By the time humans reach old age, up to a quarter of our killer T cells are devoted to fighting human cytomegalovirus. Pathogens and immune systems are in constant battle, with one just barely keeping the other in check. The coronavirus that causes COVID is much newer to humans, and severe cases have justifiably gotten the most attention during the pandemic. Scientists have made dramatic advances in understanding this virus and how to treat it.
But unraveling why it makes some of us sick, and leaves others unscathed, requires an appreciation of the delicate dance between pathogen and immune system that begins each time the virus finds a new host. The initial infectious dose—the number of virus particles that enter the body—may influence the course of infection. The more particles that land in your nose, for example, the closer the virus is to overwhelming your immune system, leading in some cases to more severe illness.
The fire alarm alerts the two main branches of the human immune system: the fast but nonspecific innate immune system, which causes inflammation and fever, and the adaptive immune system, which over a series of days will muster antibodies and T cells that more precisely target the invading virus. By slowing replication of the virus, interferons buy time for the rest of the immune system.
This is what happens when everything goes right. In the race between virus and immune system, the immune system falls behind. The virus proliferates. Lung cells die. Eventually, so many viral particles are infecting so many cells that the immune system knows something must be wrong. It begins to gear up—but too late. This is one possible explanation for the immune overreaction observed in severe and fatal cases of COVID This delayed interferon response, Rasmussen told me, reminds her of Ebola, which she studied before our current pandemic.
Ebola is a very different virus with a much higher fatality rate, but deadly cases of Ebola are also characterized by uncontrolled inflammation in the body following a delayed interferon response. And Ebola is asymptomatic in some people too—as many as a quarter of all those infected, according to one estimate.
In response to infection, your immune system springs into action. White blood cells , antibodies , and other mechanisms go to work to rid your body of the foreign invader. Indeed, many of the symptoms that make a person suffer during an infection—fever, malaise, headache, rash—result from the activities of the immune system trying to eliminate the infection from the body.
Pathogenic microbes challenge the immune system in many ways. Viruses make us sick by killing cells or disrupting cell function. Many bacteria make us sick in the same way that viruses do, but they also have other strategies at their disposal.
Sometimes bacteria multiply so rapidly they crowd out host tissues and disrupt normal function. Sometimes they kill cells and tissues outright. The protozoa that cause malaria , which are members of the genus Plasmodium, have complex life cycles.
As world health leaders try to determine how to respond to the new coronavirus, virus expert Marilyn J. Roossinck answers a few questions.
Defining a virus has been a challenge, because every time we come up with a good definition someone discovers a virus that breaks the rules.
Viruses are entities that infect cellular life. They are very diverse. Others have hundreds of genes, more than some bacteria. All viruses are ultimately parasites.
They require a host for replication. They cannot generate their own energy like cells can. When a new human virus disease appears, it is most often because the virus has jumped from a different species into humans.
The worst viruses are often the ones that have very recently jumped into the species. After jumping species, the virus goes through a process of adjustment to its new host. The real challenge, however, is to the host. As it tries to figure out how to adjust to an invasion from something completely new, the immune system overreacts.
This is what makes the host sick.
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