Lectin Switching During Dengue Virus Infection

Dejnirattisai, Wanwisa; Webb, Andrew I.; Chan, Vera; Jumnainsong, Amonrat; Davidson, Andrew; Mongkolsapaya, Juthathip; Screaton, Gavin

To formally prove that the loss of infection of DCs was a result of the loss of affinity of DC-produced virus for DC-SIGN, we went on to test infection on 3T3 cells expressing DC-SIGN and included in these assays the related C-type lectin L-SIGN ( Figure 3A ), which has also been reported to be a receptor for dengue virus. Insect-derived virus could efficiently infect both DC-SIGN-and L-SIGN-expressing cells when compared with control 3T3 cells ( Figure 3B ). Similar to the lack of observable infection of DCs, the DC-derived virus showed a much lower level of infection on DC-SIGN-expressing 3T3 cells, with ,2% infection. Surprisingly, however, this virus progeny was still able to infect cells expressing L-SIGN, with up to 13% infection observed.