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Query: UMLS:C0001175 (AIDS)
 120,706 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Experimental transmission of simian acquired immunodeficiency syndrome (SAIDS) and Kaposi-like skin lesions. 613 95

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.
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PMID:Characterization of exogenous type D retrovirus from a fibroma of a macaque with simian AIDS and fibromatosis. 620 Sep 29

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)
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PMID:Epidemiologic aspects of an outbreak of acquired immunodeficiency in rhesus monkeys (Macaca mulatta). 672 87

To evaluate the role of humoral immunity against simian immunodeficiency virus (SIV), we tested whether passive immunization with plasma from SIVmac251 vaccine-protected or healthy infected animals would protect rhesus monkeys against intravenous infection with ten 50% animal infectious doses of the cell-free homologous virus. The challenge dose of this SIVmac251 virus stock had previously caused persistent infection in all (21 of 21) nonimmunized controls. A plasma pool was obtained from a donor that had been immunized with an inactivated whole SIVmac251 vaccine produced in human T cells. This plasma pool contained low levels of SIVmac binding and neutralizing antibody but had a high titer of antibodies recognizing human cell proteins. Given 4 or 18 hr before intravenous challenge, this plasma completely protected three of eight recipients from infection and delayed virus detection in one recipient. The five unprotected animals had only a transient or undetectable p27 antigenemia and low virus load in their PBMCs, and all survived at least 7 months after infection. By contrast, no protection was observed in 6 monkeys given inactivated, pooled plasma or purified immunoglobulin (Ig) from healthy SIVmac251-infected animals. This plasma pool and the Ig preparation contained high levels of SIV-binding and neutralizing antibody but no reactivity to human cellular components. Five of the six recipients had persistent antigenemia after challenge and four died acutely from simian AIDS in 4-7 months. These studies suggest that passive transfer of antibody to human cellular antigens can confer protection against SIVmac whereas passive transfer of neutralizing antibodies without human cellular antibodies does not protect against the homologous virus and may enhance infection.
AIDS Res Hum Retroviruses 1995 Jul
PMID:Passive immunization of rhesus macaques against SIV infection and disease. 754 12

Mycobacterium avium complex (MAC) in simian immunodeficiency virus (SIV)-infected macaques is a frequent opportunistic infection that shares many features with the condition in human AIDS patients. A retrospective analysis of necropsies on 135 macaques with SIV-induced simian AIDS that received neither antiretroviral nor antimicrobial therapy revealed that 17% (23/135) were infected with MAC. MAC developed in 31.3% (21/67) of the animals inoculated with uncloned SIVmac251 versus 1.9% (1/53) and 6.7% (1/15) of the animals inoculated with the molecular clones SIVmac239 and SIVmac239/316EM, respectively (P = .001). This is the first example in which the risk of infection with a specific opportunistic organism was affected by the infecting strain of immunodeficiency virus. In addition, animals with MAC had a longer mean survival after primary infection and lower CD4 cell counts at death than animals that did not develop this opportunistic infection. The SIV-inoculated macaque is a valuable model in which to study the pathogenesis of MAC in the immunocompromised host.
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PMID:Mycobacterium avium complex in macaques with AIDS is associated with a specific strain of simian immunodeficiency virus and prolonged survival after primary infection. 756 Dec 1

Some macaques infected with SRV-2 developed SAIDS and RF, a Kaposi's sarcoma (KS)-like tumor. We investigated the immunophenotypic markers of this SAIDS-associated retroperitoneal fibromatosis (RF). RF tumor is characterized by proliferation of spindle cells accompanying inflammatory cell infiltrates, fibroblasts, and endothelial cells. RF spindle cells in tumor tissues revealed several immunobiologic characteristics similar to vascular smooth-muscle cells or myofibroblasts based on positive immunoreactivity of smooth-muscle alpha-actin and desmin. The majority of cultured RF spindle cells also expressed specific markers for vascular smooth muscle. These results suggest that the RF spindle cells are derived from vascular smooth-muscle cells. Furthermore, RF tissues and cells were persistently infected with SRV-2, which may play an important role in viral etiology of AIDS-associated neoplasm in this macaque model.
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PMID:Immunocytochemistry of Kaposi's sarcoma-like tumor cells from pigtailed macaques with simian AIDS. 756 10

Proliferative lesions were found on the squamous epithelium of the tongue, esophagus, or penis or haired skin of the lip, hand, or thorax of 8 simian immunodeficiency virus-infected rhesus monkeys that died of simian AIDS. The lesions were focal and consisted of hyperkeratosis, parakeratosis, and acanthosis in the skin, with additional ballooning degeneration in the tongue, esophagus, and penis. The epithelial surfaces were frequently colonized by Candida species or gram-positive cocci. Intranuclear inclusion bodies were seen in cells in the middle and superficial layers. Herpesvirus virions were found in inclusion-bearing cells by transmission electron microscopy. An Epstein-Barr-like virus was identified in inclusion-bearing cells by immunohistochemistry and in situ hybridization. No virus was detectable in basal layers of the epithelium. These lesions resemble oral hairy leukoplakia in AIDS patients and may thus provide a useful primate model to study permissive epithelial infection by Epstein-Barr-like viruses.
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PMID:Squamous epithelial proliferative lesions associated with rhesus Epstein-Barr virus in simian immunodeficiency virus-infected rhesus monkeys. 762 99

Human immunodeficiency virus type 1 (HIV-1) typically evolves from a macrophage-tropic, noncytopathic virus at early asymptomatic stages of infection to a T-cell-tropic, cytopathic, and syncytia-inducing virus population as humans progress to AIDS. This suggests that changes in virus phenotype may influence disease. Because simian immunodeficiency virus (SIV) infection in macaques is a common model system for HIV-1 pathogenesis, we determined whether SIV infection in macaques that develop simian AIDS is associated with a similar shift in viral tropism, replication, and cytopathic properties. The virus that infected the monkeys (SIVMneCL8) and predominated at early times in infection is a macrophage-tropic virus that replicates with relatively low efficiency in human T cell lines. The variant populations that arise in macaques as they progress to AIDS are more infectious for human T cell lines, exhibiting enhanced replication in CEM x 174 cells and an expanded host range that includes Molt-4 Clone 8 cells. Infections starting with equal doses of the viruses demonstrated that the late variants are cytopathic and syncytia-inducing compared to SIVMneCL8, but the variants replicate less efficiently in primary macaque macrophages. V3 sequences were generally conserved between the early and the late variants, suggesting that changes in SIVMne tropism, replication, and cytopathicity were apparently not due to alterations in V3. This study demonstrates important similarities in the phenotypic viral changes that accompany development of AIDS in SIV and HIV-1 infections and suggest that SIV may provide a model system for determining whether the rapidly replicating, T-cell-tropic cytopathic variants present late in infection and disease are indeed important in determining progression to AIDS.
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PMID:Progression to AIDS in macaques is associated with changes in the replication, tropism, and cytopathic properties of the simian immunodeficiency virus variant population. 788 56

Simian immunodeficiency virus infection of macaques is a model for human immunodeficiency virus infection of humans. In vivo-titrated stocks of SIV are essential for the utilization of this model for vaccine development. The elicitation of anti-human cell antibodies by some vaccines prepared in human cells and the related protective effects of the vaccine produced in human cells suggest a need for new macaque-derived SIV stocks. Here we describe the titration and characterization of two stocks of SIVmac that were produced in primary rhesus macaque cells. The first virus is SIVmac251, isolated from tissues of macaque 251, and the second is a molecular clone designated as SIVmac239. A 50% rhesus monkey infectious dose (MID50) was titrated for each virus stock by intravenous inoculation. An additional five macaques were inoculated with 10 MID50 of the SIVmac251 stock and were followed for disease outcome. All five monkeys developed antigenemia by 14 days postchallenge. Two of the five monkeys developed strong anti-SIV humoral immunity, whereas three developed little or no humoral immunity. As has been observed previously, the rapidity of disease progression correlated with the lack of a strong antibody response. The three animals with low humoral immunity died within 7 months of challenge, with antigenemia, cachexia, hypoproteinemia, hypoalbuminemia, weight loss, and intractable diarrhea, while maintaining their circulating CD4 numbers. One animal died at 1.5 years of more typical simian AIDS.
AIDS Res Hum Retroviruses 1994 Feb
PMID:Titration and characterization of two rhesus-derived SIVmac challenge stocks. 819 74

Rhesus macaque monkeys infected with the simian immunodeficiency virus develop a syndrome mimicking AIDS in humans. We have demonstrated previously that sera from individuals infected with human immunodeficiency virus type 1 inhibit the proliferation of lymphocytes from healthy noninfected subjects and that this phenomenon is associated with the development of clinical AIDS. We have also shown that sera from monkeys infected with SIV also have such inhibitors. In this body of work, we attempted to document the onset of these inhibitors in relation to the time of SIV infection. Twenty rhesus macaques were injected with one of two tissue strains of SIV or media. Blood was drawn on a set schedule and the serum samples frozen at -70 degrees C. The animals were monitored and observed for up to 42 weeks. All test animals were autopsied. Sera from all the draws were assayed against the same populations of human peripheral blood mononuclear cells in the same experiment using suboptimal amounts of phytohemagglutinin (PHA). Sera from those animals that subsequently developed SAIDS were more likely to demonstrate serum inhibition. This inhibition could be seen as early as 8-10 weeks after infection. By week 14, the assay could differentiate animals into SAIDS or healthy groups with a sensitivity of 67% and a specificity of 89%.
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PMID:Serum inhibitors precede the development of SAIDS. 834 Sep 1


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