Identification and localization of the structural proteins of anguillid herpesvirus 1

ABSTRACT: Many of the known fish herpesviruses have important aquaculture species as their natural host, and may cause serious disease and mortality. Anguillid herpesvirus 1 (AngHV-1) causes a hemorrhagic disease in European eel, Anguilla anguilla. Despite their importance, fundamental molecular knowledge on fish herpesviruses is still limited. In this study we describe the identification and localization of the structural proteins of AngHV-1. Purified virions were fractionated into a capsid-tegument and an envelope fraction, and premature capsids were isolated from infected cells. Proteins were extracted by different methods and identified by mass spectrometry. A total of 40 structural proteins were identified, of which 7 could be assigned to the capsid, 11 to the envelope, and 22 to the tegument. The identification and localization of these proteins allowed functional predictions. Our findings include the identification of the putative capsid triplex protein 1, the predominant tegument protein, and the major antigenic envelope proteins. Eighteen of the 40 AngHV-1 structural proteins had sequence homologues in related Cyprinid herpesvirus 3 (CyHV-3). Conservation of fish herpesvirus structural genes seemed to be high for the capsid proteins, limited for the tegument proteins, and low for the envelope proteins. The identification and localization of the structural proteins of AngHV-1 in this study adds to the fundamental knowledge of members of the Alloherpesviridae family, especially of the Cyprinivirus genus.     

Healing of Cortical Bone Grafts in the Dog The Role of Azathioprine

Sixteen unrelated beagles, randomly divided into groups of four, were used in evaluating the role of therapeutic immunosuppression in the healing of fresh cortical bone allografts over a 16-week period. The four groups included: nontreated allograft, treated allograft, nontreated autograft, and treated autograft. A 2.7-cm tibial cortical graft was fixed orthotopically using a dynamic compression plate. Healing was evaluated by radiography and by gross and histologic studies at 2, 4, 8, and 16 weeks after surgery. The treated dogs were immunosuppressed with azathioprine for eight weeks postsurgery. The conclusions were that: temporary immunosuppression did not significantly alter healing of fresh cortical bone autografts; healing of fresh cortical bone allografts in immunosuppressed dogs was similar to healing of fresh cortical bone autografts; slight differences were observed in the healing of bone grafts in all groups after eight weeks; and cellular reaction typical of graft rejection was found in nontreated allografts, but healing still occurred.     

Current Techniques for Evaluation of Spinal Cord Injury

Spinal cord injuries have been evaluated in the past chiefly on the basis of subjective tests. New electronic techniques are now coming into clinical use which allow objective testing of afferent and efferent conduction through long spinal cord tracts. With continued research, it is probable that diagnosis and prognosis of spinal cord injuries can be made with a high degree of confidence.     

Fibrotic Myopathy of the Semitendinosus Muscle in Four Dogs

Fibrosis of the semitendinosus muscle resulted in a characteristic gait abnormality in four male German shepherd dogs. Blood chemistry, electrophoresis, and electromyographic studies were performed. Surgery was undertaken in each case to relieve the restricting fibrous tissue. The lameness returned with reappearance of the fibrous band within six months. The etiology of fibrotic myopathy is unknown, but electromyographic studies and electrophoresis results suggest a myopathy due to chronic inflammation. Histopathologic exam reveals replacement of degenerating muscle fibers with connective tissue.     

SIMULATED NATURAL INFECTION OF CHICKENS WITH AUSTRALIAN LENTOGENIC NEWCASTLE DISEASE VIRUS AND SUBSEQUENT CHALLENGE WITH VIRULENT VIRUS

A total of 291 eight-week-old chickens were exposed to chickens infected with either of two Australian lentogenic strains (V4 and AVL NDV-1) of Newcastle disease virus (NDV). At 3 weeks after exposure, all chickens exposed to V4 infected chickens had developed haemagglutination-inhibition (HI) antibody. All chickens exposed to AVL NDV-1 virus infected chickens had developed HI antibody 5 weeks later. This sudden late appearance of HI antibody, to titres higher than those observed with V4 chickens, was explained by V4 virus being introduced to the AVL NDV-1 group of chickens. When groups of these chickens were challenged with Roakin virus (mesogenic NDV) at 3 weeks and Fontana 1083 virus (viscerotropic velogenic NDV) and Texas GB virus (neutrotropic NDV) at 3, 5, 10 and 21 weeks only three chickens developed clinical illness one of which died. These chickens were one AVL NDV-1 chicken contact challenged with Fontana 1083 virus at 3 weeks, one V4 chicken oronasally challenged with Texas GB virus at 5 weeks and one V4 chicken challenged oronasally with Fontana 1083 virus at 10 weeks. Susceptible non-vaccinated chickens died soon after challenge. Challenge by oronasal infection with 10(7.0) ELD50 of virus or contact with susceptible infected chickens enabled virulent virus to be isolated from most chickens and was accompanied by a large anamnestic increase in serum HI antibody.