Abstract
Monocytes-macrophages and lymphocytes are recruited to the respiratory tract in response to influenza virus challenge and are exposed to the virus during the establishment of immune defenses. The susceptibility of human lymphocytes to infection was assessed. The presence of monocytes-macrophages was required to attain infection of both resting and proliferating lymphocytes. Lymphocyte infection occurred in the context of immune cell clusters and was blocked by the addition of anti-intercellular adhesion molecule-1 (ICAM-1) antibody to prevent cell clustering. Both peripheral blood-derived and bronchoalveolar lymphocytes were susceptible to infection. Both CD4+ and CD8+ T lymphocytes were susceptible to influenza virus infection, and the infected CD4+ and CD8+ lymphocytes served as infectious foci for other nonpermissive or even virus-permissive cells. These data show that monocytes-macrophages and both CD4+ and CD8+ lymphocytes can become infected during the course of an immune response to influenza virus challenge. The described leukocyte interactions during infection may play an important role in the development of effective anti-influenza responses.
Highlights
Murine models have been used to demonstrate the rapid and substantial recruitment of peripheral blood mononuclear cells (PBMC), both monocytes-macrophages and lymphocytes, to the lung after influenza virus challenge [1,2,3,4]
The results indicate that macrophage-to-lymphocyte transfer of influenza virus occurs in the context of the immune cell cluster that is a critical component of the developing antiviral host response
Elutriated purified resting lymphocytes were free of monocytes-macrophages, and even the proliferating lymphocyte preparations contained
Summary
Murine models have been used to demonstrate the rapid and substantial recruitment of peripheral blood mononuclear cells (PBMC), both monocytes-macrophages and lymphocytes, to the lung after influenza virus challenge [1,2,3,4]. These recruited cells play important roles in defense against and recovery from the virus infection [2,5,6], demonstrated by studies using adoptive transfer [7,8] or host immunosuppression [9,10,11]. Exposure to influenza virus results in enhanced expression of the lymphocyte function-associated antigen-1 (LFA-1) and its ligand intercellular adhesion
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