2) COVID-19 impacts cognitive functioning through several pathways. The virus may directly infect brain cells or enter the central nervous system indirectly.
A major driver of cognitive effects is the cytokine storm - when the immune system overreacts and releases ...
3) ... too many inflammatory proteins.
This neuroinflammation can disrupt brain cell communication and survival. Cytokines like IL-6 are particularly implicated.
The cytokine storm may also weaken the blood-brain barrier, allowing more viruses to enter the brain.
4) This exacerbates neuroinflammation and neuronal death. Specific brain regions like the hippocampus seem especially vulnerable.
Some patients develop conditions like NeuroCOVID and frontal syndrome during the acute phase.
5) Symptoms involve problems with short-term memory, executive function, and attention. Severity often correlates with blood marker levels of inflammation.
Long COVID can yield prolonged psychiatric effects due to chronic stress and neuroinflammation.
6) This may worsen pre-existing neurological disorders or increase risk of conditions like Alzheimer's. Early diagnosis and treatments seeking to dampen inflammation may help mitigate cognitive consequences.
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2) COVID-19 can cause various ocular symptoms including conjunctivitis, keratitis, scleritis, uveitis, retinal changes, and neurological involvement. Common early symptoms are conjunctivitis and eye pain.
3) Rarely, severe cases present with retinal hemorrhages, cotton wool spots, or retinal artery/vein occlusions likely due to virus-induced hypercoagulability. Cranial nerve palsies, optic neuritis, and vision loss due to occipital strokes are neurological manifestations.
2) The kynurenine pathway metabolizes the essential amino acid tryptophan into neuroactive compounds like kynurenine, kynurenic acid, and quinolinic acid. It is activated by inflammation and produces both neuroprotective and neurotoxic metabolites.
3) The SARS-CoV-2 virus that causes COVID-19 can significantly alter levels of metabolites in the kynurenine pathway (KP), which metabolizes the essential amino acid tryptophan.ย
During acute infection, inflammation raises levels of cytokines like IFN-ฮณ ...
2) A case in China involved a female farmer who became severely ill after exposure to sick poultry. Genetic analysis found she was infected with a clade 2.3.4.4b H5N1 strain. Interestingly, prior SARS-CoV-2 infection may have increased her susceptibility.
3) Clinical tests confirmed dual infection with H5N1 and persisting SARS-CoV-2. Epidemiological data implicated direct poultry contact as the source. Close contacts did not become ill, suggesting limited human-to-human transmission so far.
2) This study examined the evolution of SARS-CoV-2 in 8 patients with persistent infections lasting over 17 days. Whole genome sequencing was performed on respiratory samples collected at various times from each patient.
3) The results show rapid intra-host evolution occurred, with lineages forming based on each individual patient. One unvaccinated patient in particular showed a longer phylogenetic branch length compared to other isolates over their 56-day infection period ...
2) The study investigated the effects of microplastics (MPs) on the host response to SARS-CoV-2 infection in a mouse model. MPs were found to dysregulate innate inflammatory responses to the virus.
3) At 2 days post-infection, MPs suppressed proinflammatory signatures like phagocytosis and interferon responses. This likely reduced macrophage and dendritic cell activation early in infection.