The immune system through the ages

The components of the immune system develop in utero and like a computer, some components are immediately functional (the innate components) but other components must learn the programs and details necessary to function (antigen adaptive components). Like other systems, including military and municipal, the innate and antigen specific components develop into an immune system that helps maintain and surveil the other body processes and systems for aberrations, provide surveillance and protection of the mucoepithelial borders and protection from microbial invasion. Inability, excesses, or errors in these processes cause disease. Aging of the immune system brings immunosenescence, inflammaging, more errors, and decreased surveillance which increases risk for new infections (e.g. COVID-19, influenza), recurrence of latent infections, cancer and autoimmune and inflammatory diseases. With greater understanding of the surveillance, effector and regulatory deficits upon aging, better therapies can be developed.

Why Is a Child Not a Miniadult for Infections?

The presentation of an infectious disease in a child is likely to differ from an adult and will differ at different ages of the child. In addition to differences in immune response, there are significant differences in anatomy, physiology, metabolism, and behavior that affect susceptibility, course of disease, severity, and treatment. This is the first of a series of reviews that examine differences in disease presentation for different demographics. This short review will look at some of the parameters that ask, "Why is a child not a miniadult for infections?"

Three properties of SARS-CoV-2 that promote COVID-19

Much of COVID-19 disease can be attributed to the stable structure of the envelope, which facilitates its transmission;the spike protein and its receptor which determine which tissues get infected and are susceptible to viral and immune cytolysis;and evasion of initiation of type 1 and 3 interferons, which gives the virus a replicative head start and ability to spread while simultaneously compromising the antiviral immune response. © Wolters Kluwer Health, Inc. All rights reserved.