Regardless of the agent, the inflammatory response is interconnected with infection. Mostly the initial response to infection is severe sepsis and characterized by a pro-inflammatory state, which then progresses to an anti-inflammatory state that develops and favors secondary infections (Florescu and Kalil, 2011) [1]. T-helper 1 (Th1) cells activated by microorganisms increase transcription of pro-inflammatory cytokines such as tumor necrosis factor (TNF-α), interferon-γ (INF-γ), and interleukin-2 (IL-2) (Hotchkiss and Karl, 2003; Brown and Jones, 2004; Russell, 2006) [[2], [3], [4]]. Different cytokines, TNF-α, interleukins, lymphokines, monokines, IFN-γ, colony-stimulating factor (CSF) and transforming growth factors, released from endothelial cells and subsequently from macrophages can induce lymphocyte activation and infiltration at the sites of infection and will exert direct antiviral effects. Subsequently, with the shift toward an anti-inflammatory state, activated T-helper 2 (Th2) cells secrete interleukin-4 (IL-4) and interleukin-10 (IL-10) (Hotchkiss and Karl, 2003; Russell, 2006) [2,4]. Sometimes, T cells can become anergic and fail to proliferate as wells producing cytokines (Hotchkiss and Karl, 2003) [2]. Type I IFN has a potent anti-influenza virus activity, it induces transcription of several interferon-stimulated genes, which in turn restrict viral replication (Garcia-Sastre, 2011) [5]. However, the influenza virus developed several mechanisms to evade IFN response as NS1 protein, IFN-antagonist produced by the virus, PB1-F2 proteins that inhibit IFN induction, the viral polymerase inhibits IFN function, and M2 protein prevents toll-like receptor (TLR) induction (Garcia-Sastre, 2011) [5]. Influenza virus can also trigger the deregulation of the innate immune system with excessive cytokines release leading to potentially harmful consequences (Teijaro et al., 2011) [6]. Abnormal immune response to influenza can lead to endothelial damage through the remodeling of the cellular cytoskeleton, loss of intercellular junctional integrity, cellular apoptosis, deregulation of coagulation, the consequent alteration of microvascular permeability, tissue edema, and shock (Steinberg et al., 2012) [7]. This increase in permeability of the endothelium is mainly due to the intercellular pathways and to a lesser extent through the transcellular leak (Steinberg et al., 2012) [7]. Such vascular hyperpermeability and multi-organ failure with severe edema, shock, acute lung injury, and even acute encephalopathy have been described in severe influenza infections (Wang et al., 2010; Armstrong et al., 2013) [8,9]. Novel drugs and vaccines such as peramivir, baloxavir marboxil, and 4 egg-based quadrivalent inactivated influenza vaccines have been added recently [10]. These changes require better and more efficient diagnostic and therapeutic approaches to avoid a fatal progression. I would like to report a child patient with H1N1 influenza, who developed rapid fatal viral septicemia.
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