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Butel C.,Montpellier University | Mundeke S.A.,Montpellier University | Mundeke S.A.,University of Kinshasa | Drakulovski P.,Montpellier University | And 6 more authors.
International Journal of Primatology | Year: 2015

Simian immunodeficiency virus (SIV) infects many primate species. Chimpanzees (Pan troglodytes) can develop an immune disease similar to human acquired immunodeficiency syndrome (AIDS). Immunosuppressed patients often suffer from opportunistic diseases such as microsporidiosis and cryptosporidiosis. We report on the occurrence of infections with microsporidia and Cryptosporidium spp. in wild-living chimpanzees, gorillas (Gorilla gorilla gorilla), bonobos (Pan paniscus), and four monkey species from the Cercopithecinae subfamily (Cercocebus agilis, Cercopithecus cephus, Cercopithecus nictitans, and Lophocebus albigena) and assess whether these infections may be good indicators of SIV-related immunosuppression. We analyzed 399 fecal samples collected in Cameroon and Democratic Republic of Congo for the presence of cross-reactive HIV antibodies using a line immunoassay (INNO-LIA®). We amplified via polymerase chain reaction (PCR) a 200–500 bp DNA fragment for the genus Encephalitozoon and the genus Enterocytozoon respectively (microsporidia), and an 820 bp DNA fragment of various Cryptosporidium species. Twenty-nine percent (45/155) of the chimpanzees samples analyzed were SIV+, whereas samples from the other primate species were SIV–. Phylogenetic analyses showed that 11 fecal samples [one SIV+, four SIV– chimpanzees, three gorillas, a bonobo, an agile mangabey (Cercocebus agilis), and a moustached monkey (Cercopithecus cephus)] are infected with microsporidia. DNA sequences of amplicons derived from eight fecal samples clustered together with Encephalitozoon hellem and three branched close to E. intestinalis. We also amplified Cryptosporidium spp. in two SIV+ chimpanzee samples and in two gorilla samples. We found no significant association between SIV infection status in chimpanzees and the presence of microsporidia or Cryptosporidium, suggesting that detection of microsporidia and Cryptosporidium is not a reliable marker for immunosuppressive status in SIV-infected primates. © 2015, Springer Science+Business Media New York. Source

Aghokeng A.F.,Virology Laboratory CREMER IMPM IRD | Aghokeng A.F.,Montpellier University | Mpoudi-Ngole E.,Virology Laboratory CREMER IMPM IRD | Chia J.E.,Virology Laboratory CREMER IMPM IRD | And 3 more authors.
Journal of Clinical Microbiology | Year: 2011

The ViroSeq HIV-1 genotyping system is used in many African countries for drug resistance testing. In this study, we used a panel of diverse HIV-1 groupMisolates circulating in Cameroon to show that the performance of this assay can be altered by the sequence variation of non-B HIV-1 strains that predominate in African settings. Copyright © 2011, American Society for Microbiology. Source

Djoko C.F.,Global Viral Forecasting | Djoko C.F.,University of Yaounde I | Wolfe N.D.,Global Viral Forecasting | Wolfe N.D.,Stanford University | And 16 more authors.
EcoHealth | Year: 2012

Hunting and butchering of wildlife in Central Africa are known risk factors for a variety of human diseases, including HIV/AIDS. Due to the high incidence of human exposure to body fluids of non-human primates, the significant prevalence of simian immunodeficiency virus (SIV) in non-human primates, and hunting/butchering associated cross-species transmission of other retroviruses in Central Africa, it is possible that SIV is actively transmitted to humans from primate species other than mangabeys, chimpanzees, and/or gorillas. We evaluated SIV transmission to humans by screening 2,436 individuals that hunt and butcher non-human primates, a population in which simian foamy virus and simian T-lymphotropic virus were previously detected. We identified 23 individuals with high seroreactivity to SIV. Nucleic acid sequences of SIV genes could not be detected, suggesting that SIV infection in humans could occur at a lower frequency than infections with other retroviruses, including simian foamy virus and simian T-lymphotropic virus. Additional studies on human populations at risk for non-human primate zoonosis are necessary to determine whether these results are due to viral/host characteristics or are indicative of low SIV prevalence in primate species consumed as bushmeat as compared to other retroviruses in Cameroon. © 2012 International Association for Ecology and Health. Source

Ayouba A.,Montpellier University | Njouom R.,Center Pasteur du Cameroun | Chia J.E.,Virology Laboratory CREMER IMPM IRD | Ahuka-Mundeke S.,Montpellier University | And 6 more authors.
Infection, Genetics and Evolution | Year: 2015

•African green monkeys (AGM) are the most widely distributed monkeys in Africa.•Four out of 6 AGM species are infected by an SIVagm in a species-specific manner.•SIVagm prevalence can reach 50-60% in some AGM communities.•A C. tantalus monkey from Cameroon infected with a SIVagmSAB/SIVagmTAN mosaic virus is identified.•The evolution of AGM and SIVagm is more complex than previously thought. African green monkeys (AGMs) represent the most widely distributed non-human primates species in Africa. SIVagm naturally infects four of the 6 AGMs species at high prevalence in a species-specific manner. To date, only limited information is available on molecular characteristics of SIVagm infecting Chlorocebus tantalus.Here, we characterized the full-length genome of a virus infecting a naturally infected captive C. tantalus from Cameroon by amplifying and sequencing sub-genomic PCR fragments. The isolate (SIVagmTAN-CM545) is 9923. bp long and contained all canonical genes of a functional SIV. SIVagmTAN-CM545 showed a mosaic structure, with gag, pol, nef and accessory genes closely related to SIVagmSAB infecting Chlorocebus sabaeus monkeys from west Africa, and the env gene, closely related to SIVagmTAN infecting tantalus monkeys from Central Africa. Thus SIVagmTAN-CM545 is SIVagmSAB/SIVagmTAN recombinant.These unexpected findings suggest that the evolution of SIVagm is more complex than previously thought and warrant further studies. © 2014 Elsevier B.V. Source

Aghokeng A.F.,Virology Laboratory CREMER IMPM IRD | Aghokeng A.F.,Montpellier University | Kouanfack C.,Central Hospital | Eymard-Duvernay S.,Montpellier University | And 7 more authors.
Journal of the International AIDS Society | Year: 2013

Introduction: The current expansion of antiretroviral treatment (ART) in the developing world without routine virological monitoring still raises concerns on the outcome of the strategy in terms of virological success and drug resistance burden. We assessed the virological outcome and drug resistance mutations in patients with 36 months' ART experience, and monitored according to the WHO public health approach in Cameroon. Methods: We consecutively recruited between 2008 and 2009 patients attending a national reference clinic in Yaoundé - Cameroon, for their routine medical visits at month 36+2. Observance data and treatment histories were extracted from medical records. Blood samples were collected for viral load (VL) testing and genotyping of drug resistance when HIV-1 RNA ≥ 1000 copies/ml. Results: Overall, 376 HIV-1 infected adults were recruited during the study period. All, but four who received PMTCT, were ART-naïve at treatment initiation, and 371/376 (98.7%) started on a first-line regimen that included 3TC + d4T/AZT + NVP/EFV. Sixty-six (17.6%) patients experienced virological failure (VL ≥ 1000 copies/ml) and 53 carried a resistant virus, thus representing 81.5% (53/65) of the patients who failed. Forty-two out of 53 were resistant to nucleoside and non-nucleoside reverse-transcriptase inhibitors (NRTIs + NNRTIs), one to protease inhibitors (PI) and NNRTIs, two to NRTIs only and eight to NNRTIs only. Among patients with NRTI resistance, 18/44 (40.9%) carried Thymidine Analog Mutations (TAMs), and 13/44 (29.5%) accumulated at least three NRTI resistance mutations. Observed NNRTI resistance mutations affected drugs of the regimen, essentially nevirapine and efavirenz, but several patients (10/51, 19.6%) accumulated mutations that may have compromised etravirine use. Conclusions: We observed a moderate level of virological failure after 36 months of treatment, but a high proportion of patients who failed developed drug resistance. Although we found that for the majority of patients, second-line regimens recommended in Cameroon would be still effective, accumulated resistance mutations are of concern and may compromise future treatment strategies, stressing the need for virological monitoring in resource-limited settings. © 2013 Aghokeng AF et al; licensee International AIDS Society. Source

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