The maedi-visna virus (MVV) is classified as a lentivirus of the retro
viridae family. The genome of MVV includes three genes: gag, which enc
odes for group-specific antigens; pol, which encodes for reverse trans
criptase, integrase, RNAse H, protease and dUTPase and env, the gene e
ncoding for the surface glycoprotein responsible for receptor binding
and entry of the virus into its host cell. In addition, analogous to o
ther lentiviruses, the genome contains genes for regulatory proteins,
i.e. vif, rev and tat. The coding regions of the genome are flanked by
long terminal repeats (LTR) which play a crucial role in the replicat
ion of the viral genome and provide binding sites for cellular transcr
iption factors. The organs targeted by MVV are, in descending order of
importance, the lungs, mammary glands, joints and the brain. In these
organs, the virus replicates in mature macrophages and induces slowly
progressing inflammatory lesions containing B and T lymphocytes. The
clinical signs of MVV infection, i.e. dyspnea, loss of weight, mastiti
s and arthritis, are related to the location of these lesions. Infecti
on with MVV induces the formation of antibodies which can be detected
by agar gel immunodiffusion, ELISA and the serum neutralization assay.
As neither antiviral treatment nor vaccination is available, diagnost
ic tests are the backbone of most of the schemes implemented to preven
t the spread of MW. However, since current serological assays are stil
l lacking in sensitivity and specificity, molecular biological methods
are being developed permitting the detection of virus in peripheral b
lood, milk and tissue samples. Future research will have to focus on b
oth the development of new diagnostic tests and a better understanding
of the pathogenesis of MW infection. (C) Inra/Elsevier, Paris.