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C Coulibaly

Publications and source records attributed to C Coulibaly.

At least 19 recordsLinked to original sources
PubMed2004

A natural asymptomatic herpes B virus infection in a colony of laboratory brown capuchin monkeys (Cebus apella).

Herpes B virus (BV) infection of macaques persists in the natural host, but is mainly asymptomatic. However, BV can cause fatal disease in humans and in several non-macaque species such as capuchin monkeys (Cebus apella). The BV infection described here in a colony of capuchin monkeys was persistent but asymptomatic. Initially the infection was detected serologically in five out of seven animals. However, using polymerase chain reaction (PCR) developed specifically for BV, we found the virus in all seven clinically healthy animals. It is probable that the infection was transferred from BV-infected macaques housed in different cages but in the same room for several years. We have no evidence to indicate that similar asymptomatic infections may occur in other New World species but the possibility should not be discounted. We recommend that the housing of capuchin monkeys in close proximity to macaques should be avoided and that greater caution should be used when handling capuchin monkeys and possibly other New World species that have been in contact with macaques. All may act as a source of BV infection in humans, hence routine, repeated testing of all primates is essential.

Animal Technicians↗
PubMed2002

Productive infection of a mink cell line with porcine endogenous retroviruses (PERVs) but lack of transmission to minks in vivo.

Porcine endogenous retroviruses (PERVs) are considered a special risk for xenotransplantation because they are an integral part of the porcine genome and are able to infect cells of numerous species including humans in vitro. Among these cells, the mink lung epithelial cell line Mv1Lu could be productively infected with PERV. Provirus integration was detected by PCR, expression of viral proteins was shown by immunostaining and reverse transcriptase was detected in cell supernatants. PERV produced from mink cells could infect both, uninfected mink Mv1Lu cells and uninfected human 293 cells, with considerably higher virus production by human cells. Typical type C retroviruses were observed in PERV-infected mink cells using electron microscopy together with numerous multivesicular body (MVB)-like structures containing small virus-like particles, not present in uninfected mink cells. These MVBs could be stained with PERV-specific serum. In an attempt to establish a small animal model, PERV grown on mink cells was inoculated into adult and newborn American minks. Neither antibody production against PERV nor integration of viral DNA or production of viral proteins in tissues of different organs could be detected 12 weeks post virus inoculation, indicating that PERV infection had not occurred.

Animals↗
PubMed2002

Virus safety in xenotransplantation: first exploratory in vivo studies in small laboratory animals and non-human primates.

For xenotransplantation, the transplantation of animal cells, tissues and organs into human recipients, to date, pigs are favored as potential donors. Beside ethical, immunological, physiological and technical problems, the microbiological safety of the xenograft has to be guaranteed. It will be possible to eliminate all of the known porcine microorgansims in the nearby future by vaccinating or specified pathogen-free breeding. Thus, the main risk will come from the porcine endogenous retroviruses (PERVs) which are present in the pig genome as proviruses of different subtypes. PERVs will therefore be transmitted, with the xenograft, to the human recipient. PERVs can infect numerous different types of human primary cells and cell lines in vitro and were shown to adapt to these cells by serial passaging on uninfected cells. Furthermore, PERVs have high homology to other retroviruses, such as feline leukemia virus (FeLV) or murine leukemia virus (MuLV), which are known to induce tumors or immunodeficiencies in the infected host. To evaluate the potential risk of a trans-species transmission of PERV in vivo, naive and immunosuppressed rats, guinea pigs and minks were inoculated with PERV and screened over a period of 3 months for an antibody reaction against PERV proteins or for the integration of proviral DNA into the genomic DNA of the host's cells. Furthermore, we inoculated three different species of non-human primates, rhesus monkey (Macaca mulatta), pig-tailed monkey (Macaca nemestrina) and baboon (Papio hamadryas) with high titers of a human-adapted PERV. To simulate a situation in xenotransplantation, the animals received a daily triple immunosuppression using cyclosporine A, methylprednisolone and RAD, a rapamycin derivative, presently under development by Novartis. None of the small laboratory animals or the non-human primates showed production of antibodies against PERV or evidence of integration of proviral DNA in blood cells or cells of several organs, 3 months after virus inoculation, despite the observation that cells of the animals used in the experiment were infectible in vitro. This apparent difference in the outcome of the in vitro and the in vivo data might be explained by an efficient elimination of the virus by the innate or adaptive immunity of the animals.

Animals↗
PubMed2002

A spontaneous uterine sarcoma in a rhesus monkey (Macaca mulatta).

In primates, little has been reported about malignant mesenchymal uterine tumours. A case of a spontaneous metastasising uterine sarcoma in a 17-year-old rhesus monkey is presented. Clinically, transient abdominal pain, spasms, nausea, anaemia, a firm uterus and bloody vaginal discharge were noted. In a diagnostic laparoscopy, both massive adhesions in the lesser pelvis and 10 ml of ascites fluid were detected. In necropsy, in addition to peritonitis with massive adhesions, a cauliflower-shaped, irregular, tough, greyish-white uterine tumour was seen. Two cherry-sized tumour metastases were noticed in the greater omentum. In histology, both in the uterus and the metastases, a sarcoma with a low amount of connective tissue and well-differentiated cell nuclei was identified.

Animals↗
PubMed1999

Simian immunodeficiency virus (SIV) from sun-tailed monkeys (Cercopithecus solatus): evidence for host-dependent evolution of SIV within the C. lhoesti superspecies.

Recently we reported the characterization of simian immunodeficiency virus (SIVlhoest) from a central African l'hoest monkey (Cercopithecus lhoesti lhoesti) that revealed a distant relationship to SIV isolated from a mandrill (SIVmnd). The present report describes a novel SIV (SIVsun) isolated from a healthy, wild-caught sun-tailed monkey (Cercopithecus lhoesti solatus), another member of the l'hoest superspecies. SIVsun replicated in a variety of human T-cell lines and in peripheral blood mononuclear cells of macaques (Macaca spp.) and patas monkeys (Erythrocebus patas). A full-length infectious clone of SIVsun was derived, and genetic analysis revealed that SIVsun was most closely related to SIVlhoest, with an amino acid identity of 71% in Gag, 73% in Pol, and 67% in Env. This degree of similarity is reminiscent of that observed between SIVagm isolates from vervet, grivet, and tantalus species of African green monkeys. The close relationship between SIVsun and SIVlhoest, despite their geographically distinct habitats, is consistent with evolution from a common ancestor, providing further evidence for the ancient nature of the primate lentivirus family. In addition, this observation leads us to suggest that the SIVmnd lineage should be designated the SIVlhoest lineage.

Amino Acid Sequence↗
PubMed1998

Simian immunodeficiency virus of African green monkeys is apathogenic in the newborn natural host.

Several studies have demonstrated that newborn animals are more susceptible to disease development following infection with retroviruses than adults. Adult African green monkeys (AGMs) infected with SIVagm do not develop AIDS-like disease and the objective of the study was to determine whether experimental infection of newborn AGMs with SIVagm would result in pathogenesis. Neonatal AGMs were found to have a higher percentage of circulating CD4+ lymphocytes than adults (62% versus 14%) and therefore a higher potential pool of target cells for SIVagm infection. However, no differences in the in vitro replication kinetics of SIVagm in peripheral blood mononuclear cells of adult or neonatal AGMs could be observed. In vivo, the neonatal AGMs became viremic at the earliest two months after inoculation whereas the adult AGMs had evidence of virus replication already 2 to 6 weeks after infection. None of the animals developed AIDS-like symptoms upon infection. In the heterologous cynomolgus macaque host, a newborn infected with SIVagm developed early high virus loads and died two months after birth with AIDS-like histopathologic features. It would therefore appear that in contrast to the situation with many other retroviruses, newborn AGMs are no more permissive to SIVagm infection than are adults.

Aging↗
PubMed1996

The effect of simian immunodeficiency virus infection in vitro and in vivo on the cytokine production of isolated microglia and peripheral macrophages from rhesus monkey.

Microglia are the major target for human immunodeficiency virus (HIV) infection within the central nervous system. Because only a few cells are productively infected, it has been suggested that an aberrant cytokine production by this cell population may be an indirect mechanism leading to the development of neurological disorders in HIV-infected patients. Therefore we decided to study the secretion pattern of several interleukins (IL) by microglial cells and peripheral blood macrophages isolated from uninfected and simian immunodeficiency virus (SIV)-infected Rhesus monkeys. We found that uninfected, unstimulated primate microglia produce more IL-6 and less TNF alpha than peripheral blood macrophages, but generate comparable levels of IL-1 beta and IL-8. After infection with SIV in vitro, synthesis of all cytokines tested is increased compared to uninfected cultures and to peripheral blood macrophages. Microglia isolated from infected animals produce more IL-8 and TNF alpha than the uninfected cultures and display a strongly increased capacity to secrete TNF alpha upon stimulation with lipopolysaccharide. In addition, production of IL-6 by in vivo-infected microglia increases with time in culture to very high levels despite the fact that only a few cells contained replicating virus. These findings clearly show that the cytokine production of microglia is impaired after SIV infection both in vitro and in vivo and that a low level of viral replication is sufficient for these alterations to occur. In conclusion, the results of this study further support a possible role of cytokines in the pathogenesis of neuro-AIDS.

Animals↗
PubMed1996

Simian immunodeficiency virus (SIV) gp130 oligomers protect rhesus macaques (Macaca mulatta) against the infection with SIVmac32H grown on T-cells or derived ex vivo.

The efficacy of three SIVmac32H gp130 vaccines was compared in rhesus monkeys. Three rhesus monkeys were each immunized over a period of 20 weeks with a total of 600 microgram virion-derived gp130 oligomers (O-gp130) mixed with keyhole limpet hemocyanin and emulsified with incomplete Freund's adjuvant. Three other monkeys were infected with 5 x 10(8) PFU of vaccinia virus wild type (VV-wt) while three additional animals received an equivalent dose of VV expressing the gp130 of SIVmac (VV-gp130). At Week 8, the two VV-wt animals received an additional immunization with 100 microgram O-gp130 each. All VV-infected animals then received booster immunizations at Weeks 12, 16, and 20 with a total of 300 microgram O-gp130 per animal. All animals along with two controls were challenged iv with 50 MID50 of T-cell-grown SIVmac32H at Week 22. Four weeks after the challenge and thereafter, both controls and one animal from either VV group were infected as demonstrated by polymerase chain reaction (PCR), virus isolation, and antibody response. In contrast, all O-gp130 animals and one animal each from the VV-wt and the VV-gp130 group were completely protected as shown by negative PCR and virus reisolation. One animal of the VV-gp130 group was partially protected, since it remained virus isolation negative but became PCR positive. All protected animals did not develop a secondary antibody response. Six months after the first challenge, the five completely protected animals were reimmunized twice 4 weeks apart with a total of 200 microgram O-gp130 per animal. Two weeks later, all animals were challenged with 5 MID50 of the SIVmac32H/spI prepared from the spleen of an immunized, but unprotected SIV-infected rhesus monkey. After the second challenge, all three control animals and one of the vaccinees become productively infected. In contrast, two animals were completely protected, one from the former O-gp130 and one from the former VV-gp130 group. One animal from the former VV-wt group was only DNA-PCR positive and thus partially protected. Therefore, immunization with virion-derived gp130 oligomers of SIVmac32H can confer protection against the infection with T-cell-grown SIVmac32H as well as the ex vivo isolate SIVmac32H/spI.

Animals↗
PubMed1995

Repeated exposure of rhesus macaques to low doses of simian immunodeficiency virus (SIV) did not protect them against the consequences of a high-dose SIV challenge.

As part of an in vivo titration study of the macaque simian immunodeficiency virus (SIVmac) strain 251/spl, macaques were inoculated intravenously with various dilutions of this infectious SIVmac. Seven animals received dilutions from 10(-3) to 10(-6) of SIVmac251/spl. Two monkeys infected with the 10(-3) dilution of SIVmac exhibited a productive infection as indicated by seroconversion, detection of genomic RNA and proviral DNA and positive virus isolation. These animals showed a cytotoxic T cell (CTL) response against different SIVmac proteins without any measurable T cell proliferation. The five macaques receiving higher virus dilutions did not seroconvert and were negative for both viral RNA and for infectious virus, although proviral DNA was detected in their peripheral blood mononuclear cells. In contrast to the animals receiving the 10(-3) virus dilution, these five silently infected monkeys developed an SIV-specific proliferative T cell response but SIV-specific CTL could not be observed. The SIV-specific T cell proliferation of the silently infected animals could be boosted by a second low-dose exposure with a 10(-4) or 10(-5) dilution of SIVmac251/spl. The virological status of the animals was not changed following this second virus inoculation. Four months later these macaques were challenged intravenously with 2 ml of a 10(-4) dilution of SIVmac251/32H containing 10 monkey ID50. After this challenge all SIV-pre-exposed animals and three naive controls became productively infected. In addition, all infected animals developed typical signs of an immunodeficiency within 6 months after infection. These observations indicate that macaques infected silently by a low-dose exposure to infectious virus generated a virus-specific cellular immune response. However, SIV-specific T cell proliferation alone could not protect the monkeys against an intravenous challenge with SIVmac and the subsequent development of AIDS-like symptoms.

Animals↗
PubMed1995

Reactivation of human immunodeficiency virus type 2 in macaques after simian immunodeficiency virus SIVmac superinfection.

By superinfection of human immunodeficiency virus type 2 (HIV-2) strain HIV-2ben-infected macaques with simian immunodeficiency virus (SIV) strain SIVmac, we investigated the mutual influences of an apathogenic and a pathogenic virus in vivo. Four rhesus and two cynomolgus monkeys were infected with HIV-2ben in 1988 and 1989, respectively. Virus could be reisolated from five of six animals 6 weeks after infection. The monkeys remained healthy over the next 2 to 3 years. PCR for viral RNA became negative, and virus could no longer be reisolated by coculture. All six macaques were superinfected with the pathogenic SIVmac251/32H. Subsequently, five monkeys became persistently viremic, while one animal was protected against the SIVmac infection. In the peripheral blood mononuclear cells and cocultures of the five viremic animals, DNA from both HIV-2 and SIVmac was present. The plasma contained RNA from both viruses. Thus, superinfection with SIVmac activated HIV-2. A proliferative T-cell response against both HIV-2 and SIVmac was measured in all animals after superinfection. Such a response was regularly seen after infection with the apathogenic HIV-2 but never when the pathogenic SIVmac alone was administered. While naive control monkeys inoculated with SIVmac251/32H regularly develop AIDS-like symptoms soon after infection and have to be killed, none of the preinfected animals has developed AIDS-like symptoms, but two of six animals developed tumors. After the SIVmac challenge, however, apoptotic lymphocytes were detected in the peripheral blood mononuclear cells of all animals. Thus, the presence of an apathogenic viral variant seems to retard the disease occurring after infection with a pathogenic virus rather than to confirm total protection. This partial protection appears to depend on a specific proliferative T-cell response early after infection.

Animals↗
PubMed1995

vpr deletion mutant of simian immunodeficiency virus induces AIDS in rhesus monkeys.

In previous experiments, animals infected with SIVmac239 containing a point mutation in the vpr and nef genes developed AIDS-like symptoms after early reversion of the vpr and nef genes. Here we show that two animals in which the nef gene but not the vpr gene had reverted in the first few months did not develop disease during a 3-year observation period even after reversion to a functional vpr gene 70 weeks postinfection. To study the influence of a stable vpr mutation on virus load and pathogenesis, a 43-bp deletion was introduced into the vpr gene of SIVmac239on, a nef-open mutant of SIVmac239. Four rhesus monkeys were inoculated with the vpr deletion mutant (SIV delta vpr), and two control animals were infected with SIVmac239on. Both control animals had persistent antigenemia, high cell-associated virus loads, and elevated neopterin levels. They had to be euthanized 20 and 30 weeks postinfection because of AIDS-related symptoms. However, all four rhesus monkeys inoculated with SIV delta vpr showed only transiently detectable antigenemia. The cell-associated virus loads were high in three of the four animals. Two animals with AIDS-like symptoms had to be euthanized 71 and 73 weeks postinfection. The two remaining monkeys infected with SIV delta vpr were still alive 105 weeks postinfection. In contrast to the SIVmac239on-infected animals, SIV delta vpr-infected animals had strong humoral immune responses and intermittent cellular immune responses to SIV antigens. Our data show that a functional vpr gene is not necessary for pathogenesis. However, vpr-deficient SIVmac239 variants might be slightly attenuated, allowing some animals to resist progression to disease for an extended period of time.

Animals↗
PubMed1994

SIV- and HIV-2-neutralising antibodies in infected macaques measured by a novel and simple neutralisation test based on a non-commercial antigen-ELISA.

A method for the measurement of neutralising antibodies (nab) directed against SIVmac or HIV-2 was developed. The assay is based on antigen detection using a non-commercial enzyme-linked immunosorbent assay (ELISA). Studies were carried out to determine the influence of the test conditions on the nab titre. The sensitivity of the assay depended mainly on the virus dose and the length of incubation of the serum-virus-mixture. Prolongation of the culture time from 9 to 11 days increased the validity of the results. Applying this neutralisation assay on sequential serum samples from SIV mac- or HIV-2ben-infected macaques, a considerable variation was found in nab titres between individual animals. Whereas after infection with SIVmac, in vitro-neutralisation seems to correlate with protection against disease, and the lower pathogenity of HIV-2ben in macaques compared with SIVmac is not due to the differences in nab titres.

Acquired Immunodeficiency Syndrome↗
PubMed1994

Early helper T-cell dysfunction in simian immunodeficiency virus but not in human immunodeficiency virus type-2-infected macaques.

Both naive and vaccinated macaques acquired a virus-specific proliferative helper T-cell reactivity in response to infection with the nonpathogenic human immunodeficiency virus type 2 (HIV-2). In contrast, macaques infected with the pathogenic simian immunodeficiency virus of the macaque strain (SIVmac) did not develop a helper T-cell response. Furthermore, a vaccine-induced preexisting T-cell reactivity was abrogated after SIVmac infection in vaccine failures. These differences may reflect the different pathogenicity of the two closely related viruses.

AIDS Vaccines↗
PubMed1994

Comparison of humoral immunity and induction of proliferating T lymphocytes in vaccinia virus-infected rabbits and rhesus macaques.

Vaccina virus (VV) infection induces specific antibodies and cytotoxic T cells in various animal species. Therefore, helper T cells also should be induced that stimulate the humoral and cellular immune responses. We determined such helper T-cell activity in 2 species after VV infection. Rabbits and rhesus macaques were infected with the Copenhagen strain of VV or with recombinant VV expressing retroviral proteins. Animals of both species developed antibodies and specific proliferative T-cell response. This reactivity could be enhanced by booster infection with VV. The proliferating macaque cells were CD4+ and major histocompatibility complex class II-restricted. These data confirm the broad immunogenicity of VV. Expression of additional polypeptides expressed from a recombinant VV does not lead to altered immune response to VV antigens. However, strength of the helper T-cell response, as well as clinical reactions, differed between macaques and rabbits. Infection with recombinant VV as delivery vectors offers the opportunity for combined vaccination against recombinant proteins and does not diminish cellular and humoral immune responses to VV itself.

Animals↗
PubMed1994

Immunization with virion-derived glycoprotein 130 from HIV-2 or SIV protects macaques against challenge virus grown in human or simian cells or prepared ex vivo.

We have compared in the macaque model the efficacy of the virion-derived glycoprotein of HIV-2ben (HIV-2 gp130) with that of SIVmac251/32H (SIV gp130). The latter vaccination trial was in part combined with vaccinia virus (VV) priming. Both antigen preparations induced a strong humoral, but a weak cellular, immune response. The first challenge was performed with autologous virus grown on a human T cell line. More than 50% of the monkeys immunized with HIV-2 gp130 (five of nine) and 63% of the monkeys immunized with SIV gp130 (five of eight) were protected. All such protected animals received one or two booster immunizations before they were rechallenged either with heterologous HIV-2SBL6669 grown on monkey peripheral blood mononuclear cells or with an ex vivo stock of SIVmac251/32H prepared from the spleen of an SIV-infected macaque and not passaged in vitro. Immunization with HIV-2 gp130 did not protect against the second challenge, but one animal showed limited infection as indicated by positive PCR only. Challenge of the SIV gp130-immunized monkeys with the spleen-derived virus led to infection of three animals; remarkably, one of these was only PCR positive. Two animals were completely protected. Thereby we can exclude the influence of cellular proteins on protective immunity. Priming with VV was not superior to immunization with gp130 alone. Neither at the first nor at the second challenge were the virus-specific humoral and cellular immune responses of the vaccinees clearly correlated with protection. However, neutralizing antibodies may have been important in the SIV gp130-immunized animals at first challenge.

AIDS Vaccines↗
PubMed1993

In vitro and in vivo infection of rhesus monkey microglial cells by simian immunodeficiency virus.

The observation that microglial cells in brain tissue are probably a major target for human immunodeficiency virus (HIV) infection has raised interest in the pathogenic role of this cell population for the development of neuro-AIDS. Since it is very difficult to obtain microglia from normal or diseased human brain we studied microglial cells isolated from fresh brain tissue of uninfected and simian immunodeficiency virus (SIV) infected rhesus monkeys (Macacca mulatta) in comparison to peripheral blood macrophages. Besides the characterization of the phenotypes of these two cell populations, we examined the replication of SIV in the cells in addition to the effect of viral infection on the expression of cell surface molecules. We found that microglia and macrophages support replication of the wild-type SIVmac251 strain as well as the infectious clone (SIV239). Infectious virus was produced and a CPE developed. Isolated microglial cells from SIV-infected monkeys were latently infected independent of the presence of neuropathological lesions and produced infectious virus after 20-25 days in culture. In situ hybridization revealed that only a small percentage of isolated microglial cells are productively infected in vivo, yet the majority of these expressed MHC class II molecules. This indicated a state of activation that is acquired in vivo. These findings indicate that microglia are a prime target cell for SIV infection in CNS tissue.

Animals↗