TRIM44 Promotes Rabies Virus Replication by Autophagy-Dependent Mechanism

The tripartite motif (TRIM) proteins control essential biological processes, and have been shown to play important roles in viral infections. This study showed that Rabies virus (RABV) infection to neuroblastoma cells caused upregulation of TRIM47, TRIM56 and TRIM44. Although silencing of the former two did not have any significant effect on the transcription of the RABV viral genome, silencing of TRIM44 significantly inhibited the RABV genome and the virus titre. Furthermore, knockdown of TRIM44 reduced the viral titre and the expression of the glycoprotein (G), while its overexpression led to increased transcription of the RABV viral genome and the G protein. Depletion of TRIM44 in neuroblastoma cells led to a reduced expression of the RABV nucleoprotein. The addition of an autophagy inhibitor reversed the potentiating effect of TRIM44 on G protein expression and genome replication, while the addition of an autophagy inducer enhanced the TRIM44-induced expression of the RABV glycoprotein. This study highlighted the crucial role of TRIM44 in RABV replication. Further research is needed to identify other mechanisms by which TRIM44 regulates RABV infection.
(MRM)