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Why are the natural hosts of SIV resistant to AIDS?
S Norley1, B Beer, S Holzammer
1Paul-Ehrlich-Institute, Langen, Germany. norst@pei.de
Abstract:
An increasing number of African primate species have been shown to be infected in the wild with their own distinct variants of simian immunodeficiency virus. The most striking feature of these natural host systems is the lack of AIDS-like disease despite long-term infection. In the African green monkey (AGM)/SIVagm system there is no evidence that a vigorous antiviral immune response, a lack of variability or a low virus load accounts for this lack of pathogenicity. New-born AGMs appear to be even more resistant to the virus than adults, despite their immature immune system and higher pool of target cells. The fact that AGMs, unlike HIV-infected humans, lack a humoral immune response to non-denatured Gag protein and do not show trapping of virus in the lymph nodes suggested that tolerance to Gag might prevent the formation of immune complexes which would normally be filtered out by the lymphoid tissues with detrimental results. This apparent tolerance to Gag is a common feature of many, if not all, of the natural host systems and might explain why the lymph nodes and immune system in general remain intact in these primates in the face of continuous, high level virus replication.
Insights
African green monkeys infected with simian immunodeficiency virus (SIV) do not develop AIDS. This natural resistance may be due to immune tolerance to Gag proteins, preventing harmful immune complex formation.
Area of Science:
- Primate immunology
- Virology
- Infectious diseases
Background:
- African primate species harbor distinct simian immunodeficiency virus (SIV) variants.
- Natural SIV infection in African primates does not lead to AIDS-like disease, a striking contrast to human immunodeficiency virus (HIV) infection.
Purpose of the Study:
- To investigate the mechanisms underlying the lack of pathogenicity in the African green monkey (AGM)/SIVagm system.
- To explore why AGMs resist AIDS development despite long-term, high-level SIV infection.
Main Methods:
- Comparative analysis of immune responses in SIV-infected AGMs versus HIV-infected humans.
- Investigation of viral load, immune response vigor, and Gag protein immune response in AGMs.
- Examination of virus trapping in lymphoid tissues.
Main Results:
- No evidence suggests a vigorous antiviral response, low viral load, or lack of viral variability explains AGM resistance.
- New-born AGMs show increased resistance to SIV compared to adults.
- AGMs lack a humoral immune response to non-denatured Gag protein and do not exhibit virus trapping in lymph nodes.
Conclusions:
- Immune tolerance to Gag protein in AGMs may prevent detrimental immune complex formation.
- This tolerance might preserve lymphoid tissue and overall immune function in the face of persistent SIV replication.
- Mechanisms of natural SIV resistance in African primates offer insights into controlling lentiviral infections.