You Probably Have an Asymptomatic Infection Right Now

Illustration of a human body with a virus shape cut out

No, not COVID-19. Many, many viruses can infect humans without making us sick, and how they do that is one of biology’s deepest mysteries.


One of the most perplexing and enduring mysteries of the pandemic is also one of the most fundamental questions about viruses. How can the same virus that kills so many go entirely unnoticed in others?

The mystery is hardly unique to COVID-19. SARS, MERS, influenza, Ebola, dengue, yellow fever, chikungunya, West Nile, Lassa, Japanese encephalitis, Epstein-Barr, and polio can all be deadly in one person but asymptomatic in the next.   

But for most of human existence, we didn’t know that viruses could infect us asymptomatically. We didn’t know how to look for them, or even that we should. The tools of modern science have slowly made the invisible visible: Antibody surveys that detect past infection, tests that find viral DNA or RNA even in asymptomatic people, and mathematical models all show that viruses are up to much more than making us sick. Scientists now think that for viruses, a wide range of disease severity is the norm rather than the exception.

A virus, after all, does not necessarily wish its host ill. A dead host is a dead end. The viruses best adapted to humans have co-evolved over millions of years to infect but rarely sicken us. Human cytomegalovirus is a prime example, a virus so innocuous that it lives in obscurity despite infecting most of the world’s population. (Odds are that you have it.) Infections with human cytomegalovirus are almost always asymptomatic because it has evolved a suite of tricks to evade the human immune system, which nevertheless tries its best to hunt the virus down. 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. In the rare instances when human cytomegalovirus turns deadly—usually in an immunocompromised patient—it’s because this equilibrium did not hold.

The coronavirus that causes COVID-19 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.  

Let’s begin where a COVID-19 infection begins, when virus meets cell. 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.

Within hours of a typical viral infection, the first infected cells begin secreting interferons, a group of molecules that acts as “a fire alarm and sprinkler system in one,” says Angela Rasmussen, a virologist at Georgetown’s Center for Global Health Science and Security. 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.

Interferons also “interfere” with the virus in a number of ways, such as degrading viral genes, preventing cells from taking up viral particles, suppressing the manufacturing of viral proteins, and causing infected cells to self-destruct. By slowing replication of the virus, interferons buy time for the rest of the immune system.

This is what happens when everything goes right. But every successful virus has to develop ways of evading the body’s defenses, and the coronavirus that causes COVID-19 is very good at a devilish trick: Several of its genes encode proteins that seem capable of blocking interferons. By quieting the body’s fire alarm and disarming its sprinkler system, the coronavirus can set fire after fire. 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. Without timely targeted strikes from the adaptive immune system’s antibodies and T cells, the powerful but blunt innate immune response ramps up and up, destroying healthy human cells in the process. This is one possible explanation for the immune overreaction observed in severe and fatal cases of COVID-19…


F. Kaskais Web Guru

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