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At least 181 records · Page 10Linked to original sources
PubMed1978

Experimental production of respiratory tract disease in cebus monkeys after intratracheal or intranasal infection with influenza A/Victoria/3/75 or influenza A/New Jersey/76 virus.

A total of 28 cebus monkeys were inoculated intratracheally or intranasally with 10(6) 50% tissue culture infective doses of A/New Jersey/76 virus or 10(7) 50% tissue culture infective doses of A/Victoria/75 virus, and 8 additional monkeys received sterile allantoic fluid. Each of the animals became infected as evidenced by a serological response and/or shedding of the virus. Of the 10 animals inoculated intratracheally with A/Victoria/75 virus, 8 developed a systemic illness, and pulmonary infiltration was detected by X-ray in 7 of the 8. Administration of A/New Jersey/76 virus intratracheally to 10 monkeys produced a mild systemic illness in 2 animals and an upper respiratory tract illness in 6, but no illness developed in the remaining 2 monkeys; none of the animals developed X-ray evidence of lower respiratory tract disease. Intranasal administration of either virus failed to induce any illness or produced, at most, mild illness confined to the upper respiratory tract. These studies demonstrate that cebus monkeys are susceptible to respiratory tract infection with influenza A viruses and that the development of pulmonary disease is reflected in the appearance of easily recognizable radiological changes.

Animals↗
PubMed2003

Chronic Chagas' disease in rhesus monkeys (Macaca mulatta): evaluation of parasitemia, serology, electrocardiography, echocardiography, and radiology.

Severe chronic damage to the heart and gastrointestinal tract in patients with Chagas' disease are often observed 10-20 years after the acute phase. The course of long-lasting infection with the Colombian strain of Trypanosoma cruzi was studied in seven rhesus monkeys infected for 15-19 years. Subpatent parasitemia was detected in all studied animals, using hemoculture (two of seven), artificial xenodiagnosis (three of seven), and a polymerase chain reaction PCR (six of six). High titers of specific IgG antibody to T. cruzi persisted throughout the chronic phase of infection. Abnormal electrocardiographic (three of six) and echocardiographic (one of six) patterns detected in the T. cruzi-infected monkeys were possibly related to parasite-triggered myocardial damage. The results suggest that rhesus monkeys experimentally infected with T. cruzi, besides reproducing the acute phase of Chagas' disease, also develop chronic chagasic cardiomyopathy.

Animals↗
PubMed2001

Simian immunodeficiency virus replicates to high levels in naturally infected African green monkeys without inducing immunologic or neurologic disease.

African green monkeys can maintain long-term persistent infection with simian immunodeficiency viruses (SIVagm) without developing AIDS and thus provide an important model for understanding mechanisms of natural host resistance to disease. This study assessed the levels and anatomic distribution of SIVagm in healthy, naturally infected monkeys. Quantitative competitive reverse transcriptase PCR assays developed to measure SIVagm from two African green monkey subspecies demonstrated high levels of SIV RNA in plasma (>6 x 10(6) RNA copies/ml) in sabaeus and vervet monkeys. Infectious virus was readily recovered from plasma and peripheral blood mononuclear cells and shown to be highly cytopathic in human cell lines and macrophages. SIVagm DNA levels were highest in the gastrointestinal tract, suggesting that the gut is a major site for SIVagm replication in vivo. Appreciable levels of virus were also found within the brain parenchyma and the cerebrospinal fluid (CSF), with lower levels detected in peripheral blood cells and lymph nodes. Virus isolates from the CSF and brain parenchyma readily infected macrophages in culture, whereas lymph node isolates were more restricted to growth in human T-cell lines. Comparison of env V2-C4 sequences showed extensive amino acid diversity between SIVagm recovered from the central nervous system and that recovered from lymphoid tissues. Homology between brain and CSF viruses, macrophage tropism, and active replication suggest compartmentalization in the central nervous system without associated neuropathology in naturally infected monkeys. These studies provide evidence that the nonpathogenic nature of SIVagm in the natural host can be attributed neither to more effective host control over viral replication nor to differences in the tissue and cell tropism from those for human immunodeficiency virus type 1-infected humans or SIV-infected macaques.

Amino Acid Sequence↗
PubMed1977

Role of hypertension in ischemic heart disease and cerebral vascular disease in the cynomolgus monkey with coarctation of the aorta.

The role of hypertension in cardiovascular disease was studied in the hypertensive coarcted monkey during the feeding of an atherogenic and nonatherogenic diet. During the 15-month period of observation, half of the hypertensive coarcted monkeys developed cardiovascular disease which included heart failure, ischemic heart disease, stroke, and sudden death. There were no cardiovascular complications in the control normotensive monkeys except for one cholesterol-fed animal. The incidence of ischemic heart disease and sudden cardiac death was higher in monkeys with both hypertension and hypercholesterolemia than in those with hypertension or hypercholesterolemia alone. Postmortem studies revealed that the former monkeys had both hypertensive and atherosclerotic heart disease, whereas the monkeys with hypertension or hypercholesterolemia had either hypertensive or atherosclerotic heart disease. Hypertensive heart disease was characterized not only by hypertrophy of the left ventricle but also by focal myocardial degeneration and fibrosis and by focal thickening and narrowing of the small coronary arteries, particularly the sinus node artery and the atrioventricular node artery. The finding of transmural myocardial infarction in two monkeys with patient coronary arteries suggests a possible role of coronary artery spasm in ischemic heart disease in hypertension. The cerebral vascular complications of hypertension included hypertensive encephalopathy, transient "ischemic" attacks, and hemorrhagic stroke. The complications were associated with severe hypertension and with hypertensive vascular disease or hypertensive and atherosclerotic vascular disease of the cerebral arteries.

Animals↗
PubMed1992

An epidemic of non-A, non-B hepatitis in south Delhi: epidemiological studies and transmission of the disease to rhesus monkeys.

In November 1987 an epidemic of NANB-hepatitis broke out in a residential colony of South Delhi which lasted for nearly two months. The epidemic was caused due to the sewage contamination of the drinking water supply. Analysis of the epidemiological data showed that the disease was more common in the younger age group of 11-20 years and that both sexes were equally prone to the disease. The disease could be transmitted to rhesus monkeys by intravenous inoculation of the stool extracts from the patients. Experimentally infected monkeys showed elevated levels of serum aminotransferases and excreted the infectious agent in the stools. Hepatic lesions characteristic of enteric non-A, non-B hepatitis were observed in an infected monkey.

Adolescent↗
PubMed1995

Identification of a nef allele that causes lymphocyte activation and acute disease in macaque monkeys.

Residues 17 and 18 in nef of SIVmac239 were changed from RQ to YE to create a translated sequence of SRPSGDLYERLLRARGETYGRLLGEVEDGYSQSP from residues 10-43. The YXXL motifs in this context match very well with consensus sequences for SH2 binding domains and are similar to ones present in nef of the acutely lethal pathogen SIVpbj14. The YE variant of SIVmac239, unlike SIVmac239 but like SIVpbj14, replicated well in resting peripheral blood mononuclear cell cultures, caused extensive T lymphocyte activation, and produced an acute disease in rhesus and pigtailed monkeys characterized by severe diarrhea, rash, and extensive lymphoid proliferation in the gastrointestinal tract. The YEnef gene transformed NIH 3T3 cells in culture. Both 239nef and YEnef were found to associate with src in cotransfected COS cells, and both 60 kDa src and 34 kDa nef were phosphorylated at tyrosine in these cells. The extent of tyrosine phosphorylation of 239nef was considerably less than that of YEnef in these assays. These findings identify an important determinant of the SIVpbj14 phenotype, and they provide evidence of a role for nef in signal transduction and cellular activation.

3T3 Cells↗
PubMed2005

Serial electrophysiologic studies in rhesus monkeys with Krabbe disease.

Krabbe disease is a progressive leukodystrophy that results in demyelination in the central and peripheral nervous systems in humans. It has been described in a number of mammalian species including the rhesus monkey. We performed serial nerve conduction studies beginning within the first 2 months of life in four homozygous, two heterozygous, and two normal rhesus monkeys (Macaca mulatta) to characterize the peripheral neuropathy. Mean conduction velocities of the median, ulnar, and tibial nerves were significantly slower in the affected than unaffected monkeys at all ages (P < 0.0001). The conduction velocity differences became more apparent between the affected and unaffected as the monkeys aged. When compared to the unaffected monkeys, the serial conduction velocities suggested occurrence of dysmyelination followed by demyelination in the affected monkeys. These observations provide further insight into the disease process and suggest an early window of opportunity for treating Krabbe disease.

Action Potentials↗
PubMed1991

Efficacy of SIV/deltaB670 glycoprotein-enriched and glycoprotein-depleted subunit vaccines in protecting against infection and disease in rhesus monkeys.

Immunization with an inactivated whole-virus vaccine is highly effective in preventing lentivirus infection. The viral protein(s) essential to the induction of protective responses, however, have not been identified. To define the role of virion components in the induction of protective immunity, we evaluated the efficacy of glycoprotein-enriched and glycoprotein-depleted simian immunodeficiency virus (SIV) subunit vaccines prepared by lentil-lectin affinity chromatography of gradient-purified virions using the immunization and challenge regimen previously found successful with an inactivated whole-virus vaccine. Infection was determined by successful recovery of virus, the induction of SIV-specific antibody responses, and infection of naive recipients by inoculation with lymph-node-derived lymphocytes from the vaccinates. Immunization with the glycoprotein-enriched preparation prevented infection in two out of four monkeys, whereas the glycoprotein-depleted vaccine failed to prevent infection in all four vaccinates tested. However, the glycoprotein-depleted vaccine appeared to moderate the progression of SIV-induced disease compared with non-immunized infected control monkeys inoculated with the same challenge dose. These data suggest that subunit vaccines containing sufficient quantities of viral glycoproteins can protect against SIV infection, whereas subunit vaccines composed predominantly of viral core proteins cannot. The development of effective vaccines against HIV infection should include studies on the optimum presentation of the viral envelope glycoproteins to produce long-term broadly protective immune responses.

Animals↗
PubMed2006

Histological effects of intraputaminal infusion of glial cell line-derived neurotrophic factor in Parkinson disease model macaque monkeys.

Glial cell line-derived neurotrophic factor (GDNF) is a potent neuroprotection and regeneration molecule for dopamine neurons in the substantia nigra. A recent clinical study showed that intraputaminal infusions of GDNF restored the striatal dopaminergic function, resulting in improvement in patients with Parkinson disease. To investigate the efficacy and the safety of this treatment, the histological changes associated with intraputaminal GDNF infusions were investigated in non-human primate models of Parkinson disease. Two types of Parkinson disease model were constructed: unilateral infusion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridin (MPTP) into the internal carotid artery to induce hemiparkinsonism and intermittent systemic injection to induce Parkinson disease. GDNF (50 microg) was infused into the putamen on the day of the first MPTP treatment and 4 weeks later. The monkey brains were examined by immunohistochemistry 2-4 weeks after the second GDNF infusion. Losses of the nigral dopamine neurons were mild (30-50% loss) on the side of GDNF infusion, and moderate (approximately 70% loss) on the side of vehicle infusion in the Parkinson disease model. The dopamine fibers were thick and dense in the striatum around the GDNF infusion sites. Both GDNF- and vehicle-treated monkeys of the hemiparkinsonian model showed severe decrease of dopamine neurons to 10% of the intact side. Although reactive astrocytes proliferated around the GDNF infusion sites, the densities of striatal neurons involving GABAergic and cholinergic neurons were not affected. Intraputaminal infusions of GDNF have beneficial effects in parkinsonian monkeys, but dose control is required according to the severity of the disease. The specificity for dopamine neurons is quite high and there are no serious histological changes.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1981

Differential effect of sex in experimental hyaline membrane disease in newborn monkeys.

Data from forty-four infant monkeys of 135 to 150 days' gestation were reviewed for the existence of sex-related differences in the development of hyaline membrane disease, post-mortem lung mechanics, biochemistry, and histologic features. Severity of hyaline membrane disease was scored from 1 (severe) to 6 (none) from chest radiographic appearance and arterial PO2 determination. Female monkeys had a lower score (mean +/- 1 SD = 2.7 +/- 1.6) than males (3.8 +/- 1.6, less than 0.05). Females accounted for 70% of animals with scores of 1 or 2, and 33% of those with scores of 5 or 6 (p = 0.045). There was no difference in lung homogenate phospholipid (PL) concentration. Airway lavage PL and the ratio of lavage PL to homogenate PL were both decreased in the female. Surface activity of the lavage material was also less in the female. No significant differences between males and females were noted for mean maximal lung volume air-tissue ratio, as determined by light microscopy, or number of type II pneumocytes per alveolus. Premature female monkeys appeared to sustain a disadvantage in pulmonary adaptation to postnatal life.

Animals↗
PubMed1994

Estrogens, progestins, and coronary heart disease in cynomolgus monkeys.

OBJECTIVE: To determine the effects of estrogen deprivation and estrogen replacement on coronary artery atherosclerosis. DESIGN: Randomized trials using female cynomolgus monkeys as subjects. SETTING: Comparative Medicine Clinical Research Center of an academic medical center. PATIENTS: Premenopausal and postmenopausal female cynomolgus monkeys fed diets comparable in fat and cholesterol to those consumed by human beings. INTERVENTIONS: Menopause was induced by ovariectomy; coronary vasomotion was evaluated during coronary angiography. Treatments involved estrogens and progestins, and coronary artery atherosclerosis was evaluated at necropsy. MAIN OUTCOME MEASURE: Coronary artery atherosclerosis extent. RESULTS: Premenopausal stress induces ovarian dysfunction and exacerbates coronary artery atherosclerosis. Physiologic replacement of ovarian hormones reduces in half the extent of coronary atherosclerosis of surgically menopausal monkeys. Hormone replacement therapy did not enhance regression of established coronary atherosclerosis. CONCLUSION: Estrogen deprivation exacerbates and estrogen diminishes coronary artery atherosclerosis of female cynomolgus monkeys fed atherogenic diets.

Animals↗
PubMed1982

The absence of hemolytic disease in the newborn rhesus monkey (Macaca mulatta).

Hemolytic disease of the newborn has not been observed in rhesus monkeys even though the newborn's erythrocytes may be coated with maternal antibodies. Using a 51chromium-erythrocyte survival assay, we found that maternal antibodies do not mediate immune elimination of newborn's red blood cells. However, certain allogeneic or xenogeneic antibodies mediate clearance via sequestration by the reticuloendothelial system, or by intravascular hemolysis, or by a combination of these. The class of antibody plays a major role in elimination since red cells coated with IgG but not with IgM were rapidly cleared. In addition, the quantity of antibody controls the rate and extent of clearance. A comparison of rhesus alloantisera suggests that coating of multiple antigenic sites is necessary for clearance. Passive immunization with selected high-titered anti-erythrocyte alloantisera can induce some hematologic signs of erythrocyte destruction in newborn monkeys.

Animals↗