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PubMed2007

Ethological study of manual laterality in naturalistic housed chimpanzees (Pan troglodytes) from the Mona Foundation Sanctuary (Girona, Spain).

During recent years, handedness of nonhuman primates has been the subject of several studies, especially focused on our closest relatives: the chimpanzees. These studies have dealt with both wild and captive chimpanzees, and they seem to point to divergent conclusions, which have been interpreted as a by-product of the human influence in the captive samples. Here we present the results of a study of 10 chimpanzees (Pan troglodytes). In the past, they were trained in circus and marketing tasks (humanised behaviours), until they were confiscated and accepted into the Mona Foundation (in northeast Spain) in 2000, where they live in a semi-naturalistic environment. This study has been performed through observational bouts without systematic human influence, recording the actions carried out by chimpanzees when performing spontaneous activities. Our results indicate that chimpanzees that were under strong human influence in the past show the same trend in handedness as those living in freedom: few significant lateralities were observed among either individuals or tasks. So, laterality may not be influenced by humanisation. However, this conclusion must be taken as preliminary because very few individuals were studied.

Animals↗
PubMed1997

Manual specialisation and tool use in captive chimpanzees (Pan troglodytes): the effect of unimanual and bimanual strategies on hand preference.

Hand preference for tool use was assessed in a sample of captive chimpanzees (Pan troglodytes). Whether the subjects solved the tool task using either a unimanual or coordinated bimanual strategy was manipulated in the chimpanzees. No population-level hand preference was found for tool use when unimanual strategies were used by the chimpanzees. However, a population-level right-hand bias was found when coordinated bimanual actions were required of the chimpanzees. A significant correlation was found in hand use for the two hand preference testing conditions. Neither sex nor rearing was found to significantly affect the direction or strength in hand preference. These results may explain discrepancies in hand preference reported in captive and wild chimpanzees with regard to tool use and other manual activities.

Journal Article↗
PubMed1991

Gorilla class I major histocompatibility complex alleles: comparison to human and chimpanzee class I.

14 gorilla class I major histocompatibility complex (MHC) alleles have been isolated, sequenced, and compared to their counterparts in humans and chimpanzees. Gorilla homologues of HLA-A, -B, and -C were readily identified, and four Gogo-A, four Gogo-B, and five Gogo-C alleles were defined. In addition, an unusual Gogo class I gene with features in common with HLA-A and its related pseudogene, HLA-H, is described. None of the gorilla alleles is identical or even closely related to known class I alleles and each encodes a unique antigen recognition site. However, the majority of polymorphic substitutions and sequence motifs of gorilla class I alleles are shared with the human or chimpanzee systems. In particular, elements shared with HLA-A2 and HLA-B27 are found in Gogo-A and -B alleles. Diversity at the Gogo-B locus is less than at the Gogo-A locus, a trend the opposite of that seen for HLA-A and -B. The Gogo-C locus also appears to have limited polymorphism compared to Gogo-A. Two basic Gogo-C motifs were found and they segregate with distinctive sets of HLA-C alleles. HLA-A allels are divided into five families derived from two ancient lineages. All chimpanzee A alleles derived from one of these lineages and all gorilla alleles derive from the other. Unlike chimpanzee Patr-A alleles, the Gogo-A alleles do not clearly partition with one of the HLA-A families but have similarities with two. Overall, gorilla class I diversity appears from this sampling to show more distinctions from class I HLA than found for chimpanzee class I.

Alleles↗
PubMed1993

Conversion of an immunogenic human immunodeficiency virus (HIV) envelope synthetic peptide to a tolerogen in chimpanzees by the fusogenic domain of HIV gp41 envelope protein.

The fusogenic (F) domain of human immunodeficiency virus (HIV) gp41 envelope (env) protein has sequence similarities to many virus and mediates the fusion of HIV-infected cells. During a survey of the immunogenicity of HIV env peptides in chimpanzees, we have observed that HIV peptide immunogenicity was dramatically altered by the NH2-terminal synthesis of the gp41 F domain to an otherwise immunogenic peptide. We compared two hybrid peptide types comprised of T helper (Th) and B cell epitopes of HIV gp120 env protein for their immunogenicity in chimpanzees. The Th-B epitope hybrid peptides contained the HIV gp120 Th cell determinant, T1 (amino acids [aa] 428-440)-synthesized NH2 terminal to gp120 V3 loop peptides, which contain B cell epitopes that induce anti-HIV-neutralizing antibodies (SP10IIIB [aa 303-321] and SP10IIIB [A] [aa 303-327]). The F-Th-B peptide contained the HIV gp41 F domain of HIVIIIB gp41 (aa 519-530)-synthesized NH2 terminal to the Th-B peptide. Whereas Th-B peptides were potent immunogens for chimpanzee antibody and T cell-proliferative responses, the F-Th-B peptide induced lower anti-HIV gp120 T and B cell responses. Moreover, immunization of chimpanzees with F-Th-B peptide but not Th-B peptides induced a significant decrease in peripheral blood T lymphocytes (mean decrease during immunization, 52%; p < 0.02). Chimpanzees previously immunized with F-Th-B peptide did not respond well to immunization with Th-B peptide with T or B cell responses to HIV peptides, demonstrating that the F-Th-B peptide induced immune hyporesponsiveness to Th and B HIV gp120 env determinants. These observations raise the hypothesis that the HIV gp41 env F domain may be a biologically active immunoregulatory peptide in vivo, and by an as yet uncharacterized mechanism, promotes primate immune system hyporesponsiveness to otherwise immunogenic peptides.

Amino Acid Sequence↗
PubMed1999

Experimental transmission of hepatitis C virus-associated fulminant hepatitis to a chimpanzee.

Hepatitis C virus (HCV) was transmitted from a patient with fulminant hepatitis C to a chimpanzee. The patient had developed two episodes of fulminant hepatitis C, each occurring after a separate liver transplantation. Serial serum and liver samples from the patient and the chimpanzee were analyzed for HCV replication, genotype, quasispecies heterogeneity, and antibodies. In the patient, the levels of HCV replication in serum and liver correlated with the degree of hepatocellular necrosis and the clinical expression of fulminant hepatitis. The same HCV strain, genotype 1a, was recovered from both episodes of fulminant hepatitis. An unusually severe acute hepatitis was also observed in the chimpanzee. The viruses recovered from the patient and the chimpanzee were almost identical and displayed relatively little quasispecies heterogeneity. Thus, the same HCV strain induced two episodes of fulminant hepatitis in a single patient and severe hepatitis in a chimpanzee, suggesting that the pathogenicity or virulence of a specific HCV strain may be important in the pathogenesis of fulminant hepatitis C.

Adult↗
PubMed2000

Progressive infection in a subset of HIV-1-positive chimpanzees.

Chimpanzees are susceptible to infection with human immunodeficiency virus (HIV)-1; however, infected animals usually maintain normal numbers of CD4(+) T lymphocytes and do not develop immunodeficiency. We have examined 10 chronically infected HIV-1-positive chimpanzees for evidence of progressive infection. In addition to 1 animal that developed AIDS, 3 chimpanzees exhibit evidence of progressive HIV infection. All progressors have low CD4(+) T cell counts (<200 cells/microL), severe CD4:CD8 inversion, and marked reduction in interleukin-2 receptor expression by CD4(+) T cells. In comparison with HIV-positive nonprogressor chimpanzees, progressors have higher plasma and lymphoid virus loads, greater CD38 expression in CD8(+)/HLA-DR(+) T cells, and greater serum concentrations of soluble tumor necrosis factor type II receptors and beta2-microglobulin, all markers of HIV progression in humans. These observations show that progressive HIV-1 infection can occur in chimpanzees and suggest that the pathogenesis of progressive infection in this species resembles that in humans.

ADP-ribosyl Cyclase↗
PubMed2004

New insights into chimpanzees, tools, and termites from the Congo Basin.

The tool-using behaviors of wild chimpanzees comprise the most impressive assemblages and flexible repertoires of nonhuman material culture. We expand knowledge of the breadth and complexity of tool use in this species by providing the first descriptions of the form and function of two distinct tool sets used by chimpanzees in preying upon termites within the forests of the Goualougo Triangle, Republic of Congo. Further, we report the first application of remote video monitoring technology to record wild chimpanzee tool-using behavior. Based on tool assemblages recovered at termite nests, we hypothesized that chimpanzees were regularly visiting two forms of termite nests and using specific tools to extract termite prey depending on the structure of the nest. Six months of continuous remote video monitoring at six termite nests confirmed that chimpanzees use a tool set to puncture and fish at subterranean termite nests and another tool set to perforate and fish at epigeal (aboveground) nests. Our findings of strict adherence to tool forms at different nest types, tool material selectivity, repeated visits to nests with reusable wood tool assemblages, and differences in material culture between communities have broad implications for our understanding of the ecological and cultural factors that shape hominoid tool use.

Animals↗
PubMed2002

In vitro replication of SIVcpz is suppressed by beta-chemokines and CD8+ T cells but not by natural killer cells of infected chimpanzees.

Unlike humans, chimpanzees are relatively resistant to AIDS after infection with HIV-1 or simian immunodeficiency virus of chimpanzee (SIVcpz). We hypothesized that resistance to disease progression is associated with efficient suppression of virus replication possibly by beta-chemokines secreted by CD8+ lymphocytes and especially natural killer (NK) cells. In vitro suppression of virus replication can be easily studied in SIVcpz-infected chimpanzees because they produce high infectious virus titers in their peripheral blood. A study was undertaken to assess the sensitivity of SIVcpz to beta-chemokines in vitro and to investigate the role of endogenous beta-chemokines in relation to the in vitro capacity of CD8+ lymphocytes and NK cells of chimpanzees to suppress SIVcpz replication. Our results show that SIVcpz uses CCR5 as a coreceptor to gain cell entry and is sensitive to recombinant beta-chemokines in vitro. Here we report that despite their potent capacity to produce RANTES, NK cells of infected chimpanzees do not suppress SIVcpz replication in vitro, in contrast to CD8+ lymphocytes. We also show that endogenous beta-chemokines are not the predominant factors mediating in vitro suppression.

Animals↗
PubMed2005

Identification of nine human-specific frameshift mutations by comparative analysis of the human and the chimpanzee genome sequences.

MOTIVATION: The recent release of the draft sequence of the chimpanzee genome is an invaluable resource for finding genome-wide genetic differences that might explain phenotypic differences between humans and chimpanzees. AVAILABILITY: In this paper, we describe a simple procedure to identify potential human-specific frameshift mutations that occurred after the divergence of human and chimpanzee. The procedure involves collecting human coding exons bearing insertions or deletions compared with the chimpanzee genome and identification of homologs from other species, in support of the mutations being human-specific. Using this procedure, we identified nine genes, BASE, DNAJB3, FLJ33674, HEJ1, NTSR2, RPL13AP, SCGB1D4, WBSCR27 and ZCCHC13, that show human-specific alterations including truncations of the C-terminus. In some cases, the frameshift mutation results in gene inactivation or decay. In other cases, the altered protein seems to be functional. This study demonstrates that even the unfinished chimpanzee genome sequence can be useful in identifying modification of genes that are specific to the human lineage and, therefore, could potentially be relevant to the study of the acquisition of human-specific traits.

Amino Acid Sequence↗
PubMed1996

A fine-scale comparison of the human and chimpanzee genomes: linkage, linkage disequilibrium and sequence analysis.

We have performed a fine-scale comparative study of the human and chimpanzee genomes, using linkage, linkage disequilibrium and sequence analyses on microsatellite loci spanning a region of approximately 30 cM on human chromosome 4p. Our results extend the findings of previous studies that indicated virtually complete conservation between the human and chimpanzee genomes at the chromosomal and sub-chromosomal level and support the hypothesis, derived from previous analyses of mitochondrial DNA, that chimpanzee populations are more diverse than human ones. By sequencing several human and chimpanzee alleles of two microsatellites we showed that base substitutions that diminish the length of perfect repeats (but do not change allele sizes) are probably responsible for the low heterozygosity of these loci in chimpanzees; our results suggest that the evolutionary history of microsatellites should not be inferred from comparisons of mean allele lengths between populations or species.

Alleles↗
PubMed1975

Effects of cyclophosphamide on hepatitis B virus infection and challenge in chimpanzees.

The role of antibodies to the surface antigen of hepatitis B virus (HBsAg) and to the hepatitis B core antigen (HBcAg) and of cell-mediated immunity in hepatitis B virus infections and in resistance to challenge was studied in six chimpanzees. Two chimpanzees were studied during primary hepatitis B virus infection while being treated with cyclophosphamide (5-15 mg/kg im three times per week). Cyclophosphamide treatment may have predisposed these chimpanzees to chronic hepatitis B virus infections. Four other chimpanzees convalescent from primary hepatitis B virus infection (subtype ayw) were challanged with hepatitis Bvirus; two were callenged with heterologous virus (subtype adw) without immunosuppression, and two were challenged with homologous virus (subtype syw)while being treated with cyclophosphamide. Chimpanzees with residual humoral immunity, demonstrable by serum antibodies against the group determinant a and subdeterminant y of HBsAg, resisted challenge with either heterologous or homologous hepatitis B virus despite cyclophosphamide immunosuppression in the latter case. Antibodies to the hepatitis B virus core did not appear necessary for protection against hepatitis B virus infection in these chimps.

Animals↗
PubMed1981

Non-A, non-B hepatitis in chimpanzees and marmosets.

Nine of 15 specimens of human origin thought to contain non-A, non-B hepatitis agents caused hepatitis in recipient chimpanzees. Two have been further characterized. One inoculum, designated strain F, has been reported to produce unique cytoplasmic changes detected by electron microscopy in liver biopsy specimens; the other, strain H, produced distinctive nuclear changes. It is not yet clear whether these two changes result from infection by different agents; they have been useful markers of non-A, non-B hepatitis in chimpanzees. Strain F was serially passaged six times in chimpanzees, and the infectivity titer of the strain F plasma was estimated to be less than 10(2)/ml. Strain H had an infectivity titer in chimpanzees of at least 10(6)/ml. Both the strain F and strain H agents have been successfully transmitted and serially passaged in marmosets. Although hepatitis was detected in a lower percentage of marmosets than chimpanzees given either the strain F or H inoculum, the infectivity titer of the strain H agent appeared to be greater than or equal to 10(8) marmoset infectious doses/ml.

Acute Disease↗
PubMed1995

Immunization of chimpanzees with recombinant gp160, but not infection with human immunodeficiency virus type 1, induces envelope-specific Th1 memory cells.

The human immunodeficiency virus (HIV) type 1 envelope protein (recombinant [r] gp160)-induced T cell lymphokine release pattern of chimpanzees immunized with HIVIIIB rpg160 tested and compared with rpg160-induced lymphokine releases of T cells from unimmunized, HIV-1-infected chimpanzees. The results showed that infection of chimpanzees with HIV-1 did not induce rgp160-specific memory T cells (as evidenced by the lack of Th1 and 2 type lymphokine releases after rgp160 stimulation). In contrast, T cells of rgp160-immunized chimpanzees released Th1 type lymphokines upon stimulation with rgp160 of HIVIIIB, HIVMN, and HIVRF. release was comparable whether chimpanzees were immunized with rgp160 only or also challenged with HIV-1 and protected or not protected. Thus, rgp160 immunization leads to generation of Th1 type memory cells. Whether Th1 type responses contribute to protection against HIV-1 infection has yet to be clarified.

Animals↗
PubMed2003

Compositional evolution of noncoding DNA in the human and chimpanzee genomes.

We have examined the compositional evolution of noncoding DNA in the primate genome by comparison of lineage-specific substitutions observed in 1.8 Mb of genomic alignments of human, chimpanzee, and baboon with 6542 human single-nucleotide polymorphisms (SNPs) rooted using chimpanzee sequence. The pattern of compositional evolution, measured in terms of the numbers of GC-->AT and AT-->GC changes, differs significantly between fixed and polymorphic sites, and indicates that there is a bias toward fixation of AT-->GC mutations, which could result from weak directional selection or biased gene conversion in favor of high GC content. Comparison of the frequency distributions of a subset of the SNPs revealed no significant difference between GC-->AT and AT-->GC polymorphisms, although AT-->GC polymorphisms in regions of high GC segregate at slightly higher frequencies on average than GC-->AT polymorphisms, which is consistent with a fixation bias favoring high GC in these regions. However, the substitution data suggest that this fixation bias is relatively weak, because the compositional structure of the human and chimpanzee genomes is becoming homogenized, with regions of high GC decreasing in GC content and regions of low GC increasing in GC content. The rate and pattern of nucleotide substitution in 333 Alu repeats within the human-chimpanzee-baboon alignments are not significantly affected by the GC content of the region in which they are inserted, providing further evidence that, since the time of the human-chimpanzee ancestor, there has been little or no regional variation in mutation bias.

Alleles↗
PubMed2005

A genomic region evolving toward different GC contents in humans and chimpanzees indicates a recent and regionally limited shift in the mutation pattern.

DNA sequences evolving differently in the human and chimpanzee genomes signal recent and regionally limited changes in the process of DNA sequence evolution. Here we present the comparison of 90 kb from the nonrecombining part of the human Y chromosome to the corresponding part of the chimpanzee genome using gorilla as out-group. Our results reveal a significant difference in the region-specific substitution process among the human and chimpanzee lineages. As a consequence, this region experiences a change in its GC content on the human lineage while it resides in compositional equilibrium on the chimpanzee lineage. Based on our analysis, we suggest a recent and species-specific shift in the region's mutation pattern as the cause of its differing evolution in humans and chimpanzees.

Animals↗
PubMed1999

Molecular evolution of the CMT1A-REP region: a human- and chimpanzee-specific repeat.

The CMT1A-REP repeat consists of two copies of a 24-kb sequence on human chromosome 17p11.2-12 that flank a 1.5-Mb region containing a dosage-sensitive gene, peripheral nerve protein-22 (PMP22). Unequal meiotic crossover mediated by misalignment of proximal and distal copies of the CMT1A-REP in humans leads to a 1.5-Mb duplication or deletion associated with two common peripheral nerve diseases, Charcot-Marie-Tooth disease type 1A (CMT1A) and hereditary neuropathy with liability to pressure palsies (HNPP). Previous molecular hybridization studies with CMT1A-REP sequences suggested that two copies of the repeat are also found in the chimpanzee, raising the possibility that this unique repeat arose during primate evolution. To further characterize the structure and evolutionary synthesis of the CMT1A-REP repeat, fluorescent in situ hybridization (FISH) analysis and heterologous PCR-based assays were carried out for a series of primates. Genomic DNA was analyzed with primers selected to differentially amplify the centromeric and telomeric ends of the human proximal and distal CMT1A-REP elements and an associated mariner (MLE) sequence. All primate species examined (common chimpanzee, pygmy chimpanzee, gorilla, orangutan, gibbon, baboon, rhesus monkey, green monkey, owl monkey, and galago) tested positive for a copy of the distal element. In addition to humans, only the chimpanzee was found to have a copy of the proximal CMT1A-REP element. All but one primate species (galago) tested positive for the MLE located within the CMT1A-REP sequence. These observations confirm the hypothesis that the distal CMT1A-REP element is the ancestral sequence which was duplicated during primate evolution, provide support for a human-chimpanzee clade, and suggest that insertion of the MLE into the CMT1A-REP sequence occurred in the ancestor of anthropoid primates.

Animals↗
PubMed1991

Antibody-dependent cellular cytotoxicity against HIV-1 in sera of immunized chimpanzees.

After immunization of chimpanzees against HIV antigens, antibodies that mediate antibody-dependent cellular cytotoxicity (ADCC) were evaluated and compared with anti-HIV-antibody levels detected by enzyme-linked immunosorbent assay (ELISA) and neutralizing antibody titers. Adult chimpanzees were immunized with different HIV-1 (LAV-BRU) antigen preparations: recombinant vaccinia virus (rVV) expressing gp160, p25 or p27nef; formalin- and beta-propiolactone-inactivated whole virus (inHIV); soluble recombinant gp160 either associated or not associated with other HIV proteins; a 25-mer peptide from the V3 region of gp120 coupled with KLH (V3-KLH). Immunization with the various rVV mixtures induced no or borderline ADCC increase above preimmune serum levels. Stronger and more sustained reactivity was elicited by inHIV. Purified HIV antigens elicited ADCC activity when the chimpanzees were naive; ADCC increased or remained at the same level when the animals had been preimmunized with rVV and/or inHIV. This type of reactivity apparently did not depend on whether gp160 alone or mixed with other proteins was used for immunization. The injection of V3-KLH resulted in only little, if any, recall ADCC response. ELISA antibody titers significantly correlated with ADCC and neutralizing antibody titers, but serum ADCC was independent of neutralizing antibody titers, an indication that the two latter serum activities are mediated by independent antibodies. Therefore, ADCC is elicited in the same manner as other antibody activities by the immunization of chimpanzees with inHIV or with purified recombinant HIV antigen preparations. The results obtained from the three chimpanzees of this series, which were subsequently challenged with infectious virus through the intravenous route, suggest that serum ADCC may be considered for vaccination purposes.

Amino Acid Sequence↗
PubMed2000

Therapeutic immunization of HIV-infected chimpanzees using HIV-1 plasmid antigens and interleukin-12 expressing plasmids.

OBJECTIVE: To assess HIV-1 DNA vaccination and co-immunization with interleukin (IL)-12 and IL-10 as immunotherapy in the HIV-1 infected chimpanzee model system. METHODS: Four chimpanzees that were infected with HIV-1-IIIB for longer than 4 years and remained symptom free were immunized with HIV-1 plasmid vaccines. Two chimpanzees were immunized with DNA plasmids that encoded env/rev, gag/pol along with a plasmid that encoded both chains of human IL-12. A third animal was immunized with HIV-1 DNA vaccine constructs and co-immunized with an IL-10 expressing plasmid. Finally a control animal received the HIV-1 DNA vaccine constructs alone. RESULTS: There was no evidence of systemic toxicity associated with the administration of the DNA vaccines or the cytokine-expressing plasmids. We observed that the IL-12/HIV-1 DNA vaccinated animals had enhanced proliferative responses to multiple HIV-1 antigens at multiple time points. The animal that was co-immunized with HIV-1 and IL-10 did not have any changes in the proliferative responses. Finally, the control chimpanzee demonstrated moderate increases in the proliferative responses to HIV-1 antigens. The animal that received HIV-1 vaccines alone and the animals co-immunized with IL-12 all had declines in viral load over the course of the study, however, the decrease in viral loads were transient in all animals. CONCLUSION: Immunization of HIV-1 infected chimpanzees with DNA based vaccines containing the env, gag and pol genes can transiently boost the env specific proliferative responses. Co-administration of IL-12 expressing plasmids further leads to transient boosting of the proliferative response to the core protein, p24 as well. However, at these doses the impact on viral load is minimal.

AIDS Vaccines↗