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PubMed1996

Antibody-dependent cellular cytotoxicity to clinical isolates of HIV-1 and SIVcpz: comparison of human and chimpanzees.

OBJECTIVE: To investigate differences in the antibody-dependent cellular cytotoxicity (ADCC) responses between HIV-1-infected humans and chimpanzees. DESIGN: The breadth of the ADCC responses in the two populations were tested against autologous and heterologous HIV-1 and SIVcpz clinical isolates as well as against reference isolates. METHODS: ADCC was tested in a 51Cr-release assay using human peripheral blood mononuclear cells as effector cells and infected Jurkat/Tat-cells as target cells. RESULTS: The majority of sera from chronically HIV-1-infected humans and chimpanzees had ADCC responses to HIV-1LAI. Interestingly, vaccinated chimpanzees with a low virus load during the immediate post-challenge period had low ADCC responses 3 years after challenge. In contrast, when ADCC activity to clinical isolates was evaluated, HIV-1-infected chimpanzees had more frequent heterologous (broader) responses than HIV-1-infected humans. ADCC was also tested in consecutive serum samples from two patients and two chimpanzees against autologous isolates, but was only detected to a low degree in one of the animals, although heterologous ADCC was demonstrated in all cases. The naturally infected (SIVcpz) chimpanzee did not have detectable heterologous or autologous ADCC responses. CONCLUSIONS: HIV-1-infected chimpanzees had broader ADCC reactivity to heterologous HIV-1 clinical isolates than the HIV-1-infected humans. These findings are consistent with subtle differences in host-virus relationships of these two species.

AIDS Vaccines↗
PubMed1998

Characteristics of primary infection of a European human immunodeficiency virus type 1 clade B isolate in chimpanzees.

The aim of the study was to select, from a panel of candidate European human immunodeficiency virus type 1 (HIV-1) clade B primary virus isolates, one isolate based on replication properties in chimpanzee peripheral blood mononuclear cells (PBMC). Secondly, to evaluate the in vivo kinetics of primary infection of the selected isolate at two different doses in two mature, outbred chimpanzees (Pan troglodytes). Four different low passage, human PBMC-cultured 'primary' HIV-1 isolates with European clade B consensus sequence were compared for their ability to replicate in vitro in chimpanzee versus human PBMC. The isolate which yielded the highest titre and most vigorous cytopathic effect in chimpanzee PBMC was evaluated for coreceptor usage and chosen for evaluation in vivo. Only the HIV-1Han2 isolate replicated in chimpanzee PBMC in vitro at detectable levels. This isolate was demonstrated to utilize CCR4, CCR5 and CXCR4 coreceptors and could be inhibited by beta-chemokines. Infection of chimpanzees was demonstrated by viral RNA and DNA PCR analysis, both in plasma as well as in PBMC and lymph node cells as early as 3 weeks after inoculation. Antibodies developed within 6 weeks and continued to increase to a maximum titre of approximately 12800, thereafter remaining in this range over the follow-up period of 2 years. Compared to cell line-adapted HIV-1 isolates there were slight but no dramatic differences in the kinetics of infection of chimpanzees with this particular primary isolate.

Animals↗
PubMed2006

Selective transmission of hepatitis C virus genotypes and quasispecies in humans and experimentally infected chimpanzees.

This study determined whether selective transmission of hepatitis C virus (HCV) species occurred among human and chimpanzee recipients of contaminated blood products or plasma containing multiple genotypes, subgenotypes and quasispecies. Commercially prepared factor VIII concentrate (lot DO56), produced prior to HCV testing and inactivation, was subsequently found by direct cloning to contain the following subgenotypes: 1a and 1b (73 % of clones), 2a (13 % of clones), 2b (11 % of clones) and 3a (4 % of clones). A patient transfused with factor VIII concentrate DO56 was diagnosed with clinical non-A, non-B hepatitis and subsequently found to be infected with HCV subgenotype 1b. Among five chimpanzees inoculated experimentally with the same factor VIII concentrate, two were infected only with HCV subgenotype 1a and three were infected with approximately equivalent clonal proportions of subgenotypes 1a and 1b. HCV hypervariable region 1 (HVR1) quasispecies analysis of the DO56 factor VIII concentrate and a serum specimen from the single chimpanzee that developed a chronic HCV infection following inoculation with DO56 showed 0-56 % nucleotide variation. However, specimens from chimpanzees infected in the second to fourth passages of the DO56 inoculum had 0-8 % HVR1 quasispecies nucleotide variation. The high HVR1 quasispecies variation in the factor VIII concentrate and its first passage in chimpanzees indicates the presence of multiple HCV isolates, whereas the low variation in the second to fourth chimpanzee passages suggests transmission of a single HCV isolate. These findings strongly suggest selective transmission of HCV isolates during experimental chimpanzee infection and among humans exposed to multiple HCV species.

Animals↗
PubMed2003

Analysis of 5'-end sequences of chimpanzee cDNAs.

We constructed full-length enriched cDNA libraries from chimpanzee brain, skin, and liver tissues by the oligo-capping method to establish a database of sequences of chimpanzee genes. Randomly selected clones from the libraries were subjected to one-pass sequencing from their 5'-ends. As a result, we collected 6813 chimpanzee cDNA sequences longer than 400 bp. Homology search against human mRNA sequences (RefSeq mRNAs) revealed that our collection included sequences of 1652 putative chimpanzee genes. In order to calculate the sequence identity between human and chimpanzee homologs, we constructed 5'-end consensus sequences of 226 chimpanzee genes by aligning at least three sequences for individual genes. Sequence identity was estimated by comparing these consensus sequences and the corresponding sequences of their human homologs. The average sequence identity of the 5'-end cDNAs was 99.30%. Those of the 5'-UTRs and CDSs were 98.79% and 99.42%, respectively. The results confirmed that human and chimpanzee genes are highly conserved at the nucleotide level. As for amino acids, the average sequence identity was 99.44%. The average synonymous (K(S)) and nonsynonymous (K(A)) divergences were estimated to be 1.33% and 0.28%, respectively.

5' Flanking Region↗
PubMed2006

Estimation of the species-specific mutation rates at the DRB1 locus in humans and chimpanzee.

To estimate the species-specific mutation rates at the DRB1 locus in humans and chimpanzee, we analyzed the nucleotide sequence of a 37.6-kb chimpanzee chromosomal segment containing the entire Patr-DRB1*0701 allele and the flanking nongenic region and we compared it with two corresponding human sequences containing the HLA-DRB1*070101 allele using the sequence of HLA-DRB1*04011 as an outgroup. Because the allelic pair of HLA-DRB1*070101 and Patr-DRB1*0701 shows the lowest number of substitutions between the two species, it appears that these sequences diverged close to the time of the humans-chimpanzee divergence (6 million years ago). Alignment of the nucleotide sequences for HLA-DRB1*070101 and Patr-DRB1*0701 alleles showed that they share a high degree of similarity, suggesting that the studied chromosomal segments with these sequences have not been subjected to recombination since the humans-chimpanzee divergence. Comparison of the flanking 10.6 kb of nongenic sequences revealed an average of 41.5 and 83 single nucleotide substitutions in humans and chimpanzee, respectively. Thus, the species-specific nucleotide substitution rates in the flanking nongenic region were estimated to be 6.53 x 10(-10) and 1.31 x 10(-9) per site per year in humans and chimpanzee, respectively. Unexpectedly, the estimated rate in humans was twofold lower than in chimpanzee (P < 10(-3), Tajima's relative rate test) and lower than the average substitution rate in the human genome. Because the nucleotide substitution rate in nongenic regions free from selection is expected to be equal to the mutation rate, the estimated substitution rate should correspond to the species-specific mutation rate at the DRB1 locus. Our results strongly suggest that the mutation rate at DRB1 locus differs among species.

Alleles↗
PubMed1987

Persistent infection of chimpanzees with human immunodeficiency virus: serological responses and properties of reisolated viruses.

Persistent infection by human immunodeficiency virus (HIV-1) in the chimpanzee may be valuable for immunopathologic and potential vaccine evaluation. Two HIV strains, the tissue culture-derived human T-cell lymphotropic virus type IIIB (HTLV-IIIB) and in vivo serially passaged lymphadenopathy-associated virus type 1 (LAV-1), were injected intravenously into chimpanzees. Two animals received HTLV-IIIB as either virus-infected H9 cells or cell-free virus. A third animal received chimpanzee-passaged LAV-1. Evaluation of their sera for virus-specific serologic changes, including neutralizations, was done during a 2-year period. During this period all animals had persistently high titers of antibodies to viral core and envelope antigens. All three animals developed a progressively increasing type-specific neutralizing LAV-1 versus HTLV-IIIB antibody titer during the 2-year observation period which broadened in specificity to include HTLV-HIRF, HTLV-IIIMN, and HTLV-IIICC after 6 to 12 months. The antibody titers against both viruses were still increasing by 2 years after experimental virus inoculation. Sera from all animals were capable of neutralizing both homologously and heterologously reisolated virus from chimpanzees. A slightly more rapid type-specific neutralizing response was noted for the animal receiving HTLV-IIIB-infected cells compared with that for cell-free HTLV-IIIB. Sera from all persistently infected chimpanzees were capable of mediating group-specific antibody-mediated complement-dependent cytolysis of HIV-infected cells derived from all isolates tested. Viruses reisolated from all three animals at 20 months after inoculation revealed very similar peptide maps of their respective envelope gp120s, as determined by two-dimensional chymotrypsin oligopeptide analysis. One peptide, however, from the original HTLV-IIIB-inoculated virus was deleted in viruses from all three animals, and in addition, we noted the appearance of a new or modified peptide which was common to LAV-1 as well as to HTLV-IIIB reisolated from infected chimpanzees. It thus appears that a group-specific neutralizing antibody response as well as a group-specific cytotoxic response can develop in chimpanzees after an inoculation of a single HIV variant. This finding suggests that a common, less immunodominant determinant(s) is present on a single HIV strain which could induce group-specific antibodies during viral infection and replication. The identification of this group-specific epitope and the induction of analogous immunity may be relevant to vaccine development against human acquired immunodeficiency syndrome.

Acquired Immunodeficiency Syndrome↗
PubMed1991

The inability of human immunodeficiency virus to infect chimpanzee monocytes can be overcome by serial viral passage in vivo.

Studies of lentivirus infection in ruminants, nonhuman primates, and humans suggest that virus infection of macrophages plays a central role in the disease process. To investigate whether human immunodeficiency virus type 1 (HIV-1) can infect chimpanzee macrophages, we recovered monocytes from peripheral blood mononuclear cells of HIV-1-negative animals and inoculated these and control human monocytes with a panel of four human-passaged monocytotropic virus strains and one chimpanzee-passaged isolate. HIV-1 infected human monocytes synthesized proviral DNA, viral mRNA, p24 antigen, and progeny virions. In contrast, except for the chimpanzee-passaged HIV-1 isolate, chimpanzee monocytes failed to support HIV-1 replication when cultured under both identical and a variety of other conditions. Proviral DNA was demonstrated only at background levels in these cell cultures by polymerase chain reaction for gag- and env-related sequences. Interestingly, the chimpanzee-passaged HIV-1 isolate did not replicate in human monocytes; viral p24 antigens and progeny virions were not detected. The same monocytotropic panel of HIV-1 strains replicated in both human and chimpanzee CD4+ T lymphoblasts treated with phytohemagglutinin and interleukin-2. The failure of HIV-1 to infect chimpanzee monocytes, which can be overcome by serial in vivo viral passage, occurs through a block early in the viral life cycle.

Animals↗
PubMed2002

Molecular and immunological significance of chimpanzee major histocompatibility complex haplotypes for hepatitis C virus immune response and vaccination studies.

The chimpanzee is a critical animal model for studying cellular immune responses to infectious pathogens such as hepatitis B and C viruses, human immunodeficiency virus, and malaria. Several candidate vaccines and immunotherapies for these infections aim at the induction or enhancement of cellular immune responses against viral epitopes presented by common human major histocompatibility complex (MHC) alleles. To identify and characterize chimpanzee MHC class I molecules that are functionally related to human alleles, we sequenced 18 different Pan troglodytes (Patr) alleles of 14 chimpanzees, 2 of them previously unknown and 3 with only partially reported sequences. Comparative analysis of Patr binding pockets and binding assays with biotinylated peptides demonstrated a molecular homology between the binding grooves of individual Patr alleles and the common human alleles HLA-A1, -A2, -A3, and -B7. Using cytotoxic T cells isolated from the blood of hepatitis C virus (HCV)-infected chimpanzees, we then mapped the Patr restriction of these HCV peptides and demonstrated functional homology between the Patr-HLA orthologues in cytotoxicity and gamma interferon (IFN-gamma) release assays. Based on these results, 21 HCV epitopes were selected to characterize the chimpanzees' cellular immune response to HCV. In each case, IFN-gamma-producing T cells were detectable in the blood after but not prior to HCV infection and were specifically targeted against those HCV peptides predicted by Patr-HLA homology. This study demonstrates a close functional homology between individual Patr and HLA alleles and shows that HCV infection generates HCV peptides that are recognized by both chimpanzees and humans with Patr and HLA orthologues. These results are relevant for the design and evaluation of vaccines in chimpanzees that can now be selected according to the most frequent human MHC haplotypes.

Alleles↗
PubMed2006

Evolution of the NANOG pseudogene family in the human and chimpanzee genomes.

BACKGROUND: The NANOG gene is expressed in mammalian embryonic stem cells where it maintains cellular pluripotency. An unusually large family of pseudogenes arose from it with one unprocessed and ten processed pseudogenes in the human genome. This article compares the NANOG gene and its pseudogenes in the human and chimpanzee genomes and derives an evolutionary history of this pseudogene family. RESULTS: The NANOG gene and all pseudogenes except NANOGP8 are present at their expected orthologous chromosomal positions in the chimpanzee genome when compared to the human genome, indicating that their origins predate the human-chimpanzee divergence. Analysis of flanking DNA sequences demonstrates that NANOGP8 is absent from the chimpanzee genome. CONCLUSION: Based on the most parsimonious ordering of inferred source-gene mutations, the deduced evolutionary origins for the NANOG pseudogene family in the human and chimpanzee genomes, in order of most ancient to most recent, are NANOGP6, NANOGP5, NANOGP3, NANOGP10, NANOGP2, NANOGP9, NANOGP7, NANOGP1, and NANOGP4. All of these pseudogenes were fixed in the genome of the human-chimpanzee common ancestor. NANOGP8 is the most recent pseudogene and it originated exclusively in the human lineage after the human-chimpanzee divergence. NANOGP1 is apparently an unprocessed pseudogene. Comparison of its sequence to the functional NANOG gene's reading frame suggests that this apparent pseudogene remained functional after duplication and, therefore, was subject to selection-driven conservation of its reading frame, and that it may retain some functionality or that its loss of function may be evolutionarily recent.

Animals↗
PubMed2004

Collective violence: comparisons between youths and chimpanzees.

Patterns of collective violence found among humans include similarities to those seen among chimpanzees. These include participation predominantly by males, an intense personal and group concern with status, variable subgroup composition, defense of group integrity, inter-group fights that include surprise attacks, and a tendency to avoid mass confrontation. Compared to chimpanzee communities, youth gangs tend to be larger, composed of younger individuals, occupying smaller territories and having a more complex organization. Youth gangs also differ from chimpanzee communities as a result of numerous cultural and environmental influences including complex relations with non-gang society. These relations are governed in important ways by such factors as perceived economic and personal constraints, policing, family structure, and levels of poverty, crime, and racism. Nevertheless, the concepts that sociologists use to account for collective violence in youth gangs are somewhat similar to those applied by anthropologists and biologists to chimpanzees. Thus in both cases collective violence is considered to emerge partly because males are highly motivated to gain personal status, which they do by physical violence. In the case of youth gangs, the reasons for the prevalence of physical violence in status competition compared to non-gang society are clearly context-specific, both culturally and historically. By contrast, among chimpanzees the use of physical violence to settle status competition is universal (in the wild and captivity). The use of physical violence in individual status competition therefore has different sources in youth gangs and chimpanzees. Regardless of its origin, however, its combination with an intense concern for status can explain: (1) why individual males form alliances among each other; and hence (2) how such alliances generate social power, closed groups, and a capacity for defense of territory or pre-emptive attacks on rivals. This comparison suggests that the use of physical violence to resolve individual status competition is an important predictor of collective violence at the gang level. We therefore view the similarities in aggression between humans and chimpanzees that we review here as being adaptive responses to local conditions, predicated on an inherent male concern for social status.

Adolescent↗
PubMed1999

Chimpanzees and retirement.

The subject of sanctuaries for chimpanzees has lately become the topic of a great deal of discussion (Brent, Butler, & Haberstroh, 1997; Committee on Long-Term Care of Chimpanzees, 1997; Dyke, Williams-Blangero, Mamelka, & Goodwin, 1995; Peterson & Goodall, 1993). In the United States, laboratories that use chimpanzees in research are facing a housing crisis. An increase in captive births caused by the initiation of the National Chimpanzee Breeding and Research Program in 1986 (Hobson, Graham, & Rowell, 1991), coupled with the diminished use of chimpanzees as experimental subjects, have led to a large population of chimpanzees considered to be surplus to demand (Blood, Wolfle, & Whitney, 1992). These chimpanzees, as well as an unknown number from the private sector, are candidates for what is currently being called retirement.

Journal Article↗
PubMed2003

Endocrinologic comparison of activin a secretion during pregnancy and early lactation in Japanese monkeys, chimpanzees, and humans.

Secretion of activin A in Japanese monkeys and chimpanzees during pregnancy and early postpartum periods was investigated, and the results were compared with those in humans. Plasma activin A increased throughout pregnancy in Japanese monkeys, and the level was significantly higher in the third and fourth quarters than in the first quarter. After parturition in the Japanese monkey, circulating activin A decreased to levels seen during the normal menstrual cycle. In chimpanzees, plasma activin A remained low until the third quarter of pregnancy and abruptly increased in the fourth quarter. After parturition in chimpanzees, however, circulating activin A concentrations still remained as high as levels in the fourth quarter until 42 h after parturition, then decreased to nadir levels at 1 mo after parturition, suggesting that activin A in chimpanzees may be secreted from other organs such as uterus in addition to placenta. Positive staining with inhibin/ activin alpha-, betaA-, and betaB-subunit antisera was observed in the cytoplasm of the syncytiotrophoblast of term placenta in the Japanese monkey, chimpanzee, and human. These results demonstrated that circulating activin A gradually increased from early pregnancy in Japanese monkey, whereas an abrupt increase occurred at late pregnancy in chimpanzees. These results also demonstrated that the syncytiotrophoblast of placenta is the source of activin A in Japanese monkeys and chimpanzees as well as humans.

Activins↗
PubMed2000

Oral induction of anesthesia with droperidol and transmucosal carfentanil citrate in chimpanzees (Pan troglodytes).

Five chimpanzees (Pan troglodytes) initially received oral droperidol sedation (1.25 mg for a juvenile chimpanzee, body wt = 18.5 kg, and 2.5 mg for adults, body wt >20 kg, range: 18.5-71 kg) followed by transmucosal carfentanil administration at 2.0 microg/kg. This preinduction regimen was developed to produce heavy sedation or even light anesthesia in order to eliminate the need for or at least minimize the stress of darting with tiletamine/zolazepam at 3 mg/kg i.m. This study was designed to assess the safety and efficacy of transmucosal carfentanil. Once each animal was unresponsive to external stimuli, or at approximately 25 min (range 24-34 min) after carfentanil administration, naltrexone and tiletamine/zolazepam (N/T/Z) were combined into one intramuscular injection for anesthetic induction. Naltrexone was administered at 100 times the carfentanil dose in milligrams. For comparison, two chimpanzees received only droperidol, 2.5 mg p.o., followed by tiletamine/zolazepam, 3 mg/kg i.m. The preinduction period for all animals receiving carfentanil was characterized as smooth, with chimpanzees becoming gradually less active and less responsive to external stimuli. Two animals became very heavily sedated at 24 and 35 min, respectively, and were hand injected with N/T/Z. The other three chimpanzees became sternally recumbent but retained some response to stimuli, and N/T/Z was administered by remote injection with minimal response. Rectal body temperatures, pulse and respiratory rates, arterial oxygen hemoglobin saturation, and arterial blood gases were measured at initial contact (t = 0 min) and at 10-min intervals thereafter. Respiratory depression was present in all chimpanzees, regardless of protocol. Mean hemoglobin saturation was 91% for both groups. Mean partial pressure of oxygen, arterial values for carfentanil-treated and control animals were 64.4 +/- 7.6 and 63.5 +/- 6.0 at t = 0, respectively. Only the partial pressure of carbon dioxide, arterial (Paco2) and pH showed significant differences between treated and control animals. Mean Paco2 was greater and mean pH lower for the carfentanil-treated group compared with the controls at t = 0 (58.9 +/- 3.7 and 50.3 +/- 3.1 for Paco2 and 7.33 +/- 0.02 and 7.40 +/- 0.30 for pH, respectively). The results of this study suggest that oral droperidol followed by transmucosal carfentanil can be used effectively as a premedication regimen to produce profound sedation, which limits the stress of darting during parenteral anesthetic induction with tiletamine/zolazepam in chimpanzees. The main side effect of respiratory depression appears to be adequately managed by reversing the carfentanil at the time of induction.

Administration, Oral↗
PubMed2001

Adaptation of a strain of Plasmodium vivax from India to New World monkeys, chimpanzees, and anopheline mosquitoes.

A strain of Plasmodium vivax from India was adapted to develop in splenectomized Saimiri boliviensis, Aotus lemurinus griseimembra, A vociferans, A. nancymai, A. azarae boliviensis, hybrid Aotus monkeys, and splenectomized chimpanzees. Infections were induced via the inoculation of sporozoites dissected from the salivary glands of Anopheles stephensi and An. dirus mosquitoes to 12 Aotus and 8 Saimiri monkeys; transmission via the bites of infected An. stephensi was made to 1 Aotus monkey and 1 chimpanzee. The intravenous passage of infected erythrocytes was made to 9 Aotus monkeys and 4 chimpanzees. Gametocytes in 13 Aotus monkeys and 4 chimpanzees were infectious to mosquitoes. Infection rates were markedly higher in mosquitoes fed on chimpanzees. PCR studies on 10 monkeys injected with sporozoites revealed the presence of parasites before their detection by microscopic examination. The India VII strain of P. vivax develops in Aotus and Saimiri monkeys and chimpanzees following the injection of parasitized erythrocytes, or sporozoites, or both. The transmission rate via sporozoites to New World monkeys of approximately 50% may be too low for the testing of sporozoite vaccines or drugs directed against the exoerythrocytic stages. However, the strain is highly infectious to commonly available laboratory-maintained anopheline mosquitoes. Mosquito infection is especially high when feedings are made with gametocytes from splenectomized chimpanzees.

Adaptation, Biological↗
PubMed1999

Brain weight throughout the life span of the chimpanzee.

Studies on human postmortem material report lower brain weights in older than in younger cohorts, whereas there is no apparent change with age in the rhesus monkey. In view of these contrasting results, we examined the pattern of brain weight across the life span in the chimpanzee, one of the closest biological relatives of humans. To place the study in context of the empirical life expectancy of the chimpanzee, we first performed a survival analysis on data from 275 chimpanzees that were maintained in the colony of the Yerkes Primate Center. The survival analysis revealed the maximum life spans of female and male chimpanzees to be about 59 and 45 years, respectively. We examined fresh brain weights from 76 chimpanzees ranging in age from birth to 59.4 years of age. The brains were taken from 9 infants (birth to 1 year of age), 25 juveniles (1-7 years), 13 adolescents (7-15 years), 21 young adults (15-30 years), and 8 old adults (over 30 years). Adult brain weight was achieved by the age of 7 years. The adolescent and young adult chimpanzees had the largest brain weights; in these two age groups combined, the mean brain weight (+/- standard deviation) was 368.1 g (+/-37.3) for females (n = 17) and 405.6 g (+/-39.4) for males (n = 17). This sex difference was statistically significant (P < 0.01). Simple linear regression performed on the combined material from females and males aged 7 years and older revealed a decline in brain weight with advancing age of 1.1 g/year (P < 0.05). When the effect of sex on brain weight was statistically controlled for, the loss of brain weight with age was 0.9 g/year (P = 0.07). These results suggest that brain weight declines moderately with age in the chimpanzee as it does in humans.

Age Factors↗
PubMed1999

The chimpanzee as a model of human benign prostatic hyperplasia.

PURPOSE: The etiology and natural history of benign prostatic hyperplasia (BPH), the most common benign disease in aging men, remain obscure. The canine BPH model has serious limitations but other animal BPH models have not been identified. We evaluated whether the chimpanzee, man's closest primate relative, developed spontaneous BPH. MATERIALS AND METHODS: A cross-sectional analysis of a colony (White Sands Research Center) that contained 700 chimpanzees was undertaken by sampling 63 male and female (controls) chimpanzees 8 to 35 years old. The presence of spontaneous BPH was evaluated by assessing pathological and clinical variables, including prostate volume, serum prostate specific antigen, presence of histological BPH, serum androgens and estradiol, and urodynamics studies. RESULTS: The chimpanzee had evidence of spontaneous histological BPH, and incidence and grade increased with age. Spontaneous BPH was manifested by increased prostate volume, higher serum prostate specific antigen, higher stromal/epithelial ratio and decreased urinary flow rates. As in man, serum androgens did not correlate with BPH in the chimpanzee. CONCLUSIONS: Male chimpanzees developed spontaneous histological BPH at the same relative point in their life cycle as humans which resulted clinically in larger prostates and decreased urinary flow rates. Serum hormone levels did not appear to correlate with BPH. A better understanding of the chimpanzee BPH model may lead to new therapeutic strategies for BPH in man.

Age Factors↗
PubMed2000

[Adaptations in reproduction and behavior of captive chimpanzees-- zoobiological and veterinary managements].

Monitoring of renal LH-excretion, changes in genital tumescence and menses assesses reproductive status in zookept female chimpanzees. Temporary detumescence of female sex skin in estrus is a reliable indicator for stress. Assessment of female chimpanzee reproductive status relates to local and individual variation of cycle length and temporal correlation of investigated parameters. Monitoring of neonate chimpanzee behavioural ontogeny is an essential tool of evaluating applied rearing methods since individuals were to be integrated into the adult group during adolescence. Slow and continuous transition periods between consecutive rearing phases avoid irreversible disturbed behaviour. Care by one person up to the age of 12 months, followed by a 3 year stay in a peer group guarantee normal development in zookept infant chimpanzees. 4-5 years old chimpanzees with infantile attributes and abilities to submit and appease can be integrated to adults with low risk. In female gorillas sexual cyclicity was monitored by renal excretion of LH, length of menses, sexual behaviour and--in tame females--by basal body temperature and variation of length of the urogenital cleft. Intraspecific variation of cyclicity allowed individual fertility assessment after comparison of several cycles. Analyses of behaviour gave hints to overcharged adaptability and reduced infertility under inadequate maintenance. Data on semen and testicular biopsy improve fertility evaluation in gorilla males and point to degree and time of tissue alteration and etiology. Body hygiene analogous to the human, tool use and interspecific play with chimpanzees and humans behind window screens were observed in inadequately kept gorillas. Homosexual behaviour among females was reversible with environmental and social changes. Coalitions among nonrelated females were an effective social strategy against an aggressive male. Cyclicity was disturbed drastically by social events such as physical lesions made by a male but normalized with improved social situation. Disturbed cyclicity featured prolongation of interestrus intervals and complete detumescence, oligomenorrhea and amenorrhea. Nulliparous females in their third decennium needed more than 1.5 years of social contact to a fertile male to become fullterm pregnant. During the first two months of pregnancy stillbirths and embryonic resorptions were detected. Handreared and inexperienced primiparous gorilla females accepted their infants and reared them normally after witnessing motherrearing in neighbored chimpanzee females for several years. Opportunities of free choice and decision making determine zookept pongid behaviour, that cannot be compared with prisoners' ethology. Adaptations of ontogenetic behaviour and reproduction, teleonomic patterns and zoomorphism are of zoobiological relevance. Adaptations develope during prolonged periods of time and thus results of corresponding management issues are to be assessed a posteriori.

Adaptation, Physiological↗
PubMed1991

Human markers for IgG2 and IgG4 appear to be on the same molecule in the chimpanzee.

It has been reported that all four immunoglobulin G (IgG) subclasses present in human serum are also present in chimpanzee serum, as detected with antibodies specific for the human IgG subclasses. We used monoclonal antibodies (mAb) specific for human IgG subclasses to measure concentrations of the four subclasses in the chimpanzee sera. Initial ELISA studies indicated that epitopes for all four human subclasses are present in chimpanzee sera. The concentrations of IgG1, IgG2 and IgG3 were similar in human and chimpanzee sera, but the registered concentrations of IgG4 were different. Absorption of IgG2-reactive material from chimpanzee serum with IgG2 mAb resulted in removal of IgG4-reactive material as well. Conversely, absorption of IgG4-reactive material removed IgG2-reactive material. IgG2-reactive material, isolated from chimpanzee serum using solid-phase anti-IgG2 mAb, reacted with anti-IgG4 mAb, and isolated IgG4-reactive material reacted with anti-IgG2 mAb. Three anti-IgG2 mAb and five anti-IgG4 mAb, each of which react with separate epitopes on their respective human isotype, were used in these studies. We conclude that chimpanzee serum contains only three IgG isotypes related to those of humans, one of which contains determinants related to both human IgG2 and IgG4.

Adult↗