Experimental infection of rhesus monkeys with type D retrovirus.

Journal of Virology (Impact Factor: 4.65). 12/1984; 52(2):683-6.
Source: PubMed

ABSTRACT The naturally occurring immunodeficiency syndrome of macaque monkeys is an important animal model for the acquired immunodeficiency syndrome in humans. A new type D retrovirus, distinct from Mason-Pfizer monkey virus, has been isolated from affected animals at the New England Regional Primate Research Center. We now report the results of experimental infection of macaques with retrovirus D/New England after 13 months of study. Inoculated macaques developed lymphadenopathy without follicular hyperplasia, profound neutropenia, and a transient decrease in peripheral blood lymphocyte blastogenic responsiveness. Despite our varying the strain of virus, the manner in which the virus was grown, the size of the inoculum, and the age of the inoculated animals, infected macaques have not developed opportunistic infections or profound, prolonged loss of T cell function, key features of the macaque immunodeficiency syndrome. Therefore, experimental infection of naive macaques with D/New England has not reproduced the naturally occurring macaque immunodeficiency syndrome.

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    ABSTRACT: We haveisolated a molecular cloneofthefull-length integrated provirus ofsimianacquired immune deficiency syndrome retrovirus serotype 1(SRV-1) froma fatal caseofsimianacquired immunedeficiency syndrome inajuvenile rhesus macaque.An integrated SRV-1provirus was cloned, sequenced, andfoundto contain fourlarge openreading framesencoding gag-precursorprotein, protease, polymerase, andenvelope. Theproviral clone was transfected intoD17canine osteosarcoma cells andfoundtoproduce infectious virus. A comparison ofthesequencesofthisclone witha noninfectious cloneshowed20differences, resulting in10 aminoacidchanges. Also, a cluster ofexchanges, shortinsertions, anddeletions inthe5'leader sequences resulted inextension ofthetRNALYSprimer-binding sitefrom14to19nucleotides. Virusisolated from transfected cells was showntobeinfectious andpathogenic, resulting indisease thatfollowed thesame time courseandmortality asdisease induced byuncloned, invitro cultivated virus isolated fromdiseased animals. Theseresults unequivocally showthat atypeD retrovirus (SRV-1) causesafatal immunosuppressive syndrome inrhesus monkeys. A typeD retrovirus, simian acquired immunedeficiency syndrome (SAIDS) retrovirus serotype 1(SRV-1), hascon- sistently beenassociated withSAIDSoccurring spontane- ously inrhesus monkeys (Macacca mulatta) attheCalifornia Primate Research Center (19, 20,21). Thisfatal immunosup- pressive disease wasexperimentally transmitted torhesus monkeyswithtissue culture-derived virus. Animals with terminal disease hadavariety ofclinical signs ofSAIDS,
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    ABSTRACT: Simian retrovirus type D (SRVD) is a naturally occurring betaretrovirus in nonhuman primates of the genus Macaca. Infection can lead to a variety of clinical, hematologic, and histopathologic abnormalities. We report an unusual clinical presentation of facial paralysis and histologic lymphocytic neuritis in an SRVD type 2 (SRVD2)-infected rhesus macaque (Macaca mulatta) with a catheter-associated vena caval thrombus, anemia, thrombocytopenia, and multisystemic lymphoid hyperplasia. At initial presentation, a right atrial mass was detected by echocardiography. The macaque was clinically asymptomatic but had persistent anemia, thrombocytopenia, hyperglobulinemia, and later neutropenia. It was seropositive for SRV and PCR-positive for SRVD 2. Approximately 1 mo after initial presentation, the macaque developed right facial paralysis and was euthanized. Histologic lesions included lymphoplasmacytic aggregates affecting multiple organs, consistent with SRV-related lymphoid hyperplasia. The right facial nerve showed lymphoplasmacytic inflammation. The nerve itself was negative immunohistochemically for SRV antigen, but antigen was present infrequently in pericapillary lymphoid cells within the facial nerve and abundantly within lymphoid aggregates in the adjacent parotid salivary gland, bone marrow, and soft tissue. Known neurotropic viruses could not be identified. Given the widespread inflammation in this macaque, particularly in the area surrounding the facial nerve, lymphocytic neuritis and facial paralysis likely were an indirect effect of SRV infection due to local extension of SRV-related inflammation in the surrounding tissue.
    Comparative medicine 01/2011; 61(6):538-45. · 0.76 Impact Factor

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