A program for surveillance of nonhuman primate disease.
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Animal Diseases↗
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Primate disease and breeding rates.
33 species were compared for 12 disease categories over 3 years of laboratory housing. There were low correlations between popularity, birth, death, and illness rates. Highest rates were: birth, Macaca nemestrina; illness, Pongo pygmaeus; death, Cercopithecus aethiops. Lowest rates were: birth, Lemur catta; illness, Sanguinus mystax; death, Galago crassicaudatus. Galago crassicaudatus and Macaca fasicularus had low disease and high birth rates.
Animal Diseases↗
Zoonoses in Britain: some present and potential hazards to man. Primate diseases.
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Animals↗
Preclinical lesions and their progression in the experimental spongiform encephalopathies (kuru and Creutzfeldt-Jakob disease) in primates.
Creutzfeldt-Jakob disease and kuru were studied in experimental primates. Eight animals with clinical disease lasting from 1/2 to 12 1/2 months were evaluated for histological evidence of progression of the pathological triad of neuronal vacuolation, neuronal loss and fibrous astrocytosis. The first change to appear was neuronal vacuolation, in both the body of neurones and in the neuropil. Fibrous astrocytosis was found subsequent to neuronal damage and necrosis. Neuronal loss was apparent when clinical signs were present. As the clinical disease progressed, so did the severity of neuronal loss and astrocytosis. Five animals, 1 1/2-10 1/2 months after intracerebral inoculation, before they had shown any signs of clinical disease, had histological evidence of neuronal vacuolation and astrocytosis.
Animals↗
Characterization of the rhesus monkey galactocerebrosidase (GALC) cDNA and gene and identification of the mutation causing globoid cell leukodystrophy (Krabbe disease) in this primate.
Krabbe disease or globoid cell leukodystrophy (GLD) is a severe lysosomal disorder resulting from the deficiency of galactocerebrosidase (GALC) activity. This deficiency results in the insufficient catabolism of several galactolipids that are important in the production of normal myelin. Since the cloning of the human GALC cDNA and gene many disease-causing and polymorphic changes have been identified. This autosomal recessive disease has been reported to occur in several animal species, and recently the murine and canine GALC genes have been cloned. We now describe the cloning of the GALC cDNA and gene from the rhesus monkey and the identification of the mutation causing GLD in this species. The nucleotide sequence of the coding region and the gene organization were nearly identical to human. The deduced amino acid sequence of the monkey GALC was compared to the human, dog, and mouse, and it was found to be 97, 87, and 83% identical, respectively. The mutation causing GLD in the rhesus monkey is a deletion of AC corresponding to cDNA positions 387 and 388 in exon 4. This results in a frame shift and a stop codon after 46 nucleotides. A rapid method to detect this mutation was developed, and when 45 monkeys from this colony were tested, 22 were found to be carriers. The availability of this nonhuman primate model of GLD will provide unique opportunities to evaluate treatment for this severe disease.
Amino Acid Sequence↗
Ovarian dysfunction, stress, and disease: a primate continuum.
Menopause is recognized as a period of increased risk for coronary heart disease (CHD) and osteoporosis. Vulnerability to these conditions is often attributed to the naturally occurring estrogen deficiency characteristic of this part of the life cycle. Premenopausal reductions in endogenous estrogen occasioned by functional ovarian abnormalities or failure are hypothesized to be similarly pathogenic and to accelerate development of CHD and osteoporosis prematurely, thereby increasing the health burden of older women. These functional abnormalities, which occur along a continuum from mild, luteal phase progesterone deficiency to amenorrhea, are relatively common and are often attributed to psychogenic factors (stress, anxiety, depression, or other emotional disturbance), exercise, or energy imbalance. Although numerous investigators have commented on these functional deficits, the abnormalities can be difficult to diagnose and are generally unappreciated for the contribution they may make to postmenopausal disease. Studies in nonhuman primates confirm that these deficits are easily induced by psychological stress and exercise, and that they accelerate the development of cardiovascular disease and perhaps bone loss in the presence of a typical North American diet. However, functional reproductive deficits are also reversible and are thus potentially amenable to environmental or behavioral intervention. Data from both women and nonhuman primates support the hypothesis that functional reproductive deficits are adaptive when triggered appropriately but are detrimental when activated in an environment (e.g., sedentary lifestyle, high-fat diet) permissive to the development of chronic disease.
Amenorrhea↗
Primate viral diseases in perspective.
The recent occurrence of fatal Herpesvirus simiae (B virus) infection in human subjects has again focused the attention of primatologists on this virus. B virus, however, is only one of a number of viral diseases that plays a role in primate colony management. This report is to emphasize to the primatologist a number of viruses other than H. simiae, with high morbidity and mortality rates, of importance for health management of nonhuman primate animal colonies. This concept is supported by the recent occurrence in colonies of nonhuman primates of simian hemorrhagic fever virus, SA8, herpesvirus, respiratory syncytial virus, encephalomyocarditis virus, Ebola virus, and simian immunodeficiency viruses.
Animals↗
Creation of non-human primate neurogenetic disease models by gene targeting and nuclear transfer.
Genetically modified rhesus macaques are necessary because mouse models are not suitable for a number of important neurogenetic disorders; for example, Kallmann's syndrome, Lesch-Nyhan's disease and Ataxia-Telangiectasia. Mouse models may not be suitable because there may be no mouse ortholog of the human gene of interest, as is the case for Kallmann's syndrome, or because mutant mice do not exhibit the same phenotype observed in humans, as is the the case for Lesch-Nyhan's disease and Ataxia-Telangiectasia. Non-human primate models of neurogenetic diseases are expected to more closely resemble human diseases than existing mouse models. Genetically modified rhesus macaques can be created by modifying the genome of a somatic cell and then transferring the nucleus from this cell to an enucleated oocyte. Random integration of a transgene is sufficient to create models of gain-of-function genetic diseases. Stable expression of green fluorescent protein has been achieved in rhesus macaque fibroblasts. However, gene targeting is necessary to create models of loss-of-function genetic diseases. Several technical challenges must be overcome before null mutant non-human primates can be produced. In our experience, fetal fibroblasts frequently become senescent before selection procedures can be completed. We have overcome this problem by transfecting somatic cells with human telomerase reverse transcriptase. This enzyme extends the telomeres, and lifespan, of somatic cells. Long and accurate polymerase chain reaction can be used to obtain sufficient regions of homology of isogenic rhesus genomic DNA for targeting constructs. This should improve gene targeting efficiency. Gene targeting experiments are currently underway. Null mutant rhesus macaques will likely result in breakthrough advances in the understanding of neurogenetic disease and prove invaluable for preclinical trials of new therapies.
Animals↗
DNA markers in primate models of human disease.
Nonhuman primates are particularly useful as animal models for common human diseases in which both genetic and environmental factors play important roles. The recent development of DNA markers (restriction fragment length polymorphisms, RFLPs) greatly increases the power of linkage analysis to detect major genes that affect quantitative phenotypes, including those related to diseases. This paper summarizes a strategy for using RFLPs in linkage analysis of baboon pedigrees to identify genes that control lipoprotein phenotype, which in turn is predictive of susceptibility to atherosclerosis. This strategy also can be applied to other common human diseases for which nonhuman primate models exist.
Animals↗
Effects of MHC class I on HIV/SIV disease in primates.
Data indicate that resistance to HIV-1 disease involves an array of contrasting HLA genotypic effects that are subtle, but significant, particularly when these genetic effects are considered as a whole. Numerous reports attributing a role for HLA genotype in AIDS outcomes have been reported, and a few of these have been affirmed in multiple studies. Functional studies of immune cell recognition have provided clues to the underlying mechanisms behind some of the strongest HLA associations, suggesting the means by which relative resistance or susceptibility to the virus may occur. SIV infection in non-human primates has served as an invaluable model for understanding AIDS pathogenesis (in rhesus monkeys) and viral resistance (in chimpanzee). The effect of rhesus MHC class I molecules on the evolution of SIV has been convincingly described [19], and a recent study in humans has suggested that selection pressure conferred by HLA molecules is responsible for specific genetic variation in HIV-1 [114]. HIV-1 may eventually have conspicuous evolutionary effects on HLA and other AIDS restriction genes, a prolonged process that could have occurred in chimpanzee [92]. To prevent such an outcome, it will be necessary to approach the disease from many perspectives, andapply comprehensively the knowledge gained to the successful control of the virus.
Animals↗
Spontaneous arterial disease in primates.
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Animals↗
Hydatid disease in four nonhuman primates.
Hydatid disease was detected in 4 nonhuman primates (Galago crassicaudatus, Lemur catta, and 2 Macaca mulatta) at the Oregon Regional Primate Research Center. Involvement extended from 2 1/2 to 7 1/2 years. A 6-cm cyst was surgically removed from the thoracic cavity of 1 macaque; 6 years later multiple cysts were found in its abdominal cavity. Lesions found in the primates at necropsy included compression or displacement of the lungs, hydroureter and hydronephrosis, and distension of the abdomen--all related to impingement of developing cysts.
Abdomen↗
Parkinson's disease and primate research: past, present, and future.
Scientific research involving non-human primates has contributed towards many advances in medicine and surgery. This review discusses its role in the progress made towards our understanding of Parkinson's disease and its treatment. Established medical treatments like dopamine agonists continue to need primate models to assess their efficacy, safety, and mechanism of action. The recently developed treatment of deep brain stimulation of the subthalamic nucleus required validation in primates before entering the clinic. Controversies surrounding future treatments such as gene therapy show the need for properly evaluated preclinical research using appropriate animal models before progression to clinical trials. Research on primates has played--and continues to play--a crucial part in deepening our understanding of Parkinson's disease, improving current therapies, and developing new treatments that are both safe and effective. In animal research, the "three Rs" of humane technique--reduction, refinement, and replacement--should be adhered to.
Animals↗
Phagocytes containing a disease-promoting Toll-like receptor/Nod ligand are present in the brain during demyelinating disease in primates.
Recent studies claim a central role for Toll-like receptor (TLR) ligands in stimulating autoimmune disease by activation of antigen-presenting cells in the target organ, but it is unclear if and how TLR ligands reach target organs. Most evidence comes from rodent models, and it is uncertain whether this principle holds in primates. Here we identify which cells contain peptidoglycan (PGN) in multiple sclerosis brain and in two nonhuman primate experimental autoimmune encephalomyelitis (EAE) models with different disease courses: acute (rhesus monkey) versus chronic disease (marmoset). Because persistence of TLR ligands in the central nervous system might be consequential for disease progression, we also determined the expression of two major PGN-degrading enzymes, ie, lysozyme and N-acetylmuramyl-l-alanine amidase. Distinct phagocyte subsets, including granulocytes, macrophages, and dendritic cells, contained PGN in the brain and coexpressed the inflammatory cytokine interleukin-12. The number of phagocytes carrying PGN increased in acute and chronic EAE compared with control animals, with the highest number of PGN-containing cells in acute EAE brain. Lytic enzymes were scarcely expressed in monkey and multiple sclerosis brain, favoring PGN persistence. PGN stimulated interleukin-12p70 release by leukocytes from all three primate species. The presence of PGN in the inflamed brain may have major implications because TLR2/Nod ligation potentially promotes inflammation and disease progression.
Adult↗
The major histocompatibility complex influences the ethiopathogenesis of MS-like disease in primates at multiple levels.
Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease primarily affecting the central nervous system. Of the many candidate polymorphic major histocompatibility complex (MHC) and non-MHC genes contributing to disease susceptibility, including those encoding effector (cytokines and chemokines) or receptor molecules within the immune system (MHC, TCR, Ig or FcR), human leukocyte antigen (HLA) class II genes have the most significant influence. In this article we put forward the hypothesis that the influence of HLA genes on the risk to develop MS is actually the sum of multiple antigen presenting cell (APC) and T-cell interactions involving HLA class I and class II molecules. This article will also discuss that, because of the genetic and immunologic similarity to humans, autoimmune models of MS in non-human primates are the experimental models "par excellence" to test this hypothesis.
Animals↗
SMART amplification maintains representation of relative gene expression: quantitative validation by real time PCR and application to studies of alcoholic liver disease in primates.
The small quantities of tissue available for most studies of human disease are a significant limitation for meaningful gene expression profiling. The Atlas Switch Mechanism At the 5' end of Reverse Transcript (SMART) probe amplification kit uses as little as 50 ng of total RNA to generate complex cDNA probes for DNA array and other analyses. However, the extent to which this attractive methodology maintains representation of relative gene expression has not been quantified. In this study, we demonstrate using real-time quantitative PCR analysis that the relative expression levels of a range of low- to high-abundance mRNAs are retained after SMART amplification independent of transcript abundance and full-length transcript, coding region and PCR product size. Using this technology, a mean amplification of 3800-fold was achieved in human liver samples, greatly enhancing the ability to perform replicate DNA array experiments. Probes generated with the SMART amplification method were used to detect increased expression of genes involved with inflammation, fibrosis, xenobiotic metabolism, immune function, oxidant stress and endothelium in liver from the baboon model of alcoholic liver disease.
DNA, Complementary↗