Characterization of Exogenous Type D Retrovirus from a Fibroma of a Macaque with Simian AIDS and Fibromatosis

Abstract

A novel type D retrovirus was isolated by cocultivation of explants of fibromatous tissue from a rhesus monkey (Macaca mulatta) with immunodeficiency and retroperitoneal fibromatosis. This type D virus, isolated from a macaque with simian acquired immunodeficiency syndrome (SAIDS-D/Washington), is exogenous and is partially related to the Mason-Pfizer and the langur monkey type D viruses. The SAiDS-D virus can be distinguished from all other primate retroviruses by antigenicity and molecular hybridization. Nucleic acid hybridization studies reveal that the origin of the SAIDS-D isolate may reside in Old World monkey (subfamily Colobinae) cellular DNA.

Asymptomatic Infection of the Central Nervous System by the Macaque Immunosuppressive Type D Retrovirus, SRV-1

“…SRV-1 and MPMV are closely related serotypes whereas SAIDS-D/Washington is a more distant relative (serotype 2) showing only about 60~ similarity in predicted amino acid sequences of the external envelope protein gene. This difference in envelope genes may account for the unique ability of SAIDS-D/Washington and other type D retroviruses in serogroup 2 to induce retroperitoneal fibromatosis, an aggressive proliferation of fibrous tissue in the abdominal cavity (Giddens et al, 1985;Stromberg et al, 1984). Differences in the envelope could also account for the ability of this virus to infect the brain parenchyma.…”

“…Two related type D retroviruses, Mason-Pfizer monkey virus (MPMV), the prototype type D retrovirus (Chopra & Mason, 1970) and SAIDS-D/Washington (an isolate from the Washington Primate Research Center) (Stromberg et al, 1984), have previously been detected in the CNS (Fine et al, 1975;Tsai et al, 1987). Each of these type D retroviruses was isolated from the CSF of one animal.…”

Virus Load and Sequence Variation in Simian Retrovirus Type 2 Infection

“…Disease caused by the more commonly found SRV-2 infection in macaques is characterized by diarrhea, fever, chronic weight loss, anemia, and sometimes retroperitoneal fibromatosis, a tumor of connective tissue origin (21). As in SIV infection, secondary opportunistic infections often develop in diseased monkeys (13,25).Type D retroviruses emerged as serious pathogens associated with immune deficiency between 1983 and 1985 to devastating effect in primate centers across the United States, including those in New England, California, Oregon, and Washington (7,21,30). The prevalence of type D retrovirus infection in these breeding colonies reached epidemic proportions; in the California Primate Center, for example, almost all adult macaques were infected with either SRV-1 or SRV-2 and the mortality rate among juveniles less than 2 years of age approached 50% (17).…”

“…They infect various Asian macaque species and can cause a fatal immune deficiency (7,11,12,13,22,30), similar to that induced by simian immunodeficiency virus (SIV) in macaques. Of the five simian retrovirus neutralization serotypes identified (SRV-1 to SRV-5), three (SRV-1 to SRV-3) have been molecularly cloned and genomically sequenced (27,29,34).…”

Trans-activation of Long Terminal Repeat Sequence-mediated Gene Expression Is Not a Property of Type D Retrovirus Replication

“…NE-LTR was digested with HindlII and the 1.1 kb fragment cloned into the HindllI site of pSVO-CAT (Gorman et al, 1982b) (Power et al, 1986;Sonigo et al, 1986). Also, a magnesium preference of the reverse transcriptase is shown by all retroviruses that have been found thus far to trans-activate, and the type D retroviruses also have a magnesium-preferring reverse transcriptase (Rho et al, 1981 ;Rey et al, 1984;Stromberg et al, 1984). Furthermore, type D retroviruses are similar to some of the known trans-activating retroviruses in their ability to induce a chronic immunodeficiency syndrome .…”