Summary auto-generated
This study investigates how human herpesvirus 6 (HHV-6) infection affects DC-SIGN expression on dendritic cells, which are key immune cells. DC-SIGN is an important molecule that binds and transmits various pathogens, including HIV, to target cells. The researchers infected immature dendritic cells with HHV-6 and found that surface and intracellular DC-SIGN expression decreased significantly within three days of infection. By analyzing mRNA and protein levels, they demonstrated that this downregulation occurs at the transcriptional level. The effect required active viral replication, as UV-inactivated virus and culture supernatants from infected cells did not induce downregulation. However, DC-SIGN was not required for HHV-6 binding or infection of dendritic cells, suggesting HHV-6 uses alternative receptors. This is the first demonstration that viral infection directly reduces DC-SIGN expression at the transcriptional level, with potential implications for understanding HHV-6's role in pathogenesis and its interactions with other viruses like HIV.
Key findings
- HHV-6 infection causes transcriptional downregulation of DC-SIGN on immature dendritic cells, reducing both mRNA and protein levels within three days
- Active viral replication is required for DC-SIGN downregulation, as UV-inactivated virus and culture supernatants have no effect
- DC-SIGN is not necessary for HHV-6 binding or infection of dendritic cells, indicating the virus uses alternative cellular receptors
- HHV-6-induced downregulation of DC-SIGN may affect dendritic cell function and susceptibility to other pathogens, particularly HIV
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Abstract
DC-SIGN expressed on dendritic cells (DCs) efficiently binds and transmits various pathogens, including human immunodeficiency virus, to lymphoid tissues and permissive cells. Consequently, alteration of DC-SIGN expression may affect susceptibility and resistance to pathogens. The present study shows that infection with human herpesvirus 6 (HHV-6) induces downregulation of DC-SIGN expression on immature DCs. Expression levels of DC-SIGN mRNA and intracellular protein appeared to decrease following infection with HHV-6, indicating that downregulation of surface DC-SIGN occurs at the transcriptional level. Downregulation of DC-SIGN was not induced by inoculation of UV-inactivated HHV-6 or culture supernatant of HHV-6-infected DCs, indicating that replication of HHV-6 in DCs is required for downregulation of DC-SIGN. The present study demonstrates for the first time that expression of DC-SIGN is altered at the transcriptional level by virus infection.