Small ruminant lentiviruses: Strain variation, viral tropism, and host genetics influence pathogenesis

Authors: Highland, Margaret

Submitted to: Veterinary Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/18/2017
Publication Date: 4/25/2017
Citation: Highland, M.A. 2017. Small ruminant lentiviruses: Strain variation, viral tropism, and host genetics influence pathogenesis. Veterinary Pathology. 54(3):353-354.

Interpretive Summary: This is a brief (approximately 1000 words) invited guest editorial for publication in Veterinary Pathology. The purpose of this publication is to bring attention to the agricultural importance of Small Ruminant Lentiviruses (SRLV) and provide general insight into the biology of infection by these viruses, based on what is currently reported in peer-reviewed scientific literature. This insight includes providing the reader with a perspective on how both the strain of the virus and host factors impact the type and severity of disease the virus causes in the host. Different SRLV strains can cause vastly different disease entities such as pneumonia, encephalitis, arthritis, and mastitis. The type and severity of disease induced by SRLV infection can also depend on the host species (sheep versus goat), as well as breed and/or genetic variation of the host. Understanding both SRLV strain and host differences is important in understanding best practices for diagnosing infection, understanding routes of transmission, and mitigating transmission between susceptible hosts.

Technical Abstract: Small Ruminant Lentiviruses (SRLV), which include the Maedi-Visna virus, also known as ovine progressive pneumonia virus (OPPV), and caprine arthritis and encephalitis virus (CAEV), are of global economic importance to sheep and goat producers, respectively. These viruses belong to the genus Lentivirus, of the Retroviridae family, and are characterized by a single-strand RNA genome that is associated with reverse transcriptase protein, enclosed within a capsid, and surrounded by an envelope that holds glycoproteins important for attachment and invasion of host cells of the monocyte lineage. Given the simplicity of these viruses, SRLV are biologically fascinating in their ability to induce differing disease presentations, as their viral names elude to. Infection is lifelong, and as the genus nomenclature implies ("lentus", Latin for slow), these viruses cause slowly progressive (months to years) disease, which may or may not manifest clinically within the host's lifetime. Disease manifestations include chronic progressive pneumonia, encephalitis, arthritis, and mastitis. Mammary and pulmonary tissue tropism provide routes of viral shedding and transmission from the infected host to offspring and other susceptible hosts. Unfortunately for the hosts and agricultural entities, slow progression of disease with shedding from asymptomatic hosts and characteristic low fidelity viral reverse transcriptase resulting in antigenic drift make these viruses quite successful and difficult to control. In light of the research by Pinczowski, et al., published in this issue of Veterinary Pathology, this editorial provides a general overview on ways in which host and viral genetics and tissue tropism influence pathogenesis and impact disease control measures.