Regulation of lymphocyte proliferation after influenza virus infection of human mononuclear leukocytes

N. J. Roberts, Joan Nichols

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Previous studies demonstrated that in vitro infection with influenza A viruses altered several functions of human monocytes-macrophages but did not detectably alter functions of human lymphocytes. However, both types of cells were infected, as determined by production and surface expression of viral antigens. In the current studies, human mononuclear leukocytes were infected in vitro and assayed for both influenza virus-induced proliferation and mitogen (phytohemagglutinin [PHA])-induced proliferation, as well as for ability to stimulate proliferative responses by normal autologous leukocytes. The leukocytes showed proliferation in response to the infectious virus, but concomitant depressed proliferative responses to PHA. Coculture experiments suggested suppression of PHA-induced responses by the virus-infected cells. However, upon coculture with fresh autologous leukocytes (without PHA stimulation), both virus-infected macrophages and virus-infected lymphocytes induced autologous lymphocyte proliferative responses. Altered proliferative responses to mitogen stimulation after exposure to the virus were not due to diminished interleukin-1 production or diminished expression of HLA-DR by monocytes-macrophages. The expression of influenza virus antigens and resulting induction of autologous proliferative responses, combined with depressed mitogen-induced proliferation, may be important in human antiviral defense.

Original languageEnglish (US)
Pages (from-to)179-187
Number of pages9
JournalJournal of Medical Virology
Volume27
Issue number3
StatePublished - 1989
Externally publishedYes

Fingerprint

Mononuclear Leukocytes
Virus Diseases
Orthomyxoviridae
Phytohemagglutinins
Lymphocytes
Viruses
Mitogens
Leukocytes
Macrophages
Coculture Techniques
Monocytes
Viral Antigens
Influenza A virus
HLA-DR Antigens
Interleukin-1
Antiviral Agents
Antigens
Infection

ASJC Scopus subject areas

  • Virology

Cite this

Regulation of lymphocyte proliferation after influenza virus infection of human mononuclear leukocytes. / Roberts, N. J.; Nichols, Joan.

In: Journal of Medical Virology, Vol. 27, No. 3, 1989, p. 179-187.

Research output: Contribution to journalArticle

@article{d1ad83c30b484aa683c945b9c529d641,
title = "Regulation of lymphocyte proliferation after influenza virus infection of human mononuclear leukocytes",
abstract = "Previous studies demonstrated that in vitro infection with influenza A viruses altered several functions of human monocytes-macrophages but did not detectably alter functions of human lymphocytes. However, both types of cells were infected, as determined by production and surface expression of viral antigens. In the current studies, human mononuclear leukocytes were infected in vitro and assayed for both influenza virus-induced proliferation and mitogen (phytohemagglutinin [PHA])-induced proliferation, as well as for ability to stimulate proliferative responses by normal autologous leukocytes. The leukocytes showed proliferation in response to the infectious virus, but concomitant depressed proliferative responses to PHA. Coculture experiments suggested suppression of PHA-induced responses by the virus-infected cells. However, upon coculture with fresh autologous leukocytes (without PHA stimulation), both virus-infected macrophages and virus-infected lymphocytes induced autologous lymphocyte proliferative responses. Altered proliferative responses to mitogen stimulation after exposure to the virus were not due to diminished interleukin-1 production or diminished expression of HLA-DR by monocytes-macrophages. The expression of influenza virus antigens and resulting induction of autologous proliferative responses, combined with depressed mitogen-induced proliferation, may be important in human antiviral defense.",
author = "Roberts, {N. J.} and Joan Nichols",
year = "1989",
language = "English (US)",
volume = "27",
pages = "179--187",
journal = "Journal of Medical Virology",
issn = "0146-6615",
publisher = "Wiley-Liss Inc.",
number = "3",

}

TY - JOUR

T1 - Regulation of lymphocyte proliferation after influenza virus infection of human mononuclear leukocytes

AU - Roberts, N. J.

AU - Nichols, Joan

PY - 1989

Y1 - 1989

N2 - Previous studies demonstrated that in vitro infection with influenza A viruses altered several functions of human monocytes-macrophages but did not detectably alter functions of human lymphocytes. However, both types of cells were infected, as determined by production and surface expression of viral antigens. In the current studies, human mononuclear leukocytes were infected in vitro and assayed for both influenza virus-induced proliferation and mitogen (phytohemagglutinin [PHA])-induced proliferation, as well as for ability to stimulate proliferative responses by normal autologous leukocytes. The leukocytes showed proliferation in response to the infectious virus, but concomitant depressed proliferative responses to PHA. Coculture experiments suggested suppression of PHA-induced responses by the virus-infected cells. However, upon coculture with fresh autologous leukocytes (without PHA stimulation), both virus-infected macrophages and virus-infected lymphocytes induced autologous lymphocyte proliferative responses. Altered proliferative responses to mitogen stimulation after exposure to the virus were not due to diminished interleukin-1 production or diminished expression of HLA-DR by monocytes-macrophages. The expression of influenza virus antigens and resulting induction of autologous proliferative responses, combined with depressed mitogen-induced proliferation, may be important in human antiviral defense.

AB - Previous studies demonstrated that in vitro infection with influenza A viruses altered several functions of human monocytes-macrophages but did not detectably alter functions of human lymphocytes. However, both types of cells were infected, as determined by production and surface expression of viral antigens. In the current studies, human mononuclear leukocytes were infected in vitro and assayed for both influenza virus-induced proliferation and mitogen (phytohemagglutinin [PHA])-induced proliferation, as well as for ability to stimulate proliferative responses by normal autologous leukocytes. The leukocytes showed proliferation in response to the infectious virus, but concomitant depressed proliferative responses to PHA. Coculture experiments suggested suppression of PHA-induced responses by the virus-infected cells. However, upon coculture with fresh autologous leukocytes (without PHA stimulation), both virus-infected macrophages and virus-infected lymphocytes induced autologous lymphocyte proliferative responses. Altered proliferative responses to mitogen stimulation after exposure to the virus were not due to diminished interleukin-1 production or diminished expression of HLA-DR by monocytes-macrophages. The expression of influenza virus antigens and resulting induction of autologous proliferative responses, combined with depressed mitogen-induced proliferation, may be important in human antiviral defense.

UR - http://www.scopus.com/inward/record.url?scp=0024518292&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024518292&partnerID=8YFLogxK

M3 - Article

VL - 27

SP - 179

EP - 187

JO - Journal of Medical Virology

JF - Journal of Medical Virology

SN - 0146-6615

IS - 3

ER -