Postintegration HIV-1 Infection of Cervical Epithelial Cells Mediates Contact-Dependent Productive Infection of T Cells

This study investigates how post-integration HIV-1 infection in cervical epithelial cells contributes to the contact-dependent productive infection of CD4+ T cells. Researchers found that cervical epithelial cells could become productively infected by both X4 and R5 tropic HIV-1, even though they lack the typical HIV-1 receptors (CD4, CCR5, CXCR4). The infection in epithelial cells required reverse transcription and integration of viral DNA, suggesting the virus undergoes a full life cycle within these cells.

Key findings:

1. HIV-1 Entry and Infection: HIV-1 enters cervical epithelial cells in a CD4- and coreceptor-independent manner, involving a charge-dependent interaction with heparan sulfate proteoglycans.

   
   

2. Enhanced Infection by SEVI: The presence of SEVI fibrils significantly enhanced the infection of epithelial cells, facilitating HIV entry.

   
   

3. Transmission to CD4+ T Cells: Infected epithelial cells can transmit virus to CD4+ T cells in a contact-dependent manner, using the typical CD4 and CCR5 entry mechanisms. This transfer required de novo virus production within the epithelial cells.

   
   

4. Implications for Transmission: The study suggests that cervical epithelial cells play an active role in the initial stages of HIV transmission during sexual contact by facilitating the infection of target CD4+ T cells.

   
   

These findings provide valuable insights into the mechanics of HIV-1 sexual transmission and highlight cervical epithelial cells as a potential target for prevention strategies.

https://academic.oup.com/jid/article/208/11/1756/850869?login=false