COVID-19 disease, caused by infection with SARS-CoV-2, is related to a series of physiopathological mechanisms that mobilize a wide variety of biomolecules, mainly immunological in nature. In the most severe cases, the prognosis can be markedly worsened by the hyperproduction of mainly proinflammatory cytokines, such as IL-1, IL-6, IL-12, IFN-γ, and TNF-α, preferentially targeting lung tissue. This study reviews published data on alterations in the expression of different cytokines in patients with COVID-19 who require admission to an intensive care unit. Data on the implication of cytokines in this disease and their effect on outcomes will support the design of more effective approaches to the management of COVID-19.

Systemic lupus erythematosus (SLE) is an autoimmune chronic inflammatory disease of unknown etiology, although genetic and environmental factors appear to contribute to its pathogenesis. Specifically, infectious processes are associated with SLE onset and exacerbation. However, we are far from a complete understanding of the interactions between infectious agents and the host, explaining the interest in gathering updated scientific information on this topic. According to the literature, the pathogens most frequently associated with SLE are viruses, notably human endogenous retroviruses, Epstein-Barr virus, parvovirus B19, cytomegalovirus and human immunodeficiency virus type 1, alongside certain bacterial components that can also trigger activation of the immune system. The mechanisms underlying autoreactivity remain unclear but various explanations have been proposed, including immunological changes responsible for infectious processes or molecular mimicry between host structures and those of infectious agents.

No abstract