Hyperinflammatory syndromes in adults with viral infections are well known and often characterized by increased levels of inflammatory mediators such as interleukin-2 (IL-2), IL-6, tumor necrosis factor-α (TNF-α), monocyte chemoattractant protein − 1 (MCP-1) or macrophage inflammatory protein 1-α (MIP-1α) [12, 13]. This evidence concerns the gene IL2 and viral infectious disease.