Maedi-Visna virus: current perspectives

Abstract

Maedi-Visna virus (MVV) and caprine arthritis-encephalitis virus are commonly known as small ruminant lentiviruses (SRLVs) due to their genetic, structural, and pathogenic similarities. They produce lifelong lasting infections in their hosts, which are characterized by slow progression till overt disease happens. There are four major clinical forms derived from a chronic inflammatory response due to the constant low grade production of viruses from monocyte-derived macrophages: respiratory (caused by interstitial pneumonia), mammary (which may produce a decrease in milk production due to subclinical mastitis), joint (characterized by lameness), and neurological (characterized by chronic nonpurulent meningoencephalomyelitis). There are three levels which try to eliminate the virus: cellular, body, and the flock level. However, SRLVs have ways to counteract these defenses. This review examines some of them.

Keywords: genetic resistance; immune response; molecular biology; small ruminant lentivirus.

Figure 1

Schematic representation of an SRLV particle. Notes: The viral genome, along with the enzymes necessary for transcription, integration, and maturation, is encapsidated inside the core formed by capsid proteins. This is surrounded by the matrix and by the lipid bilayer in which the envelope glycoproteins are inserted. Abbreviation: SRLV, small ruminant lentivirus.

Figure 2

Schematic representation of the gene distribution in the proviral genomes of MVV and CAEV. Notes: In the provirus, the viral DNA is flanked by the LTR, which governs transcription of the genome. In the image, the essential genes are shown in the middle and the accessory genes are shown on the right. Abbreviations: CAEV, caprine arthritis and encephalitis virus; LTRs, long terminal repeats; MVV, Maedi-Visna virus.

Figure 3

Mechanism by which APOBEC3 induces G-to-A mutations and counteraction by SRLV Vif. Notes: APOBEC3 produces deamination of C, leading to U, which is reverse transcribed into A. However, SRLV Vif is able to degrade APOBEC3, circumventing this defense mechanism. Abbreviation: SRLV, small ruminant lentivirus.

Figure 4

Mechanism of action of interferon in virus-infected cells. Notes: When the cell senses viral presence, signaling pathways are triggered, which reach the nucleus. Certain molecules can stimulate ISRE, which activates the transcription of factors rendering the cell into an antiviral state. Data from Ballesteros. Abbreviations: ISRE, interferon-sensitive response element; IRF, interferon-response factor; ISGF, interferon-stimulated growth factor; TLR, toll-like receptor.

Figure 5

Stimulation of transcription by steroid hormones (represented by yellow triangles). Notes: Steroid hormones are able to freely cross the plasma membrane and combine with the receptor (represented by gray forms). The best-studied mechanism involves that the hormone–receptor complexes cross the nuclear membrane and react with HREs, triggering transcription. Abbreviations: HREs, hormone response elements; GRE, glucocorticoid responsive element; ERE, estrogen responsive element.