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Respiratory syncytial virus induces phosphorylation of mTOR at ser2448 in CD8 T cells from nasal washes of infected infants
Author(s) -
de Souza A. P. Duarte,
de Freitas D. Nascimento,
Antuntes Fernandes K. E.,
D'Avila da Cunha M.,
Antunes Fernandes J. L.,
Benetti Gassen R.,
Fazolo T.,
Pinto L. A.,
Scotta M.,
Mattiello R.,
Pitrez P. M.,
Bonorino C.,
Stein R. T.
Publication year - 2016
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/cei.12720
Subject(s) - respiratory system , immunology , virus , virology , phosphorylation , medicine , biology , biochemistry
Summary 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‐M 282–90 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.

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