Updates on the role of TRIM proteins in AIDS: molecular mechanisms and potential for interventions

AIDS (acquired immunodeficiency syndrome) is the final stage of infection with the human immunodeficiency virus (HIV) and adversely impacts the health of affected people globally, placing an added burden on healthcare systems. Nonetheless, advanced HIV infection is still not effectively curable, so the search for new drug targets remains an important research focus. Tripartite motif (TRIM) proteins constitute an extensive family of ubiquitin E3 ligases that regulate a wide range of cellular processes. Several recent studies have shown that many of TRIM proteins can take part in host defense to combat viral infection by diverse and distinct molecular mechanisms involving interaction with the NF-κB (Nuclear Factor kappa-B) pathway, JAK(Janus Kinase)-STAT (Signal Transducer and Activator of Transcription) pathway, RLR/MDA5 (Melanoma Differentiation-Associated protein 5) pathway, as well as IRF (Interferon Regulatory Factor) pathway; it can even induce premature degradation of viral proteins. Thus, this review aims to offer an in-depth insight into the roles of TRIM proteins in the pathologic progression of advanced HIV infection, especially on HIV-1 invasion and long terminal transcription inhibition and nonhistone protein reversible ubiquitination, which may afford therapeutic targets for this challenging disease.