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Respiratory syncytial virus induces phosphorylation of mTOR at ser2448 in CD8 T cells from nasal washes of infected infants

2015; Oxford University Press; Volume: 183; Issue: 2 Linguagem: Inglês

10.1111/cei.12720

1365-2249

Ana Paula Duarte de Souza, Deise Nascimento de Freitas, Kerri E Fernandes, Mariana D’Ávila da Cunha, Krist Helen Antunes, R Benetti Gassen, Tiago Fazolo, Leonardo Araújo Pinto, Marcelo Comerlato Scottá, Rita Mattiello, Paulo Márcio Pitrez, Cristina Bonorino, Renato T. Stein,

Animal Virus Infections Studies

Respiratory syncytial virus (RSV)-specific CD8(+) T cell responses do not protect against reinfection. Activation of mammalian target of rapamycin (mTOR) impairs memory CD8(+) T cell differentiation. Our hypothesis was that RSV inhibits the formation of CD8(+) T cells memory responses through mTOR activation. To explore this, human and mouse T cells were used. RSV induced mTOR phosphorylation at Ser2448 in CD8 T cells. mTOR activation by RSV was completely inhibited using rapamycin. RSV-infected children presented higher mTOR gene expression on nasal washes comparing to children infected with metapneumovirus and rhinovirus. In addition, RSV-infected infants presented a higher frequency of CD8(+) pmTORser2448(+) T cells in nasal washes compared to RSV-negative infants. Rapamycin treatment increased the frequency of mouse CD8 RSV-M282-90 pentamer-positive T cells and the frequency of RSV-specific memory T cells precursors. These data demonstrate that RSV is activating mTOR directly in CD8 T cells, indicating a role for mTOR during the course of RSV infection.