London, Feb 17 (IANS): Headaches, memory problems, and fatigue -- commonly known to continue post a Covid-19 infection -- may be a result of inflammation in the rest of the body and not because SARS-CoV-2 infects the brain, claims a new research.

Early on in the pandemic, researchers surmised that direct infection of the brain could be the cause behind these neurological symptoms. Many studies have also proposed the effect of Covid virus on the brain symptoms. But a study by researchers at the Charite- Universitatsmedizin Berlin in Germany has now produced evidence to support the new theory.

“We took that as our hypothesis at the start, too. But so far, there has been no clear evidence that the coronavirus can persist in the brain, let alone proliferate,” said Dr Helena Radbruch, head of the Chronic Neuroinflammation working group at the Department of Neuropathology at Charite.

“For that, we would have needed to find evidence of intact virus particles in the brain, for example. Instead, the indications that the coronavirus could infect the brain come from indirect testing methods, so they aren’t entirely conclusive,” Radbruch added.

According to a second hypothesis, the neurological symptoms would instead be a kind of side effect of the strong immune response the body deploys to defend against the virus.

For the study, the team of researchers analysed various areas of the brain in 21 people who died in hospital settings, typically in an ICU, due to severe coronavirus infection. For comparison, the researchers studied nine patients who died of other causes after treatment in intensive care.

First, they looked to see whether the tissue showed any visible changes and hunted for any indication of coronavirus. Then they conducted a detailed analysis of genes and proteins to identify the specific processes that had taken place inside individual cells.

Like other teams of researchers before them, the Charite scientists found coronavirus genetic material in the brain in some cases.

“But we didn’t find neurons infected with SARS-CoV-2,” Radbruch noted. “We assume that immune cells absorbed the virus in the body and then travelled to the brain. They’re still carrying the virus, but it doesn’t infect cells of the brain. So coronavirus has invaded other cells in the body, but not the brain itself.”

Still, the researchers did note striking changes in molecular processes in some cells of the brain in those infected with Covid-19: For example, the cells ramped up the interferon signalling pathway, which is typically activated in the course of a viral infection.

“Some neurons evidently react to the inflammation in the rest of the body,” said Prof. Christian Conrad, head of the Intelligent Imaging working group at the Berlin Institute of Health at Charite (BIH) and one of the principal investigators in the study.

“This molecular reaction could be a good explanation for the neurological symptoms we see in Covid-19 patients. For example, neurotransmitters emitted by these cells in the brainstem could cause fatigue. That’s because the brainstem is home to groups of cells that control drive, motivation, and mood.”

Further, the team found that the neurons’ reaction to the inflammation is temporary, as shown by a comparison of people who died during an acute coronavirus infection with those who died at least two weeks afterward. The molecular changes are most evident during the acute infection phase, but they do normalise again afterward -- at least in the vast majority of cases.