It can be a gastrointestinal disease causing only diarrhea and abdominal pain. It can cause symptoms that may be confused with a cold or the flu. It can cause pinkeye, a runny nose, loss of taste and smell, muscle aches, fatigue, diarrhea, loss of appetite, nausea and vomiting, whole-body rashes, and areas of swelling and redness in just a few spots.
In a more severe disease, doctors have also reported people having heart rhythm problems, heart failure, kidney damage, confusion, headaches, seizures, brain inflammation, Guillain-Barre syndrome, and fainting spells, along with new sugar control problems, blood clots throughout the body, and severe immune system responses.
It’s not just a fever and coughing, leading to shortness of breath, like everyone thought at first.
Some people may have lingering effects for months afterward.
Some people can have no symptoms at all.
This makes it incredibly difficult to diagnose and even harder to treat.
“This is a disease progression we have never seen for any infection that I can think of, and I’ve been doing this for a couple of decades,” says Joseph Vinetz, MD, an infectious disease specialist at Yale School of Medicine.
How It Invades
When viral particles land in our eyes, nose, or mouth, “spike proteins” on the virus connect with a specific receptor, known as ACE2, on the surface of our cells, allowing entry. ACE2 receptors make a great target because they are found in organs throughout our bodies. Once the virus enters, it turns the cell into a factory, making millions and millions of copies of itself -- which can then be breathed or coughed out to infect others.
A lot of what we know about the infectious capability of SARS-CoV-2, the virus that causes COVID-19, closely parallels what we learned about the coronavirus that caused SARS. What makes COVID-19 uniquely dangerous is that unlike SARS, this virus is much more effective at binding to ACE2 receptors, both in the upper respiratory tract and lower down, in the lungs --- making it as easy to transmit as a cold and as damaging to the lungs as SARS.
We have also learned from SARS that iIn order to evade early detection, the coronavirus uses multiple tools to prevent the infected cells from calling out for help. The virus snips off distress signal proteins that cells make when they are under attack. It also destroys antiviral commands inside the infected cell. This gives the virus much more time to make copies of itself and infect surrounding areas before it is identified as an invader. This is part of the reason why the virus spreads before immune responses, like fever, begin.
Direct Attack
Many with mild or no symptoms are able to fend off the virus before it gets worse. These people may have symptoms only in the upper airway, at the site where they were first infected. But when someone’s body can’t destroy the virus at its entry point, viral particles march deeper into the body. The virus seems to take a few paths from there, either setting up camp in the lungs, fighting its way into the digestive tract, or doing some combination of both.
“There’s clearly a respiratory syndrome, and that’s why people end up in the hospital. Some people get a gastrointestinal illness with diarrhea, maybe some abdominal pain, which may or may not be associated with a respiratory illness,” says Vinetz.
Double-Edged Sword
Even though researchers are learning more each day about the virus and how and where it attacks the body, treatment geared toward these targets also pose significant problems. Many drugscome with a risk of destroying the delicate balance that allows the body to help fight the disease or to manage inflammation.
The ACE2 receptor that the virus uses to enter cells is a key player in lowering inflammation and reducing blood pressure. Targeting or blocking this receptor as a treatment strategy to prevent viral entry into cells may actually worsen blood pressure, increase the risk of heart failure and kidney injury, and increase inflammation that may worsen lung injury.
Drugs that target the immune response to lower the risk of a cytokine storm may also tamp down the immune response, making it hard to kill off the virus over the long run.
Using medicines to prevent clotting may end up causing severe bleeding. Cuker points out that “we don’t have a good read on bleeding … we have limited evidence about the clotting risk … we have zero evidence on bleeding risk in these patients, and it’s a real priority to understand this risk, especially because one of our strategies to treat the clotting is stepping up intensity the of anti-coagulation.”
Timing is likely to be key in treatment strategies. For example, patients may need a drug to boost the immune system early on in the disease, and then one to tamp it down if the disease progresses and cytokine markers begin to rise. In order to prepare for other potential long-term effects, scientists are looking at patients that recovered from SARS. Mental health concerns like depression, anxiety, and post-traumatic stress disorder (PTSD) are among the persistent conditions that people have experienced after recovery. These have been identified in many after COVID-19 as well.
It will take time to tease apart what long-term effects are due to organ damage from direct attack by the virus, the overactive immune response and widespread blood clotting, or side effects from treatment and prolonged hospitalization. Recently, long-term nerve damage has been identified as a possibly permanent side-effect, likely from treatment with prone positioning while on a ventilator.
One concerning finding is that while many of those who die from COVID-19 are older with other medical conditions, one survey of long-haulers in New York City found that the most were women, with an average age of 44 who were generally healthy before their bout with COVID-19. How long various effects will last, who is most at risk and whether or not full recovery is possible remains to be seen.
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