Preferred citation: Anipedia, JAW Coetzer and P Oberem (Directors) In: Infectious Diseases of Livestock, JAW Coetzer, GR Thomson,
NJ Maclachlan and M-L Penrith (Editors). B Murphy, D Knowles and M Highland, Visna-maedi, 2018.


Previous authors: D W VERWOERD AND R C TUSTIN

Current authors:
D P KNOWLES - Research Leader, DVM, PhD, DACVP, Department of Veterinary Microbiology and Pathology, Washington State University, 405 Bustad Hall, Pullman, Washington, 99164, USA
B G MURPHY - Associate Professor, DVM, PhD, Dip ACVP, VetMed PMI, 4206 VetMed, 3A One Shields Ave, Davis, California, USA
M A HIGHLAND - Veterinary Medical Officer - Researcher/Scientist, DVM, PhD, Diplomate ACVP, USDA-ARS-ADRU, Washington State University, 405 Bustad Hall, Pullman, Washington, 99164, USA


Visna-maedi, one of the so-called slow viral diseases of sheep, is caused by a non-oncogenic retrovirus of the Lentivirus genus. The Icelandic name denotes the two most common forms of the disease, maedi referring to the respiratory form of the disease (“breathlessness”, chronic interstitial pneumonia) and visna referring to the neurologic form of the disease (“wasting”, demyelinating leukoencephalomyelitis).  Two other disease syndromes, 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.15, 17

It was first described in 1915 in South Africa by Mitchell,38 who regarded the condition as an aberrant form of jaagsiekte (see Jaagsiekte), followed by reports of disease in the state of Montana (USA).11, 36 The confusion with pulmonary adenomatosis (jaagsiekte) caused by Mitchell’s report was resolved by De Kock,20 who was the first to realize that they were two distinct diseases, often coexisting in the same animal. Chronic pneumonia, named Graaff-Reinet disease after the town in which the experimental station was located, and where the diseased animals were located.

In Iceland, the introduction of visna-maedi virus (VMV) was traced to the importation in 1933 of Karakul rams from Germany, one of which carried both visna-maedi and jaagsiekte viruses.44 Sigurdson and collaborators first isolated VMV in 1960. Most of the early work on visna-maedi was done in Iceland, where it was initially considered to be two separate diseases.49


Visna-maedi virus is closely related to the caprine arthritis encephalitis virus (CAEV) of goats (see Caprine arthritis-encephalitis). Both diseases have been reviewed elsewhere.4, 8, 37, 42, 45, 48, 49 Visna-maedi virus and CAEV are genetically and pathogenically closely related.  These viruses share a predictable tropism for specific anatomic locations including joint synovium, tissues of the central nervous system (brain and spinal cord), lung, and mammary gland.  Visna-maedi virus and CAEV also share a common tropism for histiocytic cells (monocytes, macrophages and dendritic cells) and do not infect CD4 T cells as is the case with the immunosuppressive lentiviruses such as the human immunodeficiency viruses.  Well- documented cross-species transmission of CAEV and VMV between sheep and goats has resulted in a collective designation of these viruses as small ruminant lentiviruses (SRLV).37 Although capable of cross-infecting their mammalian hosts and genetically recombining, VMV and CAEV have a predisposition for either sheep or goats, respectively.

Mature virions are 80 to 100 nm in diameter.  Each virus particle contains two copies of the 8.4 to 9.2 kb long single stranded RNA genome. As is the case in all members of the Retroviridae, VMV replicates via a proviral DNA intermediate generated from the viral RNA genome through the viral reverse transcriptase enzyme.  The genome contains three well conserved genes: the env gene that encodes the envelope glycoprotein, the gag gene coding for the three core proteins surrounding the viral nucleic acid, the pol gene that codes for the viral RNA-dependent DNA polymerase (reverse transcriptase) and several other viral enzymes. The structural proteins of SRLV include the surface (SU) and transmembrane (TM) proteins (both encoded by env) and CA, MA and NC (encoded by gag).  In addition to the gag-pol-env genes present in all retroviruses, VMV has three additional open reading frames (vif, vpr-like and rev) which play a role in regulating viral replication.8, 49 The vpr-like gene was formerly referred to as tat, but is now thought to be functionally analogous to the vpr gene of the immunodeficiency viruses.


With the exception of Australasia, ovine lentiviruses have been isolated from all the major sheep-producing countries, and are often found with jaagsiekte (sheep pulmonary adenomatosis). They also occur in areas with a very low prevalence of jaagsiekte, such as the USA,12 and were responsible for large-scale mortalities in Iceland after the eradication of jaagsiekte.44 Studies of concurrent infections with the viruses causing visna-maedi and jaagsiekte reveal an increase in the seroprevalence of VMV antibodies in flocks affected by jaagsiekte. This effect was independent of other factors such as breed of sheep or size of flock. It was concluded that jaagsiekte plays a role in the replication and/or spread of VMV, although a synergistic effect of the simultaneous infections on the expression of concurrent lesions does not seem to occur.18, 29, 50

Differences in breed susceptibility to SRLV have not been found in South Africa, but have been reported elsewhere.17, 60


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