Simian acquired immunodeficiency syndrome.
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Acquired Immunodeficiency Syndrome↗
Biomedical subjects
M B Gardner
Publications and source records attributed to M B Gardner.
Immunodeficiency in rhesus monkeys associated with the original Mason-Pfizer monkey virus.
The Mason-Pfizer monkey virus (MPMV) was reisolated from a cryopreserved sample of the original MPMV-containing rhesus breast carcinoma, and complete integrated MPMV provirus was detected in chromosomal DNA of this tumor. Reanalysis of the in vivo pathogenicity and molecular character of MPMV reisolated from the rhesus breast tumor and analysis of the original MPMV after long-term in vitro propagation in human and rhesus cells show that the original MPMV produces an acquired immunodeficiency similar to that caused by the recently described simian acquired immune deficiency syndrome type D retroviruses, and the MPMV genome and its immunosuppressive effect in vivo have remained stable despite prolonged in vitro passage in human and rhesus cells.
Acquired Immunodeficiency Syndrome↗
AIDS serology testing in low- and high-risk groups.
The performance characteristics of the acquired immunodeficiency syndrome (AIDS)-retrovirus serological tests including enzyme-linked immunosorbent assay (ELISA), Western blot, and immunofluorescence assay were defined in a clinical laboratory setting by testing 1,257 serum specimens from low- and high-risk groups for AIDS. The three prototype AIDS retroviruses (lymphadenopathy-associated virus, human T-lymphotropic virus III, and AIDS-associated retrovirus) were equally suitable as target antigen for these assays. Sera from six of 74 laboratory and health care personnel and 91 of 1,014 unselected blood donors were falsely positive by ELISA (positive to negative ratio [P/N], greater than or equal to 2) based on the lack of Western blot confirmation. Only two true-positives (two [0.2%] of 1,014 blood donors) were detected in these low-risk groups. In contrast, 106 of 108 specimens with ELISA P/N ratios of 2 or greater from the high-risk groups including asymptomatic homosexual men, hemophiliacs, AIDS-related complex patients, and AIDS patients were positive by Western blot and immunofluorescence assay. Four false-negative ELISA results based on positive immunofluorescence assay and Western blot were found in the AIDS patient group. Ten of 69 AIDS patients were negative by all three serological tests. The consequence of maintaining high sensitivity for the ELISA (P/N ratio, greater than or equal to 2) as a screening test was a loss of specificity. The number of false-positive results necessitated the use of a confirmation test with greater specificity.
Acquired Immunodeficiency Syndrome↗
Evaluation of commercial AIDS screening test kits.
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Acquired Immunodeficiency Syndrome↗
Myxoid chondrosarcoma with a translocation involving chromosomes 9 and 22.
Myxoid chondrosarcoma is an uncommon neoplasm thought to be derived from mesenchymal chondrocytic cells. Although cytogenetic abnormalities have been reported in sarcomas, too few cases have been studied to determine the frequency of nonrandom chromosomal changes in mesenchymal tumors. In this article, we describe a chondrosarcoma with a nonrandom reciprocal translocation t(9;22)(q22;q11). The cellular homologue to the retrovirus transforming gene of simian sarcoma virus is located on chromosome #22, and its possible significance in this case is discussed.
Chondrosarcoma↗
Monocyte function in rhesus monkeys with simian acquired immune deficiency syndrome.
Monocyte function in rhesus monkeys with simian acquired immune deficiency syndrome (SAIDS) was compared with that in age-matched normal juvenile rhesus monkeys. The functional tests were 1) chemotaxis, 2) phagocytosis of opsonized Candida albicans, 3) killing and/or growth inhibition of Candida albicans, 4) generation of respiratory burst, and 5) monocyte-derived macrophage response (morphology and/or respiratory burst) to stimulating agents such as lymphokines, gamma interferon, endotoxin, and phorbol myristate acetate. The monkeys tested had either clinical SAIDS (alive with lymphadenopathy, splenomegaly, and lymphopenia or neutropenia) or had terminal SAIDS (moribund due to the disease). Responses of monocytes from 14 monkeys with clinical SAIDS were indistinguishable from those of 9 normal juvenile rhesus monkeys, whereas monocytes from 3 monkeys with terminal SAIDS had enhanced phagocytosis and respiratory burst capacity. Chemotaxis, candidacidal/stasis activity, and response to stimulating agents were normal in these terminal cases. Plasma from the SAIDS monkeys was as capable of opsonizing yeasts and of being able to generate chemotactic factors by endotoxin as was control plasma. SAIDS retrovirus (SRV) was detected by co-cultivation of pure monocyte-derived macrophage cultures with Raji cells, an indicator cell line which forms syncytia in the presence of SRV. Four terminal SAIDS cases and one late-stage clinical SAIDS case were virus-positive when the number of macrophages in the cultures ranged from less than 50 to about 500. Terminal SAIDS monocyte-derived macrophages in culture as long as 17 days produced SRV. These data show that in monkeys with SAIDS the major effector functions of monocytes and macrophages involved in host defense are intact (even up until death). Additionally, some of the monocytes are productively infected, and these infected monocytes are viable and adherent in culture.
Acquired Immunodeficiency Syndrome↗
Immune defects in simian acquired immunodeficiency syndrome.
We recently reported a Simian Acquired Immunodeficiency Syndrome (SAIDS) in rhesus macaques at the California Primate Research Center. Here, we studied in vitro lymphocyte response to the mitogens Concanavalin A (Con A), phytohemagglutinin (PHA) and pokeweed mitogen (PWM) with and without interleukin 2 (IL-2). Immunoglobulin (IgG and IgM) and complement (C3 and C4) concentrations were determined by radial immunodiffusion. T helper and T suppressor lymphocytes were identified with the monoclonal antibodies OKT4 and OKT8. Concentrations of IgG and IgM were significantly (p less than .05) decreased. Complement component C3 did not change but C4 was increased. The absolute lymphocyte count decreased but the OKT4:OKT8 ratio was unchanged from controls. A decreased lymphocyte response to all mitogens occurred early and became more severely depressed near death. IL-2 caused a complete or partial restoration of the response to the mitogens CON A and PHA. Both the humoral and cell mediated immune responses are affected in SAIDS. The role of IL-2 in this immune defect must be studied further.
Acquired Immunodeficiency Syndrome↗
Ultrastructural comparison of the retroviruses associated with human and simian acquired immunodeficiency syndromes.
Three isolates of human acquired immunodeficiency syndrome (AIDS) virus (lymphadenopathy-associated virus, human T cell lymphotropic virus strain III, acquired immunodeficiency syndrome-associated retrovirus) were compared with simian AIDS virus by thin section transmission electron microscopy. Simian AIDS virus was found to form intracytoplasmic A particles and to bud by both ring forms and crescent shapes. The extracellular mature simian AIDS virus exhibited a cylindrical nucleoid within a tubular or conical core shell. The simian AIDS virus was morphologically indistinguishable from Mason-Pfizer monkey virus, the prototype D type retrovirus, although the two were readily distinguished by radioimmunoassay and restriction endonuclease mapping. All three AIDS virus isolates exhibited identical ultrastructure and maturation sequences. The AIDS viruses did not form intracytoplasmic A particles and budded only with crescent-shaped nucleoids. Mature extracellular AIDS viruses contained an eccentric spherical nucleoid within a conical or tubular core shell. AIDS virus was found to show many morphologic features of the retroviral subfamily Lentivirinae. The AIDS virus isolates appear to form a new group of retroviruses.
Acquired Immunodeficiency Syndrome↗
Mammary tumors in feral mice lacking MuMTV DNA.
Two mammary tumors developed in feral mice treated with dimethylbenzanthracene. The tumors, livers, and spleens of these animals contained no MuMTV proviral DNA. Neither tumor had amplified or rearranged int-1 or int-2 loci. This demonstrates that mammary tumorigenesis can occur in mice in the absence of endogenous and exogenous MuMTV.
9,10-Dimethyl-1,2-benzanthracene↗
Virus isolation studies in simian AIDS.
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Acquired Immunodeficiency Syndrome↗
Hyperplastic and neoplastic changes in the mammary glands of feral mice free of endogenous mouse mammary tumor virus provirus.
Laboratory colonies of feral mice (Mus musculus domesticus) have been established with specific mouse mammary tumor virus (MuMTV) genotype, including colonies lacking any proviral DNA (ev-) or carrying only a single copy of MuMTV DNA (ev+). No evidence of a decline in reproductive capacity has been observed in the first 8 generations. Both the ev- and ev+ mice showed normal mammary gland development and the development of hyperplastic lesions in the older females. The mice were very resistant to spontaneous or chemically induced mammary tumors. However, the occurrence of 1 mammary tumor in an ev- mouse indicates that mammary neoplasias can occur in the absence of MuMTV DNA. The few tumors that do occur in the ev- mice provide a unique opportunity to study the neoplastic process in the absence of proviral DNA.
Animals↗
Clinical features of simian acquired immunodeficiency syndrome (SAIDS) in rhesus monkeys.
A syndrome of acquired immunodeficiency has been identified in a group of rhesus monkeys (Macaca mulatta) which died at the California Primate Research Center. Clinical evaluation of these animals revealed that 50% or more had lymphadenopathy, weight loss, and diarrhea. At least 30% had splenomegaly, fever, cutaneous abscesses and/or arthritis/myositis. Two animals had fibrosarcomas. Anemia was seen in 19 animals, lymphopenia in 14, granulocytopenia in four and thrombocytopenia in three. Hepatitis was diagnosed histopathologically in 13. Electrophoresis revealed hypoproteinemia, hypoalbuminemia and hypogammaglobulinemia. Numerous bacterial, protozoal, and viral agents were identified including cytomegalovirus and leukocyte-associated herpesvirus. Pathologic lesions included severe post-reactive depletion of lymphocytes in germinal centers and paracortical regions of lymph nodes. Clinical and pathologic changes indicate an acquired immunodeficiency syndrome which has some similarities to AIDS in humans. This disease in monkeys may provide a model for studying that disease.
Acquired Immunodeficiency Syndrome↗
The pathology of an epizootic of acquired immunodeficiency in rhesus macaques.
A syndrome of acquired immunodeficiency within a group of outdoor-housed rhesus macaques (Macaca mulatta) with unusually high mortality has been identified at the California Primate Research Center. The cause of death for most of the affected animals included septicemia and/or chronic diarrhea with wasting, often complicated by other problems. In many cases, multiple or unusual infectious agents were isolated or recognized, including cytomegalovirus, Cryptosporidium spp., and Candida albicans. Septicemias due to usually innocuous agents such as Staphylococcus epidermidis and Alcaligenes faecalis were seen. Two animals developed cutaneous fibrosarcomas. Affected animals had generalized lymphadenopathy and splenomegaly, with depletion of T-cell populations, initially follicular hyperplasia followed by depletion, and absence of plasma cells. This spontaneous disease syndrome in nonhuman primates has similarities to acquired immune deficiency syndrome (AIDS) in humans, providing an animal model for the study of the complex factors modulating the immune system.
Acquired Immunodeficiency Syndrome↗
Epidemiologic aspects of an outbreak of acquired immunodeficiency in rhesus monkeys (Macaca mulatta).
Since August 25, 1981, an outbreak of simian acquired immunodeficiency syndrome ( SAIDS ) has been recognized in a single outdoor corral housing 77 rhesus monkeys (Macaca mulatta) over a 16-month period. The etiology of this syndrome is unknown but epidemiologic evidence suggests an infectious agent. Thirty-two cases of SAIDS have been identified (31 female, 1 male), and 27 of these animals have died (case fatality rate = 84%). Three of these deaths occurred among 13 infants born in the corral . All 27 deaths were females. For animals in the original cohort, sex was not a statistically significant risk factor. For animals born in the corral females were at greater risk (p = 0.0489; Fisher's Exact Test). SAIDS mortality rates were highest for animals entering the corral at less than 30 months of age (4.4 deaths per 100 monkey months of follow-up) and for animals born into the cage (3.3 deaths per 100 monkey-months of follow-up). The mortality rate was lowest for animals entering the corral at greater than 30 months of age, (0.32 deaths per 100 monkey-months of follow-up). No significant associations were found for the factors weaning history, cage-move history, parentage, generation, and medical history, including history of bite-wound trauma. Nine of the original 64 animals entering the corral on August 25, 1981, were previously associated with a group of 110 rhesus monkeys occupying this same corral from September 1976 to August 1981. Though less dramatic, a similar pattern of morbidity and high mortality was recognized retrospectively in this group.(ABSTRACT TRUNCATED AT 250 WORDS)
Acquired Immunodeficiency Syndrome↗
Isolation and characterization of new ecotropic murine leukemia viruses after passage of an amphotropic virus in NIH Swiss mice.
Amphotropic murine leukemia viruses (MuLV-A) cause mainly lymphoma in newborn inoculated NIH Swiss mice after a long latent period of 6-12 months. Rarely, however, about 1% of the inoculated mice develop hind limb paralysis and progressive central nervous system disease. The biological properties and RNase T1-resistant oligonucleotide fingerprints of the recovered viruses from tissues of both lymphomatous and paralyzed mice inoculated with MuLV-A were analyzed. These results indicate that serial in vivo passages of MuLV-A in NIH Swiss mice lead to generation of new MuLVs of both amphotropic and ecotropic host ranges. The recovered amphotropic viruses are highly lymphomagenic and are recombinants of MuLV-A-specific oligonucleotides and endogenous mouse sequences. The ecotropic viruses fall into two groups: (1) recombinants of MuLV-A genes and NIH Swiss mouse viral or cellular sequences and (2) new ecotropic viruses with oligonucleotide fingerprints not related to any of the known MuLVs. The naturally occurring ecotropic MuLVs of the wild mice produce both lymphoma and paralysis in NIH Swiss mice. The viruses recovered from in vivo passages are mainly of ecotropic host range although dual-tropic virus activity is occasionally seen in the spleens but not in the brains or spinal cords of the lymphomatous or paralyzed mice. Oligonucleotide fingerprinting of the recovered MuLV-Es from paralyzed mice are identical to the input MuLV-Es, indicating that the parental MuLV-E alone, without recombination, is responsible for the paralytic disease.
Animals↗
Experimental transmission of simian acquired immunodeficiency syndrome (SAIDS) and Kaposi-like skin lesions.
A disease that is similar to human AIDS may occur in monkeys. Simian AIDS (SAIDS) was experimentally transmitted from 2 rhesus monkeys dying of the disease to 4 cytomegalovirus (CMV) antibody-negative rhesus monkeys. The inocula consisted of the supernatant fluid from 10% homogenates of various tissues with or without buffy-coat cells from blood. Lymphadenopathy, splenomegaly, neutropenia, polymyositis, and other signs of the disease appeared in recipients within a few weeks after inoculation. Two animals developed Kaposi-like "patch" and "plaque" skin lesions and one died of sepsis and profound lymphoid depletion. A second animal also died with lymphoid depletion. All animals became infected with CMV but antibody levels were low in two animals, appeared and then disappeared in one, and never developed in the second monkey which died.
Acquired Immunodeficiency Syndrome↗
Resistance to fibroblasts and hematopoietic cells to ecotropic murine leukemia virus infection; an Akvr-1R gene effect.
A gene named Akvr-1 segregates as a dominant allele in California wild mice (LC). Unlike Fv-1 and Fv-2 restriction alleles, the Akvr-1 confers resistance to replication of all ecotropic (N-, B-, and NB-tropic) murine leukemia viruses (MuLV-E) and prevents endogenous AKR virus-induced lymphoma/leukemia in F1 hybrids of AKR x LC. We have tested fibroblasts and hematopoietic cells from mice of defined Akvr-1 genotypes for in vitro susceptibility to various MuLV infections. Our results indicated a dominant in vitro resistance of exogenously MuLV-E infected cells carrying Akvr-1R allele although resistance was stronger in the homozygous cells than in the heterozygous cells. Moreover, resistance of cells to virus replication was not abrogated by high multiplicities of infection or by growth stimulation of hematopoietic cultures by various T- or B-cell-responsive mitogenic agents.
Animals↗
Epidemic of acquired immunodeficiency in rhesus monkeys.
A syndrome closely resembling acquired immunodeficiency syndrome (AIDS) in man has been identified in a group of 64 rhesus monkeys (Macaca mulatta) maintained outdoors at the California Primate Research Center. The syndrome is characterised by generalised lymphadenopathy, severe opportunistic infections including cytomegalovirus, chronic wasting, and high mortality. In 1 animal a multifocal cutaneous fibrosarcoma developed. This syndrome in monkeys may provide an animal model for human AIDS.
Acquired Immunodeficiency Syndrome↗