More often, people become infected a second time with a particular pathogen, and the immune system recognizes the invader and quickly extinguishes the infection. The coronavirus in particular is slow to do harm, giving the immune system plenty of time to kick into gear.
“It may be terminated fast enough that not only are you not experiencing any symptoms but you are not infectious,” Dr.[Alesandra] Sette said.
The idea that COVID-19 will eventually act like routine HCoVs is also supported by research on T-cell reactivity. Six studies demonstrated that samples from people who had no known exposure to COVID-19 nevertheless had reactive T-cell responses to the virus in between 20-50% of participants.
The studies were small and cannot predict how many in the population may have a pre-existing immune response based on exposure to related HCoVs. However, it is a possible explanation for the wide range of symptoms seen even in healthy individuals and those who are asymptomatic.
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These T-cells most likely result from previous coronavirus infections. For the same reason that antibody (serology) tests are almost useless to specifically detect previous Covid-19 infection, these preexisting T-cells could actually help a person to recover from Covid-19 infection faster. There are enough similarities between related viruses that the immune system does a poor job of distinguishing between them.
New research predicts that, like the virus that caused the Spanish flu epidemic in 1918, COVID-19 will become another seasonal bug that we build efficient long-term immunity against.
One cannot compare coronaviruses and influenza viruses. Influenza viruses mutate very rapidly due to their unique genetic structure. Their genetic material consists of eight physically separate gene cassettes (seven for influenza b viruses); different strains of virus can trade gene cassettes to become new strains. In addition, a given influenza strain tends to circulate for a few years, then disappear completely while other strains gain dominance. The 1917-1919 pandemic H1N1 virus disappeared. While currently circulating strains of H1N1 share some similarity to the 1918 virus, they are different strains. Because of the biology and high mutagenicity of influenza viruses, there is a persistent concern that a new influenza virus will form and cause a highly deadly pandemic.
In contrast to influenza viruses, coronavirus genes are all present on a single piece of genetic material. This completely eliminates one of the mechanisms (swapping of gene cassettes) that influenza uses to mutate rapidly. It is not impossible for coronaviruses to trade genes, but since all of their genes are on the same strand of genetic material, the process is more complicated and less likely to occur. Thus, in the long run, protective immunity could be passed from mother to child and childhood illness could help to decrease the severity of later illness. We don't know. Another possibility is that it could adapt to human host through mutation and lose some virulence as a result. At this time, we can use the history of other infectious agents as a guide for predicting the possible future of Covid-19, but we have no solid evidence to project its future.