Many social scientists have termed the age we live in as the age of “misinformation,” given the unbridled reign of free-for-all social media apps and whole groups formed under the banner of false/falsified information. During the COVID-19 pandemic, even though the science was clear about how the virus was transmitted, this did not prevent individuals from wearing cards that supposedly had the power to shield its wearer from the virus, something that even high-ranking officials in positions of power took part in.
The absurd notion that vaccines cause autism has stubbornly persisted in modern society, despite many an attempt to debunk these claims, and it seems that misinformation surrounding vaccines and infections have returned to public discourse once again. This is particularly disheartening — despite the much we still do not know about the COVID-19 virus, we are nevertheless in possession of facts that are beyond reproach; to throw everything into the mix as one big conspiracy by some individuals was deeply unhelpful.
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The quest for “truth” and the fear that institutions are shielding it from the public domain due to shadowy vested interest are, some would argue, part and parcel of the paradox that makes us human. We are afraid of what we do not understand or have no control over; the aching need to feel some semblance of control is perhaps the key force driving many of the anti-information campaigns that have mushroomed over the last few years.
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The infectious, transforming, anti-apoptotic and immune-evasion properties of EBV makes it a highly likely candidate for an etiologic agent in multiple sclerosis.
In this article, we will take a look at the fascinating relationship between viral infections and the pathogenesis of multiple sclerosis. While there is universal agreement that the etiology of multiple sclerosis remains unclear, scientists have been hard at work trying to unravel some of the risk factors attached to this disease. The identification of risk factors is always a good place to start in understanding where a disease might come from — if the correlation is found to be strong enough, clinicians may choose to make the leap to say it is causative, warranting further research.
“The role of infectious and viral agents is still controversial in multiple sclerosis, but there is increasing evidence that some viruses play a role in disease development,” Sedighi and colleagues wrote in Current Microbiology.
Scientists have observed that viral infections can influence a patient with multiple sclerosis in various ways. For example, viruses have been known to engage in direct toxicity, causing direct damage to a cell without the intermediary pathway of inflammation or autoimmunity. Furthermore, viruses can hide themselves in molecular mimicry due to the similarity of some viral structures to myelin.
More seriously, viruses can lead to brain damage following the infection of the central nervous system (CNS). Scientists have discovered that a large repertoire of viruses can enter the CNS, Including human herpes virus 6, SARS-Cov-2, and varicella zoster virus. In the CNS, these viruses can cause cellular damage and dysfunction, producing proinflammatory cytokines that destroy neurons and disrupt cellular activity.
Sedighi and colleagues discussed the role of various viruses in the context of multiple sclerosis. Let’s focus on SARS-CoV-2, given that it has received widespread interest.
“[Multiple sclerosis] is an interesting disease for several reasons,” they wrote. “First, the disease itself has an immunological nature. And then, disease-modifying therapy (DMT) clinical management may alter immune function and increase susceptibility to COVID-19.”
This means that patients with multiple sclerosis who are receiving active treatment (such as immunosuppressive/immunomodulatory therapies) may be at a higher risk of infection compared to the general public, a very serious issue during the height of the COVID-19 pandemic.
Some scientists have proposed that the overlapping immunological response generated the SARS-CoV-2 virus and the immune condition of the patient is partially explanatory of the levels of morbidity and mortality seen in patients with both COVID-19 and multiple sclerosis. Because this pandemic was so recent, much more research needs to be carried out to uncover further links between these 2 conditions. At present, scientists are confident that there is an association between viral infections and inflammation in the brain of a patient with multiple sclerosis, but more studies need to be conducted to assess if it has a role in neurodegeneration.
One of the more talked-about viruses with links to multiple sclerosis is the Epstein-Barr virus (EBV). It is among the most studied viruses with regards to multiple sclerosis, and evidence suggests it plays a role in driving the pathophysiological processes in multiple sclerosis.
Studies indicate that EBV-infected B cells enter the central nervous system, carrying with them antibodies from the serum to the cerebrospinal fluid. Scientists have observed a significant correlation between antibodies in the serum and the cerebrospinal fluid. Patients with multiple sclerosis infected with EBV have been found to have an increased amount and frequency of EBV antibodies.
“The infectious, transforming, anti-apoptotic and immune-evasion properties of EBV makes it a highly likely candidate for an etiologic agent in multiple sclerosis,” Houen and colleagues wrote in Frontiers in Immunology. “However, much remains to be investigated in future studies.”
Returning to our earlier point about the importance of accurate information regarding the pathophysiology of multiple sclerosis, it is absolutely right that the public is informed that there is indeed a link between viral infections and multiple sclerosis. However, while evidence surrounding this issue is still weak, we also want to prevent certain groups from claiming that multiple sclerosis is caused exclusively by infections, which is not at all evidence-based.
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Medicine is hardly cut and dried; our understanding of aspects of any given disease evolves according to the best and latest evidence. It is up to clinicians and healthcare officials to convey indisputable facts with authority and empathy, and to debunk wild speculations that do more harm than good.
This article originally appeared on Rare Disease Advisor
