Maedi-visna (MV), one of the so-called slow virus diseases of sheep, is caused by a non-oncogenic retrovirus of the subfamily Lentivirinae. The Icelandic name denotes the two most common forms of the disease, maedi (dyspnoea) referring to the progressive interstitial pneumonia, and visna (wasting) to the chronic encephalitic form. Arthritis and chronic mastitis are more rarely seen. The disease is also known as ovine progressive pneumonia or Montana sheep disease in the USA, zwoegersiekte in the Netherlands, la bouhite in France, and Graaff-Reinet disease in South Africa.16, 18

It was first described in 1915 in South Africa by Mitchell, 42 who regarded the condition as an aberrant form of jaagsiekte, followed by reports from Montana.12, 41 The confusion with pulmonary adenomatosis (jaagsiekte) caused by Mitchell’s report was resolved by De Kock,21 who was the first to realize that they were two distinct diseases, often coexisting in the same animal. The chronic pneumonia was named Graaff-Reinet disease after the town in which the experimental station was situated from where the diseased animals were obtained.

After these initial reports the disease seemed to disappear, and South Africa was thought to be free of maedi-visna until a lentivirus was isolated in 1986 from the lungs of sheep suffering from jaagsiekte.50 A preliminary serological survey revealed a wide distribution of the virus but it seems to have lost its pathogenicity, which may explain its ‘disappearance’ during the intervening years. Alternatively, the latter isolate may represent a later introduction.

In Iceland, the introduction of maedi-visna virus (MVV) was traced to the importation in 1933 of Karakul rams from Germany, one of which carried both maedi-visna and jaagsiekte viruses.48 Most of the early work on maedi-visna was done in Iceland, where it was initially considered to be two separate diseases.54

A closely related and clinically similar disease in goats called caprine arthritis-encephalitis (CAE) is dealt with in a separate chapter (see Caprine arthritis-encephalitis). Both diseases have recently been reviewed elsewhere.7, 46, 52, 53, 54


The virulent MVV isolated in Iceland is the prototype of a large group of lentiviruses that have been recovered from sheep in various parts of the world. All, including isolates of ovine progressive pneumonia virus (OPPV) in the USA, the South African ovine maedi-visna virus (SA-OMVV) and caprine arthritis-encephalitis virus (CAEV), are serologically related, but there is considerable variation in their biological properties, including their pathogenicity. All strains give rise to the formation of syncytia in cell cultures, but they vary in their ability to induce cell lysis.59

The morphogenesis and morphology of the viral particles are quite distinct from those of jaagsiekte and other retroviruses. 33, 50 Virions bud with a crescent-shaped core and have no intermediate space between core and envelope. The immature particles thus formed have an electron-dense layer immediately below the viral envelope. Mature virions are 80 to 100 nm in diameter, are membrane-bound and have eccentric cores, sometimes surrounded by a clear intermediate layer. Negatively stained particles sometimes show short surface projections, but usually the surface is smooth.

Each virus particle contains two copies of the 35S singlestranded RNA genome of plus strand polarity. As is the case in all members of the Retroviridae, it replicates via a proviral DNA intermediate. The nucleotide sequence of the genome has been determined for Icelandic, South African and British strains of the virus,58, 63, 70 confirming differences between strains and a close relationship to the human immunodeficiency virus (HIV). The genome contains three genes that encode the major structural proteins of the virus: the env gene that encodes the envelope glycoprotein, the gag gene coding for the three core proteins and the pol gene that codes for the viral RNA-dependent DNA polymerase. In addition to the gag-pol-env genes present in all retroviruses, the lentiviruses have unique additional open reading frames between the pol and env genes which play a role in regulating viral replication.7, 54

The buoyant density of MVV is 1,15 g/ml, which is similar to that of most type C oncogenic retroviruses but different from jaagsiekte retrovirus (JSRV) and type D viruses, which are denser (1,18 g/ml). The polypeptide compositions of all the ovine lentiviruses are very similar, with four major viral proteins named gp135 (envelope), p25–30, p16 and p14.7, 52,53 The different lentivirus isolates cannot be distinguished serologically by conventional techniques such as immunodiffusion (which mainly detects the gp135 antigen), immunofluorescence, and enzyme-linked immunosorbent assay (ELISA). However, using a Western-blot technique, MVV strains were found to share both the p30 and p16 antigens, whereas CAEV antiserum only cross-reacts with the p30 of MVV and can therefore be distinguished from it.50 There is no serological relationship between lentiviruses and JSRV or other retroviruses.

A significant genetic divergence was demonstrated between MV, CAE and SA-OMV viruses by means of endonuclease restriction analysis, nucleic acid hybridization techniques and nucleotide sequence studies.50, 54, 58, 59 Hybridization...

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