What question did this study set out to answer?

This research aims to understand how Rab14 influences the transport of human papillomavirus to the trans-Golgi network during infection.

May 28, 2026Open Access

Rab14 regulates the transport of human papillomavirus to the trans ‐Golgi network for infectious cell entry

Key Points

This research aims to understand how Rab14 influences the transport of human papillomavirus to the trans-Golgi network during infection.
Identified Rab14 as a critical host factor for HPV infection through knockout cell models.
Used confocal microscopy to track the transport of HPV pseudovirions to the trans-Golgi network in Rab14 knockout cells.
Reintroduced wild-type and mutant forms of Rab14 to assess their influence on HPV infection levels.
Rab14 knockout cells showed a significant resistance to HPV pseudovirion infection.
Transport of HPV pseudovirions to the trans-Golgi network was markedly reduced in Rab14 knockout cells.
Reintroduction of wild-type Rab14 restored infection levels, while mutant forms did not achieve similar results.

Abstract

Human papillomavirus (HPV) utilizes multiple host proteins to infect epithelial cells. Here we identified Rab14, a small GTPase belonging to the Rab family, as a critical host factor in HPV infection. Rab14 knockout (KO) cells exhibited resistance to HPV pseudovirion (PsV) infection. Confocal microscopy revealed that PsV transport to the trans-Golgi network (TGN) was significantly reduced in Rab14 KO cells. Reintroduction of wild-type Rab14 restored infection levels, but neither GDP-bound (S25N) nor GTP-bound (Q70L) mutants did. S25N preferentially localized to the TGN, while Q70L exhibited similar localization in the early endosome and the TGN. PsV showed reduced colocalization with S25N, whereas the opposite was observed for Q70L. These results indicate that Rab14 GTPase cycling controls HPV transport to the TGN.

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