When COVID-19 patients go to see Dr. Christian Bime, a pulmonary care expert at Banner University Medical Center-Tucson, they might walk in breathing on their own.

Within a matter of hours, they could be on life support.

"They come in to the emergency room with symptoms that could be mild or a little severe, but what we are finding is that they can get sick very, very quickly," Bime said.

While most people with COVID-19 experience mild symptoms akin to a bad cold, or no symptoms at all, some patients experience severe symptoms that can lead to death. Older people and those with underlying health conditions are more at risk for severe complications from the disease, but young, otherwise healthy people have also fallen victim.

One reason could be an immune system overreaction in some patients that essentially causes the body to attack itself, according to Mayo Clinic immunologist Jessica Lancaster.

"There has to be a very delicate balance to it," she said. "While it's helpful to recruit all your immune cells to the site of infection, at the same time, if you go too far, then the normal function of the organ starts to suffer, and that can be very disastrous."

Virus hijacks immune system response

A body's first line of defense against an infection are white blood cells that constantly conduct surveillance to look for damaged cells. These surveillance cells look for a signal sent out by damaged cells — a protein called a cytokine.

"On their face, they're not good or bad, they're just ways for cells to communicate with each other," Lancaster said.

After getting these signals, white blood cells will engulf any bacteria or viruses. Acids and different enzymes inside the cell can break down the invading object and destroy it.

"Once they dissolve the virus into little pieces, they can start using that as an identification of what it looks like and they can inform other immune cells," Lancaster said.

In the case of the novel coronavirus, a key part that would be recognized and targeted by the immune system are the spikes that cover its outer surface. These telltale spikes allow the novel coronavirus to attach to cells and infect them.

After white blood cells join the fight, they also release cytokines to signal other immune cells to come help. These cytokines trigger inflammation and allow blood to leak out of blood vessels more easily. Typically, this is a good response, because it allows immune cells from the blood to go into an infected area.

The release of more cytokines may also raise your body's temperature in an effort to kill the virus.

Normally, this reaction is temporary because other immune cells called B cells and killer T cells respond to the call for help and start the second phase of the immune system response. They are crucial for turning the tide of a severe infection because B cells produce antibodies that block the virus from being able to infect cells, while killer T cells destroy the virus' ability to replicate.

The novel coronavirus seems to hijack a body's immune response so that the initial inflammatory phase is overstimulated. This is dangerous because it can damage critical organs, according to Lancaster.

"The lungs, the heart, those things can't withstand a severe inflammatory response for too long," she said.

For the lungs in particular, leakier blood can flood the air sacs with fluid, making it harder for a patient to breathe and get oxygen needed to keep other organs functioning.

The overproduction of these inflammatory signals, or cytokines, is sometimes referred to as a "cytokine storm." In patients with severe cases of COVID-19, these cytokine storms cause havoc and somehow block T and B cells from helping effectively.

"Think of it as like if you have like all these fire trucks that all came to the site of infection, but they keep coming, like if you can think of it in a cartoonish aspect where there's just tons and tons of these responding cells all flooding your lung," Lancaster said. "They're all trying to help ... But for whatever reason, you can't bring in the final immune cells that are needed to really put down the virus."

Risk factors

It's unclear exactly why these cytokine storms happen in some patients and not others, according to Lancaster.

"You can't look at a patient and say 'OK, this patient will get a cytokine storm and this one won't,'" she said.

The initial point of infection isn't thought to play a role in the severity of the infection, but the amount of exposure does matter. If a person gets exposed to and infected with a higher amount of virus initially, there tends to be a worse outcome.

"If there's more seeds, then it can exponentially grow a lot faster," Lancaster said.

However, she believes lifestyle, age, and genetic factors could also play an important role. One reason that older people could be particularly vulnerable to the virus is changes in the immune system as people age.

Older people produce fewer new T and B cells, according to Lancaster, which means they have less of these cells available to fight new, unfamiliar viruses that they haven't encountered before.

"It seems the immune system has evolved ... to just build up memory to things that you've already seen, like it's kind of hedging its bets that you're not going to move too much," Lancaster said. "It doesn't account for the fact that we're so mobile now and that we can be encountering random new pathogens, especially as we get older."

Another vulnerability in the immune system of older people is that with age, immune cells seem to have a delay in their ability to communicate with one another. It's unclear why this occurs, but Lancaster said that a 72-hour delay in T cell response can be fatal in fighting something like the novel coronavirus, which seems to replicate quickly inside the body.

Older people also tend to have a higher base level of cytokines in their bodies, according to Lancaster, which rapidly increases as they continue to age. Certain preexisting conditions such as diabetes or heart disease can also cause a higher baseline of cytokines in a person's body, she said.

"It doesn't take much for it to be pushed over the edge," she said. "It's easy for it to be too sensitive because you have a chronic level of inflammation."

More men seem to die

Another active area of investigation is why men seem to be dying of the virus more often than women. New York City's Health Department is reporting that about 60% of its COVID-19 fatalities are men, the World Health Organization recently reported that 68% of deaths in Western Europe were men, and a study of more than 44,000 patients in China found that 2.8% of Chinese men diagnosed with the virus died, whereas only 1.7% of Chinese women diagnosed died.

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This could be because of other factors — men could be seeking help later than women, or may be engaging in riskier activities. But it could also be because, as men age, a gland called the thymus responsible for making more T and B cells deteriorates faster in men than women.

Prospect of long term immunity is unclear

The lack of new T and B cells in older people also means that they may not become immune to the virus as easily as young people do, according to Lancaster. This is because T and B cells can turn into special memory cells that learn how to fight certain viruses. Memory T and B cells are created specifically for each infection and can wipe out any reinfection of that particular virus or bacteria before it creates a problem in the body.

"Vaccines are definitely more effective when you're younger," Lancaster said. "That's why there's different vaccine schedules for the elderly ... it just seems like the ability to generate memory as you get older goes down."

It's unclear whether someone has who has recovered from COVID-19 develops any sort of long-lasting immunity to the virus, according to Lancaster.

Strange phenomena: Lymph nodes, spleens

While it's unclear why young people are also falling victim to cytokine storms, Lancaster said there are a few other strange phenomena being observed in the immune system response to the novel coronavirus.

In autopsies of patients who have died from COVID-19, Lancaster said lymph nodes and spleens, which are important for the immune system response, are being destroyed.

"That's something that's very unusual for them," she said. "To fight a cytokine storm, you wouldn't see direct damage to those organs ... It's unclear if this is due to the virus's direct actions."

Another effect the virus has on the body's immune system is that patients with COVID-19 start to lose white blood cells, especiallyT cells.

"They're finding that for some of these cases, there's no T-cells to actually come to the rescue and finish and resolve the virus," Lancaster said.

Signs of a cytokine storm in COVID-19 patients are inflammation, fever, acute respiratory distress syndrome, and an elevated levels of cytokines in the body. However, it's pretty tough to stop or reverse a cytokine storm once it's happening, according to Lancaster.

One possible treatment is to use anti-inflammatory drugs or drugs that suppress the immune system response.

"The tricky part is when you time it," Lancaster said. "You do it too quickly, then you might turn off your ability to fight the virus and that will make it so that you won't get better. If you do it too late and you have this uncontrolled storm, then you might be too late to actually stop it."

Amanda Morris covers all things bioscience, which includes health care, technology, new research and the environment. Send her tips, story ideas, or dog memes at amorris@gannett.com and follow her on Twitter @amandamomorris for the latest bioscience updates.

Independent coverage of bioscience in Arizona is supported by a grant from the Flinn Foundation.

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