| Full text | |
| Author(s): Show less - |
Cardoso, Ricardo de Souza
[1, 2]
;
Mendes Viana, Rosa Maria
[1]
;
Vitti, Brenda Cristina
[1]
;
Lunardello Coelho, Ana Carolina
[1]
;
Santos de Jesus, Bruna Lais
[1]
;
Souza, Juliano de Paula
[1]
;
Pontelli, Marjorie Cornejo
[1]
;
Murakami, Tomoyuki
[2]
;
Ventura, Armando Morais
[3]
;
Ono, Akira
[2]
;
Arruda, Eurico
[1]
Total Authors: 11
|
| Affiliation: | [1] Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Cell & Mol Biol, BR-14049900 Sao Paulo - Brazil
[2] Univ Michigan, Dept Microbiol & Immunol, Med Sch, Ann Arbor, MI 48109 - USA
[3] Univ Sao Paulo, Inst Biomed Sci, Dept Microbiol, BR-05508000 Sao Paulo - Brazil
Total Affiliations: 3
|
| Document type: | Journal article |
| Source: | Viruses-Basel; v. 13, n. 2 FEB 2021. |
| Web of Science Citations: | 0 |
| Abstract | |
Human respiratory syncytial virus (HRSV) is the most frequent cause of severe respiratory disease in children. The main targets of HRSV infection are epithelial cells of the respiratory tract, and the great majority of the studies regarding HRSV infection are done in respiratory cells. Recently, the interest on respiratory virus infection of lymphoid cells has been growing, but details of the interaction of HRSV with lymphoid cells remain unknown. Therefore, this study was done to assess the relationship of HRSV with A3.01 cells, a human CD4(+) T cell line. Using flow cytometry and fluorescent focus assay, we found that A3.01 cells are susceptible but virtually not permissive to HRSV infection. Dequenching experiments revealed that the fusion process of HRSV in A3.01 cells was nearly abolished in comparison to HEp-2 cells, an epithelial cell lineage. Quantification of viral RNA by RT-qPCR showed that the replication of HRSV in A3.01 cells was considerably reduced. Western blot and quantitative flow cytometry analyses demonstrated that the production of HRSV proteins in A3.01 was significantly lower than in HEp-2 cells. Additionally, using fluorescence in situ hybridization, we found that the inclusion body-associated granules (IBAGs) were almost absent in HRSV inclusion bodies in A3.01 cells. We also assessed the intracellular trafficking of HRSV proteins and found that HRSV proteins colocalized partially with the secretory pathway in A3.01 cells, but these HRSV proteins and viral filaments were present only scarcely at the plasma membrane. HRSV infection of A3.01 CD4(+) T cells is virtually unproductive as compared to HEp-2 cells, as a result of defects at several steps of the viral cycle: Fusion, genome replication, formation of inclusion bodies, recruitment of cellular proteins, virus assembly, and budding. (AU) | |
| FAPESP's process: | 13/16349-2 - Studies on persisting infections by human respiratory Paramyxoviruses |
| Grantee: | Eurico de Arruda Neto |
| Support Opportunities: | Regular Research Grants |