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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(+)CD62L(high) central memory (T(CM)) cells were fast response population to virus infection when compared with GrB(+)CD62L(low) 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.

international immunology

Apoptosis of lymphocytes and monocytes infected with influenza virus might be the mechanism of combating virus and causing secondary infection by influenza