HIV-specific antiretroviral targets (ART targets)

HIV-specific antiretroviral targets refer to the collection of viral proteins and host-cell receptors essential for the replication cycle of the Human Immunodeficiency Virus (HIV). The primary viral targets are the three enzymes encoded by the pol gene: reverse transcriptase (RT), which synthesizes DNA from the viral RNA template; integrase (IN), which incorporates the viral DNA into the host cell's genome; and protease (PR), which processes viral polyproteins into mature, infectious virions [1, 5, 10]. Other targets include the viral envelope glycoproteins (gp120 and gp41) and the capsid protein (CA), which are critical for viral entry and structural assembly, respectively [12, 13]. Antiretroviral therapy (ART) utilizes combinations of drugs targeting these distinct stages to suppress viral replication, restore immune function, and prevent progression to AIDS [3, 11]. For instance, nucleoside and non-nucleoside inhibitors block reverse transcriptase, while strand transfer inhibitors prevent the action of integrase [2, 6]. Protease inhibitors interfere with the final maturation of the virus, and entry inhibitors block the interaction between the virus and host receptors like CCR5 [1, 12]. While highly effective, these targets present significant therapeutic challenges, most notably the rapid evolution of drug-resistant mutations due to the error-prone nature of viral replication [8, 9]. Long-term management also requires monitoring for toxicities such as metabolic syndrome and renal impairment associated with chronic drug exposure [14, 15]. The continuous identification of novel targets, such as the HIV capsid, remains a priority to overcome resistance and improve patient outcomes [13].

Other names

HIV drug targetsAntiretroviral therapy targetsHIV-1 viral proteinsHighly active antiretroviral therapy targets

Inhibition of HIV-1 reverse transcriptase (polymerase and RNase H activities), HIV-1 protease (proteolytic cleavage), HIV-1 integrase (strand transfer), viral entry (gp120/gp41 binding or CCR5 antagonism), and capsid assembly/disassembly.