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Editor’s Note: Find the latest news and guidance from COVID-19 at Medscape’s Coronavirus Resource Center.
We have underestimated and misunderstood COVID-19 since it first appeared.
And as we learn more, it is clear that COVID-19 can be more than a respiratory illness. He has joined the ranks of other “great imitators,” diseases that can resemble almost any condition.
It can be a gastrointestinal illness that only causes diarrhea and abdominal pain. It can cause symptoms that can be mistaken for a cold or flu. It can cause pinkeye, runny nose, loss of taste and smell, muscle aches, fatigue, diarrhea, loss of appetite, nausea and vomiting, rashes all over the body, and areas of swelling and redness in just a few spots.
In a more serious illness, doctors also reported that people have heart rhythm problems, heart failure, kidney damage, confusion, headaches, seizures, Guillain-Barré syndrome, and fainting, along with new sugar control problems.
It is not just fever and cough, which leads to shortness of breath, as everyone thought at first.
This makes it incredibly difficult to diagnose and even more difficult to treat.
“This is a disease progression that we’ve never seen for any infection you can think of, and I’ve been doing this for a couple of decades,” says Joseph Vinetz, MD, an infectious disease specialist at Yale Medical School. .
How it invades
When viral particles land in our eyes, nose, or mouth, the “spike proteins” in the virus connect to a specific receptor, known as ACE2, on the surface of our cells, allowing entry. ACE2 receptors are 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 upon millions of copies of itself, which can then be breathed or coughed up to infect others.
To evade early detection, the coronavirus uses multiple tools to prevent infected cells from asking for help. The virus cuts out the distress signal proteins that cells produce when under attack. It also destroys antiviral commands within the infected cell. This gives the virus much more time to make copies of itself and infect surrounding areas before being identified as an invader. This is part of the reason why the virus spreads before immune responses, such as fever, begin.
Direct attack
Many with mild or symptom-free symptoms can 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 point of entry, the viral particles go deeper into the body. The virus seems to take a few paths from there, whether it’s setting up a camp in the lungs, making its way to the digestive tract, or making a combination of both.
“Clearly there is a respiratory syndrome, and that is why people end up in the hospital. Some people get a gastrointestinal illness with diarrhea, perhaps some abdominal pain, which may or may not be associated with a respiratory illness,” Vinetz says.
Once the virus is deeply embedded in the body, it begins to cause more serious illness. This is where a direct attack can occur on other organs that have ACE2 receptors, including the heart muscle, kidneys, blood vessels, liver, and potentially the central nervous system. This may be one of the reasons for the wide variety of symptoms that COVID-19 can cause.
“It is highly unlikely that any other organ could be affected by a direct invasion without serious disease,” Vinetz adds.
The brain and nerves can also be victims of direct attacks. Kenneth Tyler, MD, chair of the Department of Neurology at the University of Colorado School of Medicine, cautions that direct attack on the central nervous system (CNS) is still being resolved at this time. There are many routes that a virus could take to invade the CNS.
A somewhat contested view is that loss of smell could indicate that the nerve responsible for smell is infected and can carry the virus to the CNS, including the brain. “This can be shown to occur in experimental models with non-human coronaviruses and is a potential route of invasion for some other viruses. However, to date there is no evidence to establish that this actually occurs with SARS-CoV-2,” said the official. name of the virus that causes COVID-19.
Early findings, including those from autopsy and biopsy reports, show that viral particles can be found not only in the nostrils and throat, but also in tears, feces, kidneys, liver, pancreas, and heart. A case report found evidence of viral particles in the fluid around the brain in a patient with meningitis.
Collateral damage that kills
Severe damage to the lungs can be a triggering factor that activates and overstimulates the immune system through a barrage of signaling chemicals, known as cytokines.
The flooding of these chemicals can trigger what is known as a “cytokine storm”. This is a complex interaction of chemicals that can lower blood pressure, attract more killer immune and inflammatory cells, and further injure the lungs, heart, kidneys, and brain. Some researchers say cytokine storms may be the cause of sudden decompensation, leading to critical illness in patients with COVID-19.
A new finding suggests that there may be another deadly culprit. Many doctors are discovering that abnormal coagulation, known as thrombosis, can also play a role in fatal COVID-19. Doctors are seeing clots everywhere: large vessel clots, including deep vein thrombosis (DVT) in the legs and pulmonary embolism (PE) in the lungs; clots in the arteries, which cause strokes; and small clots in small blood vessels in organs throughout the body. Early autopsy results also show widely dispersed clots in multiple organs.
Adam Cuker, MD, a hematologist at the University of Pennsylvania Hospital who specializes in bleeding disorders, says these clots are occurring at high rates even when patients are taking blood thinners for clot prevention. In a study from the Netherlands, 31% of patients hospitalized with COVID-19 had clots while taking anticoagulants.
Cuker says that “new studies validate what we’ve all been seeing with our eyes, which is that ‘boy, it seems these patients are clotting a lot’. … And it could be that the rate of thrombotic events is even higher than what we really recognize. ” Although the reason for clotting is still unclear, it appears to be playing a much more important role in death than previously understood.
Beyond the collateral damage from cytokine storms and clotting, other things like low blood pressure from serious illness, low oxygen levels, use of respirators, and drug treatments themselves can damage organs throughout the world. body, including the heart, kidneys, liver, brain, and other organs.
Double-edged sword
Although researchers learn more and more about the virus and how and where it attacks the body, treatment aimed at these targets also poses significant problems. Many drugs carry the risk of destroying the delicate balance that allows the body to help fight disease or control inflammation.
The ACE2 receptor that the virus uses to enter cells is a key player in reducing inflammation and reducing blood pressure. Targeting or blocking this receptor as a treatment strategy to prevent viral entry into cells can worsen blood pressure, increase the risk of heart failure and kidney injury, and increase inflammation that can worsen lung injury.
Medications that target the immune response to reduce the risk of a cytokine storm can also lower the immune response, making it difficult to eliminate the virus in the long term.
Using medications to prevent clotting can end up causing severe bleeding. Cuker notes that “we don’t have a good read on bleeding … we have limited evidence on the risk of clotting … we don’t have evidence on the risk of bleeding in these patients, and it’s a real priority to understand this risk, especially since of our coagulation management strategies are intensifying anticoagulation intensity. “
Timing is likely to be key in treatment strategies. For example, patients may need a drug to boost the immune system early in the disease, and then one to lower it if the disease progresses and cytokine markers start to rise.
It’s just the tip of the iceberg
Cuker says that what we know about coagulation and almost everything else when it comes to COVID-19 “is just the tip of the iceberg.”
Sanober Amin, MD, PhD, a dermatologist in Texas, agrees. She has been tracking the wide variety of skin findings that dermatologists around the world have noticed on social media.
He recently posted images on social media that show the wide variety of skin findings he’s been seeing and hearing. His post received a massive response. Amin says that “dermatologists around the world, from Turkey to France, from Canada to the United States, are sharing information about rashes they have seen in people with COVID-19.”
Some rashes appear to be consistent with what is called a viral rash, which is a term for a general rash that can occur with almost any virus. But, says Amin, “some skin findings are more consistent with superficial clotting in the blood vessels near the skin.”
This is what some have begun to call “COVID toes”, also called hinge. Dermatologists are seeing more cases of these small clots in the fingers and toes, especially in children.
It is difficult to know which skin conditions are related to COVID-19 because many people without “typical” symptoms are not being evaluated, says Amin. Researchers will still need to determine what symptoms may be caused by the virus and what may be only unrelated early findings.
Questions without answer
For now, much of the information we have on the symptoms of COVID-19 comes from hospitalized patients who are very ill at the time they are seeking care and may not be able to share information on the first signs and symptoms they may have had. .
Due to delayed testing in the US. In the US, we don’t yet know the full scope of mild and moderate versions of the disease, or what effects the disease has on people who have many symptoms but are not sick enough. to be hospitalized
An open-ended question is what the long-term effects may be for survivors. What is life like after being on a ventilator or suddenly needing dialysis? Will we see lasting and permanent declines in heart, lung, and kidney function, or will patients eventually recover?
We also don’t know how people will get rid of infections. If the new coronavirus ends up being an acute infection, like other coronaviruses, most recovered people should develop at least short-term immunity. It is also possible that the virus persists as a latent infection, such as chickenpox, which remains dormant in the body, only to reappear periodically as shingles, or become a chronic infection, such as hepatitis B, that lives inside the body during a prolonged period of time, causing long-term damage.
“It’s definitely going to be an acute infection … there’s no way it’s latent or chronic, by no means … I think so … we’ll see,” Vinetz says.
Sources:
medRxiv: “COVID-19 Seroprevalence Antibody in Santa Clara County, California”.
Joseph Vinetz, MD, professor, Infectious Diseases Section, Yale School of Medicine, New Haven, CT.
Science: How does the coronavirus kill? Doctors trace the ferocious rampage through the body from head to toe. “
Brain, behavior and immunity: “Nervous system involvement after infection with COVID-19 and other coronaviruses”
The lancet: “Guillain-Barré syndrome associated with SARS-CoV-2 infection: causality or coincidence?”
medRxiv: “Covid-19 Pulmonary and Cardiac Pathology: The First Series of Autopsies from New Orleans.”
Kenneth Tyler, MD, chair, Department of Neurology, University of Colorado School of Medicine; Faculty, American Academy of Neurology, Boulder, CO.
International Journal of Infectious Diseases: “A first case of meningitis / encephalitis associated with Sars-Cornoavirus-2”.
Adam Cuker, MD, associate professor of medicine, University of Pennsylvania Hospital.
bioRxiv: “SARS-CoV-2 invades host cells through a new route: the CD147 tip protein.”
Sanober Amin, MD, PhD, dermatologist, Grapevine, TX.
Gastroenterology: “COVID-19: Gastrointestinal manifestations and possible fecal-oral transmission”.
The New England Journal of Medicine: “Viral load of SARS-CoV-2 in upper respiratory samples from infected patients”.
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