- What attributes of the virus, host, and host-virus interaction determine presentation of HIV-associated neurobehavioral disorders?
- What are the actual mechanisms by which the host-virus factors generate neural injury and neurobehavioral disorders?
- What is the role of co-pathogens and comorbidities in neuroAIDS?
- How can treatments be optimized to prevent or ameliorate neuroAIDS?
- What is the effect of HIV neurocognitive complications on everyday functioning; do treatments that correct neurocognitive abnormalities restore productivity and quality of life?
From the aspect of the virus, what are the relationships of molecular diversity (e.g., of HIV-1 envelope sequences) and neurovirulence? What are the mechanisms for increased molecular diversity in brain or CSF derived virus versus plasma or lymph nodes? Are there clade-specific differences in neurotropism and neurovirulence, and what are the molecular mechanisms underlying these? Examples of questions from the host side may include questions such as the importance of polymorphisms in genes encoding various neuroinflammatory signaling molecules (e.g., MCP-1, STF-1) or their co-receptors in facilitating vulnerability to neuroAIDS. From an international perspective, if such host genotype vulnerabilities are found, are they distributed differently in various populations, such as those from North America/Europe, India, China, or Africa?