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A large epidemiological study in the UK today finds no association between COVID-19 and Guillain-Barré syndrome (GBS), an autoimmune condition linked to other bacterial and viral infections.
GBS is a rare neurological disease that attacks the peripheral nervous system, usually the feet, hands, and extremities, causing numbness, weakness, pain, and sometimes fatal paralysis or permanent neurological effects. The most common trigger for GBS is infection with Campylobacter jejuni, a bacterial strain that causes gastroenteritis or digestive tract infection.
Many other infections can also trigger GBS, raising concerns about a possible increase in GBS during the COVID-19 pandemic. Epidemiological studies have confirmed a causal relationship between the recent Zika virus epidemics and the corresponding surge in GBS cases. Small international studies have suggested an association between infection with SARS-CoV-2, the virus that causes COVID-19, and an increased risk of GBS.
No increase in GBS during the pandemic
Researchers from University College London (UCL) assessed the incidence of GBS in the UK National Immunoglobulin Database from January 1 to May 31 of each year from 2016 to 2019 and compared the case rates with those reported during the same period in 2020.
The annual incidence of GBS in UK hospitals ranged from 1.66 to 1.88 per 100,000 people during the years 2016 to 2019. In contrast, the incidence of GBS fell from 40% to 50% between March and May 2020, compared to the same period in previous years. Significantly fewer GBS cases were reported in March, April, and May 2020 (93, 70, and 56, respectively) compared to the mean number of cases in 2016-19 for the same months (132, 116, and 113, respectively).
The researchers suggest that the blocking measures may have reduced the transmission of other GBS triggering pathogens and could explain the decline in cases seen in 2020.
“Our epidemiological study shows that there was no increase in GBS incidence during the first wave of COVID-19,” lead author Stephen Keddie said in a UCL news release yesterday. “Rather, there was a decline and therefore a causal link between COVID-19 and GBS cannot be established.”
SARS-CoV-2 lacks GBS-bound proteins
The scientists also studied the structure of the SARS-CoV-2 protein to determine whether, as Campylobacter—It has human-like antigens that could cause an autoimmune response leading to GBS.
“Our analysis shows that SARS-CoV-2 does not contain any additional known or proven immunogenic material that drives GBS,” Keddie said in the statement. “Therefore, concerns that the COVID vaccine could cause GBS in significant quantities are almost certainly unfounded.”
1976 Swine Flu Vaccine Spector
Public perception and fears about GBS are influenced by a small historical increase in the risk of GBS associated with the swine flu vaccine in the US from 1976, which was later found to be lower than previously known. I thought initially. Concerns about vaccine-related GBS risk persist despite comprehensive surveillance for influenza vaccine-related increases showing only one additional GBS case per million influenza vaccines. In contrast, the risk of flu-related complications is 17 per million cases.
Post-vaccine illnesses may be due to chance
The researchers highlight the risk that mass vaccination programs can be blamed for the incidence of GBS and other diseases that occur, by chance, in the weeks after immunization, raising unfounded fears about the risks of the vaccine.
“These cases may cause concern in patients, politicians and regulators and fuel concerns against vaccination, although it is likely that most, if not all, of the cases are related to vaccination by chance,” said Michael Lunn, PhD, from UCL’s Queen Square Neurology Institute, author of a linked comment, said in the press release.
“Such a serious illness can result in suspension or withdrawal of the vaccine as a ‘knee-jerk’ safety reaction, but this should not happen unless there is a statistically demonstrated link through careful and proven monitoring,” added Lunn . “We must accept small risks with any vaccination program of this scale, and these are much lower than the risk of COVID infection.”
In the commentary, Lunn and his co-authors emphasize that “The temporal association between vaccination and the onset of GBS even in large numbers of individuals within a huge population of billions is not adequate evidence of causality. Under conditions such as In GBS, where minds are pre-programmed to jump to the cause of assumptions through cognitive biases, this is a particularly vital message to convey. “
