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Apoptosis of lymphocytes and monocytes infected with influenza virus might be the mechanism of combating virus and causing secondary infection by influenza.
- Source :
- International Immunology; Nov2009, Vol. 21 Issue 11, p1251-1262, 12p, 1 Diagram, 7 Graphs
- Publication Year :
- 2009
-
Abstract
- Influenza affects most of the world's population annually, often causing a secondary infection, but pathological mechanisms of influenza virus infection remain unclear. We have found that influenza viruses have a selective preference for infecting monocytes and mature immune effector cells. This paper provides evidence that influenza virus infection increases the expression of granzyme B (GrB) in monocytes, activated T and B cells. All GrB+ cells had cytolytic function. GrB+CD62Lhigh central memory (TCM) cells were fast response population to virus infection when compared with GrB+CD62Llow population. The influenza virus-infected PBMC could be killed by GrB+ cells. We propose the following mechanism for influenza: (i) influenza virus within the respiratory tract overcomes humoral defenses; (ii) free virus is directly engulfed by the immune system effector cells and free virus also infects epithelial cells; (iii) virus-infected epithelial cells and the immune system cells are killed by cytotoxic cells. These indicated that an immune system that was combating a virus infection needs to sacrifice some of its immune system cells. Therefore, influenza viruses might temporally destroy the human immune system's line of defense, resulting in susceptibility to a secondary infection. This might be a prevalent mechanism existing in cell-mediated immune responses. [ABSTRACT FROM PUBLISHER]
- Subjects :
- APOPTOSIS
LYMPHOCYTES
MONOCYTES
INFLUENZA viruses
ORTHOMYXOVIRUSES
IMMUNE system
Subjects
Details
- Language :
- English
- ISSN :
- 09538178
- Volume :
- 21
- Issue :
- 11
- Database :
- Complementary Index
- Journal :
- International Immunology
- Publication Type :
- Academic Journal
- Accession number :
- 45211478
- Full Text :
- https://doi.org/10.1093/intimm/dxp087