INFECTION | BRAIN
First Case of Covid-19 Encephalitis: A Possibility of Virus Latency and Reactivation
New evidence that SARS-CoV-2 infiltrates the brain (and its ramifications)
“They’re just not thinking that the brain could be the site of the problem,” says Mattew Anderson, associate professor of pathology at Beth Israel Deaconess Medical Center, Boston, regarding the potential neuroinvasion of SARS-CoV-2 that causes COVID-19.
That’s where I’ve left off previously in “4 Clues That SARS-CoV-2 Invades the Brain”[published 14/3/2020; updated 26/3/2020]. In brief, all previous coronaviruses such as SARS and MERS are known to be neuroinvasive. SARS-CoV-2, being a coronavirus itself, is likely to be no different.
And, indeed, it’s not.
A New Case
What Professor Anderson said makes sense. People characterize SARS-CoV-2 as a pneumonia disease, as the name — severe acute respiratory syndrome coronavirus 2 — implies. Not many would investigate if SARS-CoV-2 infects the nervous system or, more precisely, the brain.
But Chinese researchers at Qingdao University have detected the presence of SARS-CoV-2 genes in the cerebrospinal fluid (i.e., brain fluid) of a 56-year-old patient with Covid-19 in Beijing Ditan Hospital. “The patient was diagnosed with viral encephalitis, and the patient’s central nervous system was attacked by SARS-CoV-2,” say the neurologist professor, Jing Gao and his colleagues. Fortunately, the patient has recovered after treatment.
Encephalitis is when microbial pathogen infects the brain and cause inflammation therein, leading to neurological symptoms such as seizures, headache, fever, nausea, confusion, fatigue, loss of bodily sensations, speech and hearing impairments, etc.
“This is the first evidence that SARS-CoV-2 has directly invaded the nervous system,” they emphasized.
Nonetheless, this is the only reported case of encephalitis caused by SARS-CoV-2 to date. Considering the vast majority who only develop respiratory symptoms, SARS-CoV-2 is still more appropriately thought of as a respiratory pathogen; and Covid-19 as a respiratory disease.
Only in rare cases would SARS-CoV-2 invades and damages the brain. Several other factors must be involved such as weakened brain immunity. There’s probably a higher likelihood that encephalitis is contracted from other microbial pathogens instead, such as herpes simplex virus (HSV-1).
Virus Latency
One worrisome fact is that viruses integrate itself into the host genome permanently, as far as scientists know. This is a mechanism viruses evolved to hide from the host immune system. Whether this applies to SARS-CoV-2 has not been shown but highly probable, considering the fundamental life cycle of viruses. As Yan‐Chao Li, associate professor at Norman Bethune College of Medicine, Jilin University explains,
“Since SARS‐CoV-2 may conceal itself in the neurons from the immune recognition, complete clearance of the virus may not be guaranteed even the patients have recovered from the acute infection.”
Virus Reactivation
As follows, under conditions of a weakened immune system, the latent or sleeping virus may reactivate and become infectious again. Conditions of immunosuppression are manifold, including chronic diseases such as obesity and diabetes, chronic emotional stress, other microbial infections, medical drugs/chemotherapy, or poor lifestyle habits. As the Chinese researchers who documented the encephalitis case questioned,
“If the SARS-CoV-2 is latent in the nervous system for a long period of time, will the cured patients reappear with neurological diseases?”
There’s no definitive answer to that. Because current technology is incapable of quantifying virus reactivation in the living brain. “The frequency and effects of viral reactivation in the central nervous system are not known and is extremely difficult to investigate,” explains the Italian virologist, Robert Mancuso, who studies another “brain sleeping virus” called herpes simplex virus type 1 (HSV-1) that normally cause cold sores and genital herpes, and also encephalitis in some cases.
“As of today, it is impossible to measure HSV-1 reactivation in the brain in vivo,” Mancuso continues. In vivo is Latin for “within the living.” Unless brain autopsies are subjected to extensive laboratory testing, yet the result might not even reflect what had happened in the living brain.
Cured patients, therefore, might reappear with neurological symptoms — like how individuals re-develop cold sores periodically as a result of HSV-1 reactivation. But nobody knows when it would happen (if it does), what is the minimum virus load, to what extent the immune system would have to be suppressed, and what genetic or environmental factors have to be present to complement the virus reactivation.
Perhaps the best we can do is to maintain a vigilant immune system with healthy lifestyle habits — as to not give viruses opportunities to reactivate. If by any chance, the virus reactivates, a potent immune system is still key in clearing the threat and repairing any damage done.
