Toll-like receptor 4 in acute viral infection: Too much of a good thing

Although a well-regulated inflammatory response is a vital defense mechanism against viral infection, too much inflammation can be detrimental.Excessive inflammatory responses, which are characterized by elevated levels of a broad array of pro-inflammatory cytokines and chemokines, have been observed in a wide variety of viral diseases associated with serious morbidity and mortality.Examples of this include acute lung injury caused by infections with respiratory syncytial virus (RSV), influenza A virus (IAV), or severe acute respiratory syndrome coronavirus (SARS-CoV).Excessive inflammatory responses induced by viral infections are not restricted to the lung but can be systemic, as reported for Ebola virus (EBOV) disease and severe dengue [1][2][3][4][5].The reasons leading to an unbalanced inflammatory response in certain viral infections are not well understood and are most likely multifactorial.Here, we explore the role of toll-like receptor 4 (TLR4) in the induction of damaging inflammatory responses during acute viral infections.