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Since the beginning of the epidemic in the 1980s, human immunodeficiency virus type 1 (HIV-1) has infected more than 70 million and killed approximately 35 million people globally. Although widespread use of combination antiretroviral therapy (cART) has effectively increased the life span of many infected individuals in the Western world, HIV-1 continues to be a major public health issue in both developed and resource-poor settings [1]. In addition to causing acquired immunodeficiency syndrome (AIDS), HIV-1 infection also causes serious neuropathology. Like all other retroviruses, upon entry into the host cell, HIV-1 converts its single-stranded RNA genome into double-stranded DNA that integrates into the host genome. To produce new viral particles or virions, HIV-1 proteins—together with the viral RNA— assemble at the plasma membrane, where a new immature virus forms. Virions then mature through processing of precursor group-specific antigen (Gag) polyprotein by HIV-1 protease at or after budding from the cell surface [2].

"APP"reciating the complexity of HIV-induced neurodegenerative diseases