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Do parasites protect against SARS-CoV-2?

Do parasites protect against SARS-CoV-2?

By Dr. Liji Thomas, MDMay 19 2020

The world has rarely seen such a readily transmissible infection as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) over the last century. Within five months, the virus has created a Tsunami of COVID-19 positive cases, comprising almost 4.88 million people and causing 322,000 deaths.

However, the spread of the virus is slower than expected in Africa. A new study by researchers at Makerere University and the London School of Hygiene & Tropical Medicine and published on the preprint server medRxiv* in May 2020 is focused on finding any possible link between the low risk of infection and parasitic infections.

The Role of Inflammation in Severe COVID-19

The disease manifestations in COVID-19 range from asymptomatic to critically ill requiring mechanical ventilatory support. Severe COVID-19 manifests with a hyperimmune response that is marked by high levels of pro-inflammatory cytokines like IL-6, IL-2, and TNF-α often termed the cytokine storm or cytokine release syndrome. High levels of IL-6 are associated with increased severity of disease in COVID-19. Some studies show that when patients with severe disease are treated with monoclonal antibodies that block the IL-6 signaling pathway, the duration of stay in the intensive care unit (ICU) is shortened, and there is an earlier resolution of disease.

Immunomodulators in Parasitic Infestation

Parasitic infestations are widespread in Africa. Many parasites live for years in their hosts, without producing significant symptoms. This is due to the interplay of immunity vs. tolerance. In other words, sterilizing immunity, or the development of an immune response strong enough to eliminate the pathogen, is rarely achieved. Still, the parasite count and distribution are kept in check, allowing the host to live a mostly healthy life.

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Not all multiple sclerosis-like diseases are alike

An antibody appears to make a big difference between Multiple Sclerosis and other disorders affecting the protective myelin sheath around nerve fibres, report Tohoku University scientists and colleagues in the journal Brain. The finding suggests that some of these 'inflammatory demyelinating diseases' belong to a different category than Multiple Sclerosis, and should be treated according to their disease mechanism.

Multiple Sclerosis is a well-known demyelinating disease of the central nervous system, but is not the only one by far. In inflammatory demyelinating diseases,?targeted myelin sheaths -- the protective layers surrounding nerve fibres in the central nervous system -- becoming damaged, slowing or even stopping the transmission of nerve impulses. This leads to various neurological problems.

Scientists have found that some, but not all, patients with inflammatory demyelinating diseases have auto-immune antibodies against myelin oligodendrocyte glycoprotein (MOG), which is thought to be important in maintaining the myelin sheath's structural integrity. This antibody is rarely detected in patients with typical Multiple Sclerosis, but is found in patients diagnosed with optic neuritis, myelitis, and acute disseminated encephalomyelitis (ADEM), for example. Scientists had not yet been able to show that high levels of this antibody mean it is specifically targeting and damaging MOG.

Tohoku University neurologist Tatsuro Misu and colleagues in Japan analysed the brain lesions of inflammatory demyelinating disease patients with and without detectable MOG antibodies, and found the two groups were quite different.

Autopsies were taken from brain lesions of people diagnosed with Multiple Sclerosis and neuromyelitis optica spectrum disorder (NMOSD), which predominantly targets the optic nerve and spinal cord. These patients did not have detectable MOG antibodies. Typical Multiple Sclerosis lesions showed solitary, slowly expanding demyelination with a profound loss of myelin sheath proteins, and the presence of activated debris-clearing macrophages at their periphery. NMOSD lesions showed reductions in nerve cells called astrocytes and in myelin-producing cells called oligodendrocytes, and loss in the innermost layers of myelin sheath proteins.

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Study: Certain inflammatory demyelinating diseases belong to different category than multiple sclerosis

Study: Certain inflammatory demyelinating diseases belong to different category than multiple sclerosis

Reviewed by James Ives, M.Psych. (Editor)May 19 2020

An antibody appears to make a big difference between Multiple Sclerosis and other disorders affecting the protective myelin sheath around nerve fibers, report Tohoku University scientists and colleagues in the journal Brain.

The finding suggests that some of these 'inflammatory demyelinating diseases' belong to a different category than Multiple Sclerosis, and should be treated according to their disease mechanism.

Multiple Sclerosis is a well-known demyelinating disease of the central nervous system, but is not the only one by far. In inflammatory demyelinating diseases, targeted myelin sheaths - the protective layers surrounding nerve fibres in the central nervous system - become damaged, slowing or even stopping the transmission of nerve impulses. This leads to various neurological problems.

Scientists have found that some, but not all, patients with inflammatory demyelinating diseases have auto-immune antibodies against myelin oligodendrocyte glycoprotein (MOG), which is thought to be important in maintaining the myelin sheath's structural integrity.

Continue reading
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