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Published on: September 20, 2010
Transfer of neuropathogenic simian immunodeficiency virus with naturally infected microglia
1Department of Neuropharmacology, Scipps Research Institute, La Jolla, California 92037, USA.
Abstract:
The central nervous system (CNS) is a target for human immunodeficiency virus infection, and, in individuals with acquired immune deficiency syndrome, this can lead to a devastating dementia. Only certain viral variants appear capable of invading the CNS and infecting microglia and brain macrophages. To determine whether the virus entering the brain may be particularly pathogenic to the CNS, we isolated microglia from the brains of simian immunodeficiency virus-infected rhesus monkeys. Serial transfer of these cells into naive animals indicated that productive simian immunodeficiency virus infection could indeed be transferred. Furthermore, CNS infection occurred within a relatively short time span and was associated with viral gene expression in the brain and pathology characteristic of human immunodeficiency virus encephalitis. While demonstrating that neuropathogenic variants partition into the CNS, our approach will allow the dissection of functional neuropathogenic elements present in these viruses.
Insights
Certain simian immunodeficiency virus (SIV) variants infect the central nervous system (CNS), causing dementia. This study shows SIV-infected microglia from rhesus monkeys can transfer CNS infection, revealing neuropathogenic viral elements.
Area of Science:
- Neurovirology
- Immunology
- Pathology
Background:
- The human immunodeficiency virus (HIV) targets the central nervous system (CNS), leading to dementia in acquired immune deficiency syndrome (AIDS).
- Specific viral variants are implicated in CNS invasion, infecting microglia and brain macrophages.
Purpose of the Study:
- To investigate if viruses entering the CNS exhibit particular neuropathogenicity.
- To determine if simian immunodeficiency virus (SIV)-infected microglia can transfer CNS infection.
Main Methods:
- Isolation of microglia from SIV-infected rhesus monkey brains.
- Serial transfer of isolated microglia into naive animals to assess infection transfer.
- Monitoring for CNS infection, viral gene expression, and neuropathology.
Main Results:
- Productive SIV infection was transferable via isolated microglia.
- CNS infection was established rapidly following microglia transfer.
- SIV infection was associated with viral gene expression and pathology resembling HIV encephalitis.
Conclusions:
- Neuropathogenic SIV variants selectively accumulate within the CNS.
- This model facilitates the study of functional neuropathogenic viral elements responsible for CNS disease.
