1 Introduction The central nervous system (CNS) has long been regarded as a pharmacological sanctuary site for human immunodeficiency virus (HIV), making the pharmacokinetic (PK) characterization of antiretroviral therapy (ART) in this compartment crucial for optimizing treatment strategies [1]. Suboptimal CNS ART exposure, combined with viral and host factors, can result in reduced antiviral pressure and the potential for ongoing viral replication in the CNS compartment [2, 3].
