Immunodepression induced by influenza A virus (H1N1) in lymphoid organs functions as a pathogenic mechanism.

In recent years,the frequency ofinfluenza epidemicsaround the worldhas posed a great threat to the lives of people, especially those in developing countries. However, it is unclear which organs are the targets of influenza A viruses (IAVs) and whathistopathology is caused by IAVs.In this study, BALB/c female mice were infected with H1N1 by nasal inoculation for five days. After euthanasia, the brain, heart, lungs, thymus, liver, spleen, hilar lymph nodes, pancreas, kidneys, and adrenal glands were collected.Among these organs, only thelungs, thymus, spleen, and hilar lymph nodes showed lesions. Lung histopathology was characterized by widening of the septum, lymphocyte infiltration, alveolar effusion, and alveolar hyaline membrane formation. The thymus and spleen exhibited atrophy due to the apoptosis of numerous lymphocytes. Although the hilar lymph nodes were enlarged, lymphocyte apoptosis still occurred. The nucleocapsid protein (NP) of IAVs was present not only in the lungs but also in the thymus, spleen, and hilar lymph nodes. In peripheral blood, CD19+ B lymphocyte levels clearly decreased whileCD3+ CD8+ T and CD3+ CD4+ T lymphocyte levels temporarily decreased butsubsequently increased. These results demonstrate that H1N1 in thelungs could reach lymphoid organs, inducethe depletion of B and T lymphocytes in peripheral blood and lymphoid organs, and suppress adaptive immunity.