Details

Autor(en) / Beteiligte

• Silveira, Guilherme F
• Wowk, Pryscilla F
• Cataneo, Allan H D
• Dos Santos, Paula F
• Delgobo, Murilo
• Stimamiglio, Marco A
• Lo Sarzi, Maria
• Thomazelli, Ana Paula F S
• Conchon-Costa, Ivete
• Pavanelli, Wander R
• Antonelli, Lis R V
• Báfica, André
• Mansur, Daniel S
• Dos Santos, Claudia N Duarte
• Bordignon, Juliano
• Diamond, Michael S.

Titel

Human T Lymphocytes Are Permissive for Dengue Virus Replication

Ist Teil von

• Journal of virology, 2018-05, Vol.92 (10)

Ort / Verlag

United States: American Society for Microbiology

Erscheinungsjahr

2018

Link zum Volltext

Quelle

Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals

Beschreibungen/Notizen

• Dengue virus (DV) infection can cause either a self-limiting flu-like disease or a threatening hemorrhage that may evolve to shock and death. A variety of cell types, such as dendritic cells, monocytes, and B cells, can be infected by DV. However, despite the role of T lymphocytes in the control of DV replication, there remains a paucity of information on possible DV-T cell interactions during the disease course. In the present study, we have demonstrated that primary human naive CD4 and CD8 T cells are permissive for DV infection. Importantly, both T cell subtypes support viral replication and secrete viable virus particles. DV infection triggers the activation of both CD4 and CD8 T lymphocytes, but preactivation of T cells reduces the susceptibility of T cells to DV infection. Interestingly, the cytotoxicity-inducing protein granzyme A is highly secreted by human CD4 but not CD8 T cells after exposure to DV Additionally, using annexin V and polycaspase assays, we have demonstrated that T lymphocytes, in contrast to monocytes, are resistant to DV-induced apoptosis. Strikingly, both CD4 and CD8 T cells were found to be infected with DV in acutely infected dengue patients. Together, these results show that T cells are permissive for DV infection and , suggesting that this cell population may be a viral reservoir during the acute phase of the disease. Infection by dengue virus (DV) causes a flu-like disease that can evolve to severe hemorrhaging and death. T lymphocytes are important cells that regulate antibody secretion by B cells and trigger the death of infected cells. However, little is known about the direct interaction between DV and T lymphocytes. Here, we show that T lymphocytes from healthy donors are susceptible to infection by DV, leading to cell activation. Additionally, T cells seem to be resistant to DV-induced apoptosis, suggesting a potential role as a viral reservoir in humans. Finally, we show that both CD4 and CD8 T lymphocytes from acutely infected DV patients are infected by DV. Our results raise new questions about DV pathogenesis and vaccine development.