INTRODUCTION

frederik widen¹ and carlos g. das neves²

¹National Veterinary Institute (SVA) and Swedish University of Agricultural Science, Uppsala, Sweden

²Norwegian School ofVeterinary Science, Department of Food Safety and Infection Biology, Section of Arctic Veterinary Medicine, Tromso, Norway

Herpesvirales is a vast order of currently approximately 130 large enveloped DNA virus species divided into three families.

Morphologically, herpesviruses are distinct from all other viruses, with a linear, double-stranded DNA genome of 125—250kbp contained within an icosadeltahedral capsid of 100 to 110 nm and containing 162 capsomers. This capsid is surrounded by an amorphous-looking, protein matrix, with variable thickness, called the tegu­ment and then by a trilaminar envelope containing lipids and proteins, bringing the total size of the virion from 120 nm up to almost 300 nm. The presence of lipids in the envelope has practical implications, as it renders her­pesviruses sensitive to detergents and lipid solvents. There are numerous spikes of glycoproteins protruding from the envelope. These spikes are more numerous and shorter than in other virus families. The variation in the size of the genome is to some extent attributed to the presence of internal and terminal repeats. Common to all herpesvi­ruses is that they are complex and contain genes for a large number of enzymes necessary for their replication, that viral DNA synthesis and capsid formation takes place in the nucleus of the infected cell, and that infected cells are destroyed owing to the virus replication and release of virus progeny, together with the ability of herpesviruses to establish latent infections.

The order Herpesvirales can be divided into three fami­lies: the family Herpesviridae contains the viruses of mammals, birds and reptiles; the family Alloherpesviridae contains fish and frog viruses; and the family Malacoherpes- viridae contains the bivalve virus. The family Herpesviridae, which includes approximately 79 known virus species so far, is further subdivided into three subfamilies: A lphaher- pesvirinae, Betaherpesvirinae and Gammaherpesvirinae.

Alphaherpesviruses are characterized by a rather broad host range, short replication cycle, rapid destruction of infected cells and a rapid spread in the host. Furthermore, they have the ability to establish life-long latent infection in sensory ganglia, or sometimes in other ganglia. Alphaher­pesviruses are known to cause several acute diseases of veterinary importance.

Infectious Diseases of Wild Mammals and Birds in Europe, First Edition. Edited by Dolores Gavier-Widen, J. Paul Duff, and Anna Meredith. © 2012 Blackwell Publishing Ltd. Published 2012 by Blackwell Publishing Ltd.

By contrast, betaherpesviruses, often called cytomegalo­viruses, have a restricted host range, long replication cycle and a slow spread of infection, with latent or persistent infections possible in a range of tissues, e.g. lymphoreticu- lar cells, secretory glands and kidneys. Infection usually results in significant enlargement of certain cell types, known as cytomegaly. Infections are often widely distrib­uted in the host population and usually not clinically apparent, except when such a virus appears in a previously uninfected herd.

Gammaherpesviruses usually have a host range restricted to the host’s family or order. Viruses of this subfamily have specificity for either B- or T-lymphocytes and may cause lymphoproliferative disease. Latency of gammaherpesvi­ruses may be established in lymphoid tissue. Infections with viruses from this subfamily generally cause few clini­cal signs in the main host but may cause severe disease in other related species, as exemplified by malignant catarrhal fever.

The ability of herpesviruses to cause latent infections is of great epidemiological importance, as it is generally not possible to determine or confirm if an animal is latently infected owing to the almost complete absence of gene expression, viral replication or host immune response during latency. Thus, diagnostic assays usually do not detect latent infections. A latent infection can, however — under certain conditions such as in the presence of con­current disease, stress, immunosuppression or hormonal changes — reactivate, resulting in a productive infection with excretion of viral particles, transmission and infection of susceptible animals.