numerous intranuclear viral inclusions within astrocytes and some neurons. The presumptive diagnosis of HHV-1-induced encephalitis was strengthened by nested PCR amplification of a segment of the herpesvirus DNA polymerase gene. Sequences from this region have been found to be unique to each herpesvirus species, thus identifying HHV-1 as the likely etiologic agent in this case. Positive HHV-1 serology from several years before the terminal episode suggested that the disease was most likely due to recrudescence of latent HHV-1 infection.     

Neurological disease in cattle in southern Brazil associated with Bovine herpesvirus infection.

The occurrence of neurological disease in cattle caused by Bovine herpesvirus in 11 farms from southern Brazil between 1987 and 2007 is described. Twenty-two animals were necropsied. Major clinical signs included excessive salivation, nasal and ocular discharge, circling, recumbency, depression, incoordination, grinding of teeth, and paddling movements. Necropsy findings in 10 of 22 cattle included hyperemia and softening of the rostral portions of the telencephalic cortex, with flattening of gyri, and malacia. Cattle in 10 cases did not show any gross lesions. Histological examination in most cases revealed nonsuppurative and necrotizing meningoencephalitis with acute neuronal necrosis, edema, eosinophilic intranuclear inclusion bodies in astrocytes and neurons, and infiltration of gitter cells. No histologic lesions could be detected in 4 cases. The initial diagnosis was based upon the clinical, epidemiological, and pathological findings. The diagnosis was confirmed by virus isolation in cell culture followed by virus identification by a glycoprotein C-based polymerase chain reaction. Seven isolates were identified as Bovine herpesvirus 5, and 4 were identified as Bovine herpesvirus 1.     

Experimental reactivation of equid herpesvirus 1 (EHV 1) following the administration of corticosteroids

Eight ponies were experimentally infected with equid herpesvirus 1 (EHV 1) (subtype 1). All animals showed clinical and serological evidence of infection and virus was isolated from nasal swabs and leucocytes. These ponies were kept in isolation for a further three months during which time complement fixing antibody decreased at least four-fold. Following immunosuppression with dexamethasone and prednisolone subtype 1 virus was recovered from six of the eight animals within 14 days. Five of these six ponies were viraemic and three of them shed virus in nasal secretions; only four displayed significant rises in complement fixing antibody and only two in neutralising antibody. Clinical abnormalities were not detected during reactivation.     

牛疱疹病毒1型主要囊膜糖蛋白研究进展

牛疱疹病毒(BHV-1)属于α疱疹病毒亚科的DNA病毒,可引起牛高热、上呼吸道感染和母牛流产。该病毒能在牛的感觉神经节内建立潜伏感染,因此,对于该病毒感染的预防和治疗较为困难。BHV-1除了引起初始感染外,还可通过免疫抑制引起动物继发感染,导致动物死亡。研究发现,病毒入侵牛机体时,病毒囊膜糖蛋白在病毒与细胞间相互作用的过程中发挥了重要作用。论文对牛疱疹病毒1型主要囊膜糖蛋白(包括gB、gD、gN)的结构特征和生物学特征加以归纳总结,为该病毒的感染特性研究和预防提供参考。     

Infection of the Bovine Udder with Bovine Herpesvirus

Infectious bovine rhinotracheitis — infectious pustular vulvovaginitis (bovine herpesvirus) grown in tissue culture was used as inoculum in trials to infect the lactating bovine udder. Six experiments were undertaken in which one or more quarters were infused with 1 ml. of tissue culture fluids containing 10⁶ to 10⁷ tissue culture infectious doses (TCID) of virus. In four of the experiments the inoculated quarters showed marked evidence of infection in the form of acute inflammation, swelling, reduced milk secretion and profound changes in the physical appearance of the milk. In each case virus was recovered in high titres in the milk from about the second until the tenth to fifteenth days following exposure. Uninfected quarters remained normal in appearance and virus could not be recovered from the milk.

In three of the experiments it was shown that serum and milk antibodies appeared shortly after the disappearance of virus from the milk. One experiment involving two animals showed that about 1000 TCID of virus were required to produce infection. In one experiment a cow having a pre-inoculation serum titre for bovine herpesvirus proved resistant to infection.

The experiments indicate that the bovine udder is readily susceptible to bovine herpesvirus in non-immune animals, and that the virus produces an acute, limited infection leading to a temporary disfunction of the gland. It appears that natural invasion of the udder through the teat canal is not readily accomplished by the virus.

     

The seal death in Danish waters 1988. 2. Virological studies.

Mass abortions and high mortality were observed in harbour seals in Danish waters during 1988. Severe pneumonia and emphysema were typical clinical and post-mortem findings. Virological studies were carried out to identify the cause of the epidemic. Although seal herpesvirus (SeHV) was isolated in 23 of 114 animals this virus was subsequently found not to be the primary cause of the disease. Following the observation of seroconversion against canine distemper virus (CDV) in diseased seals (Osterhaus & Vedder 1988) a CDV-like morbillivirus (phocine distemper virus, PDV) was identified in organs of diseased animals. It is concluded that the epidemic was caused by introduction of PDV into a highly susceptible population presumably free from morbillivirus infection. The origin of PDV remains unknown but evidence of prior morbillivirus infection has been found in arctic and antarctic seal populations.     

Herpesviruses of carnivores.

This review focuses on felid herpesvirus 1 (FHV-1), the most studied of the carnivore herpesviruses. Canid herpesvirus (CHV-1) and phocid (seal) herpesvirus 1 (PhHV-1) are also included where information is available. FHV-1 is a member of the Varicellovirus genus of the Alphaherpesvirinae, which appears to be closely related phylogenetically to both CHV-1 and PhHV-1. FHV-1 infects both domestic and some wild Felidae, such as cheetahs, and is predominantly a respiratory pathogen of cats. As in other herpesviruses, infection with FHV-1 is characterised by a latent carrier state, during which intermittent shedding of infectious virus may occur. Typical of an alphaherpesvirus, the primary site of FHV-1 latency is neurological tissue (trigeminal ganglion), though recent studies using the polymerase chain reaction have suggested that some latency may occur in non-neurological sites. Latently infected carriers are epidemiologically important as sources of infection for susceptible animals. Though conventional modified live and inactivated vaccines have been available for a number of years, they do not protect against infection nor the development of latency. Recently, work has focused on molecular characterisation of FHV-1, detecting genes such as glycoproteins or regulatory genes. Such work will enable better understanding of the interaction of FHV-1 with the natural host. Deletion mutants of some of these genes may also have potential as vaccine strains.     

Molecular evidence of bovine herpesvirus 1 and 5 in cattle with suspected rabies in Rio Grande do Sul state,Brazil

Rabies and herpetic encephalitis are the main viral infections in bovines with neurological symptoms. Bovine rabies has a high prevalence in Central and South America, while bovine encephalitis associated with herpesvirus is especially important in South America. Viral isolation is the classical way to confirm herpesvirus infection, but molecular evidence of the presence of the virus in affected animals is gaining importance in the diagnosis of the disease in the laboratory. This study investigated the presence of herpesvirus type 1 and 5 (BoHV-1 and BoHV-5) in 182 encephalon of rabies-suspected cattle in Rio Grande do Sul state (RS), Brazil using multiplex real-time polymerase chain reaction (mRT-PCR). The rabies virus was investigated by direct fluorescent antibody assay and intracerebral suckling mouse inoculation. The genomes of BoHV-1 and BoHV-5 were detected in 17% of samples. BoHV-5 and BoHV-1 were detected in 100% and 19% of BoHV positive samples, respectively, indicating the circulation of the pathogens in cattle herds in RS. The high Ct values and the absence of isolation suggest viral latency. Coinfection of herpesvirus and the rabies virus was detected in 28% of samples, although no significant association between pathogens was observed. Rabies was detected in 57.7% of suspected samples, confirming the importance of the disease in the state. Concerning the method by which samples were conserved, no significant difference was observed between the number of positive results in frozen and refrigerated samples.     

Outbreak of malignant catarrhal fever in Welsh Black cattle in Carmarthenshire

An outbreak of malignant catarrhal fever (MCF) resulted in the deaths of 12 cattle in a herd of 77 animals during seven weeks in 1999; in addition, one cow developed a milder disease which was confirmed as MCF by PCR for ovine herpesvirus 2 DNA and an immunofluorescent antibody test for antibodies to the virus, but recovered. Further PCR and serological testing revealed the infection in three other animals, none of which developed clinical disease. Hypocuprosis and the possibility of a genetic predisposition were identified as factors which may have contributed to the outbreak.     

Bovid herpesvirus 2 latency: failure to recover virus from central sensory nerve ganglia.

Latent bovid herpesvirus 2 was sought in sensory ganglia, epithelium and lymph nodes from cattle having antibodies against bovid herpes virus 2. Tissues from eight animals were maintained in vitro as explants for 49-72 days during which all expended media was tested for virus. Three animals were pretreated with corticosteroids prior to slaughter. Infectious bovine rhinotracheitis virus was recovered from one animal, but bovid herpesvirus 2 was not detected.     

Isolation and characterisation of cervine herpesvirus-1 from red deer semen

AIM: This communication describes the isolation of herpesvirus during routine export examination of semen collected from red deer stags in New Zealand. METHODS: Virus isolation was carried out using bovine embryonic lung (BEL) cells and viruses were characterised by direct immunofluorescense, restriction-fragment-length polymorphism analysis (RFLP), polymerase chain reaction (PCR) analysis and nucleotide sequencing. RESULTS: Herpesvirus was isolated from red deer semen on 2 different occasions from different animals. In both cases the virus was identified as cervine herpesvirus-1 (CvHV-1), based on RFLP, PCR and sequence analysis. Nucleotide sequence analysis of the glycoprotein-D gene showed 99.7% homology to the Banffshire strain of CvHV-1 and 89.5%, 89.2%, 85.3% and 79.6% homology to bovine herpesvirus 1.2 (BoHV-1.2), bovine herpesvirus 1.1 (BoHV-1.1), cervine herpesvirus-2 (CvHV-2) and caprine herpesvirus-1 (CpHV-1), respectively. CONCLUSION: This is the first time that CvHV-1 has been isolated in New Zealand. Its inclusion in serological surveys will allow the prevalence of CvHV-1 in the red deer population to be assessed in this country. The clinical significance of CvHV1 infection in New Zealand red deer herds has yet to be determined.     

The DNA of an IPV strain of bovid herpesvirus 1 in sacral ganglia during latency after intravaginal infection

Two calves were inoculated intravaginally with a strain of bovid herpesvirus type 1 (BHV-1, IBR/IPV) isolated from a cow with infectious pustular vulvovaginits (IPV). The animals were killed during a latent stage of infection as characterized by seroconversion, absence of virus shedding and recrudescence of virus shedding after dexamethsone treatment.IPV-virus DNA was detected in 9 out of 20 sacral ganglia of the 2 calves. Of the sections, 7.2% (n = 250) contained 1 cell with IPV-virus DNA, which was restricted to the nucleus of neurons. In agreement with findings on herpes simplex virus infections, the viral DNA of BHV-1 is harbored in the local sensory ganglia.Virological and serological implications of the latent IPV infection are discussed.     

Interferon-gamma response of PBMC indicates productive pseudorabies virus (PRV) infection in swine

In Chinese Meishan/German Landrace cross-bred swine F2 generation interferon gamma (IFN-gamma) production by peripheral blood mononuclear cells (PBMC) was determined directly ex vivo at different time points after survival of a virulent pseudorabies virus (PRV) infection. This reactivity was compared with the reactivity of na?ve PBMC. Significant IFN-gamma production was determined in ELISA and ELISPOT only after in vitro PBMC re-stimulation with PRV and not with the closely related bovine herpesvirus BHV-1. The PRV-specific IFN-gamma secretion from re-stimulated PBMC showed high levels 6 days after infection, before the presence of serum antibodies, and it persisted at a high level over a 3 months period. The response of a group of eight piglets infected intranasally with PRV varied. Only two animals showed the expected typical fever response. PRV specific IFN-gamma production by PBMC clearly indicated that infection had occurred. Early significant IFN-gamma production by primed PBMC turned out to be a reliable and specific ex vivo marker for cellular response against productive PRV infection in swine before antibody formation.     

EHV-1 and EHV-4 infection in vaccinated mares and their foals

A silent cycle of equine herpesvirus 1 infection was described following epidemiological studies of unvaccinated mares and foals on a Hunter Valley stud farm. Following the introduction of routine vaccination with an inactivated whole virus equine herpesvirus 1 (EHV-1) and equine herpesvirus 4 (EHV-4) vaccine in 1997, a subsequent study identified excretion of EHV-1 and EHV-4 in nasal swab samples tested by PCR from vaccinated mares and their unweaned, unvaccinated foals. The current sero-epidemiological investigation of vaccinated mares and their young foals found serological evidence of EHV-1 and EHV-4 infection in mares and foals in the first 5 weeks of life. The results further support that EHV-1 and EHV-4 circulate in vaccinated populations of mares and their unweaned foals and confirms the continuation of the cycle of EHV-1 and EHV-4 infection.     

T-cell lymphoproliferative disorder in an aged rhesus macaque

A CD8+ T-cell leukemia was diagnosed in an aged female rhesus macaque. Although leukemia and lymphoma in nonhuman primates are commonly associated with simian T-lymphotropic virus, gibbon ape leukemia virus, oncogenic herpesviruses, and types C, D, and E retroviruses, this monkey was not infected with any of these viruses. However, the monkey did have antibodies against herpesvirus saimiri. This likely represents cross-reactivity of the herpesvirus saimiri assay with rhesus monkey rhadinovirus (RRV) antibodies; RRV was first described in rhesus macaques that were identified as having antibodies against herpesvirus saimiri. Rhesus rhadinovirus is a gamma herpesvirus, related antigenically to herpesvirus saimiri and Kaposi's sarcoma-associated herpesvirus (KSHV), which have been linked to lymphoproliferative disorders in primates and humans, respectively. Moreover, an oncogene has been recently identified in the RRV genome that is equivalent in position to the herpesvirus saimiri and KSHV oncogenes. Presently, the association of RRV infection with disease in nonhuman primates is unknown.     

Vulvovaginitis of goats due to a herpesvirus

Two concurrent outbreaks of genital disease in goats were associated with infection by a herpesvirus that was isolated from vulval and vaginal lesions of affected does. Serum neutralising antibody to the virus was present both in goats with the clinical disease and some unaffected goats. Of 19 goat herds examined only 4 had serum neutralising antibody positive goats with low (5%) to high (60%) incidence of infection. The virus isolate was characterised as a herpesvirus on its physico-chemical and morphological features. It contained DNA and was inactivated at low pH and by treatment with lipid solvents and trypsin. The virus particles were icosahedral, consisting of a nucleocapsid surrounded by an envelope membrane and measured approximately 150 nm in diameter. The virus was serologically related to a New Zealand isolate of caprine herpesvirus (NZ-CpHV), associated with similar genital disease, and was distinct from bovine herpes virus-1 (BHV-1) showing a one way neutralisation pattern.     

The protective antigens of equine herpesvirus type 1.

Equine herpesvirus type 1 was cultivated in swine testis cell cultures and partially purified by differential centrifugation and centrifugation in a linear sucrose density gradient. The viral envelope was separated from the nucleocapsid by treatment with Rexol 25J followed by sucrose gradient centrifugation. The envelope and nucleocapsid preparations were then electrophoresed in polyacrylamide gel after solubilization with sodium dodecyl sulphate. Hamsters were immunized with various preparations of the partially purified virus, including live or inactivated equine herpesvirus type 1 and viral envelope and nucleocapsid, all derived from the Kentucky D strain of the virus. Challenge of the immunized hamsters, with a hamster-adapted strain of equine herpesvirus type 1 demonstrated protection only in those animals which had been vaccinated with envelope-containing materials. When vaccination was carried out with fractions of electrophoresed envelope or nucleocapsid, protection was induced only by polypeptides of high molecular weight containing a glycoprotein component of the envelope of equine herpesvirus type 1.     

Encephalitis induced by bovine herpesvirus 5 and protection by prior vaccination or infection with bovine herpesvirus 1.

Calves were intranasally challenged with bovine herpesvirus 5 (BHV5) and followed for the development of viral infection, clinical encephalitis, histologic lesions in the brain, and viral sequences in the trigeminal ganglia. Calves that were previously vaccinated with bovine herepesvirus 1 (BHV1, n = 4) or previously infected with BHV1 (n = 5) or that had not been exposed to either virus (n = 4) were compared. No calf developed signs of encephalitis, although all calves developed an infection as indicated by nasal secretion of BHV5 and seroconversion to the virus. Histologic lesions of encephalitis consisting of multifocal gliosis and perivascular cuffs of lymphocytes were observed in calves not previously exposed to BHV1. BHV5 sequences were amplified from the trigeminal ganglia of calves previously vaccinated and from calves not previously exposed to BHV1; calves sequentially challenged with BHV1 and later BHV5 had exclusively BHV1 sequences in their trigeminal ganglia. Administration of dexamethasone 28 days after BHV5 challenge did not influence clinical disease or histologic lesions in either previously unexposed calves (n = 2) or previously immunized calves (n = 2), although it did cause recrudescence of BHV5, as detected by nasal virus secretion.