TY - JOUR
T1 - Reduced activation and proliferation of human lymphocytes exposed to respiratory syncytial virus compared to cells exposed to influenza virus
AU - Fleming, Elisa H.
AU - Ochoa, Eliana E.
AU - Nichols, Joan E.
AU - O'Banion, M. Kerry
AU - Salkind, Alan R.
AU - Roberts, Norbert J.
N1 - Funding Information:
NIH Institutional Training, Grant number: T32-AI07526; Robert D. Watkins Minority Fellowship from the American Society for Microbiology (E.H.F.); Sealy Center for Vaccine Development; NIH, Grant numbers: AI 23774, 15547; National Institute of Allergy and Infectious Diseases; Endowment Fund (N.J.R.)
Funding Information:
This work was supported by an NIH Institutional Training Grant (T32-AI07526) and a Robert D. Watkins Minority Fellowship from the American Society for Microbiology (E.H.F.), by the Sealy Center for Vaccine Development, and by NIH grants (AI 23774 and 15547) from the National Institute of Allergy and Infectious Diseases, and the Paul R. Stalnaker, M.D. Endowment Fund (N.J.R.).
Publisher Copyright:
© 2017 Wiley Periodicals, Inc.
PY - 2018/1
Y1 - 2018/1
N2 - Both respiratory syncytial virus (RSV) and influenza A virus (IAV) may infect human peripheral blood mononuclear leukocytes (PBMC) during the immune response to viral challenge as the cells are recruited to the respiratory tract. The current studies demonstrated differences in PBMC responses to the two viruses very early after exposure, including reduced fos protein and CD69 expression and IL-2 production by RSV-exposed T lymphocytes. Exposure to RSV resulted in reduced lymphocyte proliferation despite evidence of a virus-specific T lymphocyte frequency equivalent to that for influenza virus. Reduced RSV-induced proliferation was not due to apoptosis, which was itself reduced relative to that of influenza virus-exposed T lymphocytes. The data indicate that differential immune responses to RSV and influenza virus are determined early after exposure of human PBMC and support the concept that the anamnestic immune response that might prevent clinically evident reinfection is attenuated very soon after exposure to RSV. Thus, candidate RSV vaccines should be expected to reduce but not prevent clinical illness upon subsequent infection by RSV. Furthermore, effective therapeutic agents for RSV are likely to be needed, especially for high-risk populations, even after vaccine development.
AB - Both respiratory syncytial virus (RSV) and influenza A virus (IAV) may infect human peripheral blood mononuclear leukocytes (PBMC) during the immune response to viral challenge as the cells are recruited to the respiratory tract. The current studies demonstrated differences in PBMC responses to the two viruses very early after exposure, including reduced fos protein and CD69 expression and IL-2 production by RSV-exposed T lymphocytes. Exposure to RSV resulted in reduced lymphocyte proliferation despite evidence of a virus-specific T lymphocyte frequency equivalent to that for influenza virus. Reduced RSV-induced proliferation was not due to apoptosis, which was itself reduced relative to that of influenza virus-exposed T lymphocytes. The data indicate that differential immune responses to RSV and influenza virus are determined early after exposure of human PBMC and support the concept that the anamnestic immune response that might prevent clinically evident reinfection is attenuated very soon after exposure to RSV. Thus, candidate RSV vaccines should be expected to reduce but not prevent clinical illness upon subsequent infection by RSV. Furthermore, effective therapeutic agents for RSV are likely to be needed, especially for high-risk populations, even after vaccine development.
KW - human lymphocytes
KW - influenza virus
KW - lymphocyte activation
KW - lymphocyte proliferation
KW - respiratory syncytial virus
KW - Antigens, Differentiation, T-Lymphocyte/genetics
KW - Cell Proliferation
KW - Influenza A virus/immunology
KW - T-Lymphocytes/immunology
KW - Lymphocyte Activation
KW - Humans
KW - Antigens, CD/genetics
KW - Respiratory Syncytial Virus, Human/immunology
KW - Lectins, C-Type/genetics
KW - Leukocytes, Mononuclear/immunology
KW - Interleukin-2/genetics
KW - Apoptosis
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U2 - 10.1002/jmv.24917
DO - 10.1002/jmv.24917
M3 - Article
C2 - 28856681
AN - SCOPUS:85034040648
SN - 0146-6615
VL - 90
SP - 26
EP - 33
JO - Journal of Medical Virology
JF - Journal of Medical Virology
IS - 1
ER -