Table1.

Factors contributing the pathogenesis of HIV associated neurological disorders

Host Factors	Age	Decreased mortality rates and increased life expectancies Vulnerable to neuronal injury associated with HIV infection
	Neuroinflammation	Release of host chemokine and cytokine products and neurotoxin anti-viral products
	HAART	Long term adherence to antiretroviral treatment and increased life expectancies
	Substance Abuse	Narcotics, methamphetamine, and cocaine are associated with increase risk of HAND
	Co-morbid conditions	Increase risk of infection by other pathogens such as HCV
	Metabolism	Central obesity, dyslipidemia, and insulin resistance
Viral Factors	HIV-1 Genes and proteins
	Tat	Compromises a variety of homeostatic processes in the brain, including neuronal viability, synapse formation and neuro-inflammatory profiles
	GP120	Induces the production of pro-inflammatory cytokines Increase in apoptosis in both neuronal cells, Induce ROS production, Disrupt ion regulation and glutamate homeostasis
	VPR	Impair the neural mitochondria, inhibiting axonal stability It can disrupt calcium regulation and induce pro-inflammatory cytokine expression in both neuronal cells
	NEF	Decrease metabolic activity and increase apoptosis Oxidative stress Up-regulation of IP-10 Up-regulation of CCL2, chemoattractant for circulating monocytes