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Simian Immunodeficiency Virus Infection of Chimpanzees () Shares Features of Both Pathogenic and Non-pathogenic Lentiviral Infections


The HIV-1/AIDS pandemic is the result of cross-species transmission of simian immunodeficiency virus (SIVcpz) from chimpanzees to humans. Many African primates are infected with SIV, but those studied in captivity generally do not develop disease. However, wild chimpanzees infected with SIVcpz are at increased risk of death and may develop an AIDS-like disease. It has therefore been suggested that the viral features which SIVcpz and HIV-1 share, that differentiate them from other species’ SIV, may be critical in the development of disease in both humans and chimpanzees. Here, we present a long-term follow-up of 7 SIVcpz infected chimpanzees, housed in primate centres in the US and Europe, under similar conditions to other studied models. These animals did not develop an AIDS-like disease, after up to 25 years of infection, and showed features similar to other species where disease rarely develops, such as limited immune activation in the blood. However, they also had significantly reduced CD4+ T-cells and disruption to the secondary lymphoid tissues, normally associated with pathogenic primate lentiviral infections. Thus, while SIVcpz infection of chimpanzees shares features of both pathogenic and non-pathogenic infections, disease has not developed in captivity.


Vyšlo v časopise: Simian Immunodeficiency Virus Infection of Chimpanzees () Shares Features of Both Pathogenic and Non-pathogenic Lentiviral Infections. PLoS Pathog 11(9): e32767. doi:10.1371/journal.ppat.1005146
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.ppat.1005146

Souhrn

The HIV-1/AIDS pandemic is the result of cross-species transmission of simian immunodeficiency virus (SIVcpz) from chimpanzees to humans. Many African primates are infected with SIV, but those studied in captivity generally do not develop disease. However, wild chimpanzees infected with SIVcpz are at increased risk of death and may develop an AIDS-like disease. It has therefore been suggested that the viral features which SIVcpz and HIV-1 share, that differentiate them from other species’ SIV, may be critical in the development of disease in both humans and chimpanzees. Here, we present a long-term follow-up of 7 SIVcpz infected chimpanzees, housed in primate centres in the US and Europe, under similar conditions to other studied models. These animals did not develop an AIDS-like disease, after up to 25 years of infection, and showed features similar to other species where disease rarely develops, such as limited immune activation in the blood. However, they also had significantly reduced CD4+ T-cells and disruption to the secondary lymphoid tissues, normally associated with pathogenic primate lentiviral infections. Thus, while SIVcpz infection of chimpanzees shares features of both pathogenic and non-pathogenic infections, disease has not developed in captivity.


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