Remains of SARS-CoV-2 and other related remains have been observed in the olfactory nerve formula of patients with severe COVID-19, according to a report from Italy.
A minimally invasive autopsy with endoscopic nasal dissection showed viral remains and CD163 microglia cells in the olfactory complex of two COVID patients, Patrizia Morbini, MD, PhD, University of Pavia and CO-authors of JAMA Otolaryngology reported.
“Our discovery is because it is the first evidence of a direct SARS-CoV-2 infection in the cells of the sniffing bulb in the central nervous system,” Morbini said.
“Recent imaging studies have shown that this nerve formula mastery is altered in a subset of COVID patients, while we have directly documented the presence of viral debris and related severe inflammation,” he told MedPage Today. “So far, another case report has shown viral remains in the formula vessel cells of the central nervous system, but not particularly in the olfactory bulb.”
The discovery suggests that SARS-CoV-2 “may have the ability to infect nerve formula cells, as has been shown for other coronaviruses in experimental contexts, and may enter the central nerve formula through nerve fibers from the nerve receptors of the olfactory mucosa, which is especially attractive given the nons unusual olfactory symptoms of COVID patients” Added.
In the scent bulb of the first patient, who died of COVID-19 pneumonia in the ICU, Morbini and his co-authors bodies of intracytoplasmic viral inclusion, interstitial viral detriites and marked infiltration of positive CD163 positive/ CD68 negative microglia cells.
At the time the patient COVID-19, who died of cardiopulmonary amylosis from transtiretine, discovered viral remains in the mobile membrane of hairy respiratory mobiles in the olfactory mucosa. Researchers also saw mobile CD163 microglials and CD3/CD8 perivascular lymphocytes in the olfactory bulb, but without ultrastructural evidence of viral remains.
CD163 is a prospective biomarker of inflammation. It is induced through pro-inflammatory cytokine storms in systemic inflammatory disorders such as Ebola virus infection, Morbini and his colleagues noted. “An imaginable role of CD163-positive microglia in virus-mediated inflammation and neuropathogenia has already been proposed in patients with HIV and HIV-related encephalitis and in varying degrees of neurocognitive impairment and may also be the result of sRAS-CoV-2 induced hyperinflation,” they wrote.
“Our effects recommend that passive diffusion and axonal shipping through the olfactory complex may be a major route for SARS-CoV-2 access to the central nervous system, as has been shown in the past in animal studies with a strain of humans. coronavirus, human coronavirus OC43, ” they added.
The report presents “only one observation, which is a wonderful limitation in clinical wording, but we believe it adds data to the confusing symbol of COVID protests,” Morbini said.
A mechanism for how the virus is causing smell loss in such a high number of COVID-19 patients can’t be made based on this finding, said Eric Holbrook, MD, director of the rhinology division of Massachusetts Eye and Ear in Boston. “This paper alone does not alter clinical care or our understanding of COVID-19 and its role in causing smell loss,” he told MedPage Today.
“There are already many clinical studies demonstrating the highest percentage of patients positive for COVID-19 that expand loss of smell. This is now well known, and for this reason, the symptom of a sudden loss of smell and/or taste deserves to be an early warning for an infection imaginable with COVID-19,” Holbrook added. “Recognizing this arrangement between the public and fitness service providers can help restrict the spread of the virus through the onset of isolation and early testing.”
More studies are needed on other people to perceive how the virus damages the olfactory system, he said.
“In most patients, loss of smell is transient and returns after 10 to 14 days, but there is a significant proportion of patients who have long-term loss of smell for several months,” he said.
“This difference is obviously not similar to the severity of the disease in general,” Holbrook said. “We want to perceive what the differences are between those computers and how the virus interacts with the olfactory formula before we can propose solution strategies.”
Judy George covers neurology and neuroscience for MedPage Today, writing about brain aging, Alzheimer’s disease, dementia, MS, rare diseases, epilepsy, autism, headaches, strokes, Parkinson’s disease, ALS, concussions, CTE, sleep, pain, etc.
Morbini reported non-public rates for MSD and Roche outside the doors of the work presented. No additional disclosures were reported.
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