Small Ruminant Lentiviruses and Human Immunodeficiency Virus: Cousins that Take a Long View

Abstract

Small ruminant lentiviruses (SRLV) and human immunodeficiency viruses (HIV) are related retroviruses that cause multisystem disease usually over a long period of time. The viruses show similarities and differences in biological and pathogenic features. The basic retroviral genomic organization is complicated by the presence of a variable number of accessory genes in both viruses, though the structure is more complex in HIV. Both are mucosal pathogens, and infect cells of the monocyte-macrophage lineage. The main difference in cell tropism is that, unlike HIV, SRLV do not infect lymphocytes. A major feature of both pathogens is restricted replication and virus latency, which are partly responsible for the establishment of chronic infection usually lasting for life. The pathologies observed are similar in the early stages of both infections, and possibly following highly active anti-retroviral therapy (HAART). While the pathogenesis of HIV-induced disease during symptomatic stages is mainly due to secondary infections and neoplastic conditions, the early and post-HAART stages are associated with chronic inflammatory changes that resemble those found in SRLV diseases which are thought to be mediated by anti-virus immune responses.

Genetic subgroup of small ruminant lentiviruses that infects sheep homozygous for TMEM154 frameshift deletion mutation A4Δ53

“…Infections persist for the lifetime of the host, causing chronic inflammation and a slow progression to disease [5,6]. Common symptoms of SRLV infection in sheep include interstitial pneumonia with dyspnea, indurative mastitis, and cachexia [7].…”

Genome-Wide Association Identifies Multiple Genomic Regions Associated with Susceptibility to and Control of Ovine Lentivirus

“…Ovine lentivirus (OvLV), like the human immunodeficiency virus (HIV), is a macrophage-tropic lentivirus that leads to persistent, lifelong infection of the host [1], [2]. Seroprevalence of OvLV is 24–26% in U.S. domestic sheep, with positive animals in approximately half of all U.S. flocks [3], [4].…”

Retroviral Infections in Sheep and Goats: Small Ruminant Lentiviruses and Host Interaction

“…It is believed that SRLV proviral DNA escapes detection by the immune system by persisting in monocytes, thus allowing viral dissemination to target tissues. Furthermore, SRLVs may interfere with the function of effector cells implicated in the defense against the virus, such as macrophages and dendritic cells, altering the type of immune responses that are induced [5,11,17,55,56]. …”