COVID-19 is a global pandemic caused by SARS-CoV-2 infection and is associated with both acute and chronic disorders affecting the nervous system. Acute neurological disorders affecting patients with COVID-19 range widely from anosmia, stroke, encephalopathy/encephalitis, and seizures to Guillain-Barre Syndrome. Chronic neurological sequelae are less well defined although exercise intolerance, dysautonomia, pain, as well as neurocognitive and psychiatric dysfunctions are commonly reported. Molecular analyses of cerebrospinal fluid and neuropathological studies highlight both vascular and immunologic perturbations. Low levels of viral RNA have been detected in the brains of few acutely ill individuals. Potential pathogenic mechanisms in the acute phase include coagulopathies with associated cerebral hypoxic-ischemic injury, blood-brain barrier abnormalities with endotheliopathy and possibly viral neuroinvasion accompanied by neuro-immune responses. Established diagnostic tools are limited by a lack of clearly defined COVID-19 specific neurological syndromes. Future interventions will require delineation of specific neurological syndromes, diagnostic algorithm development, and uncovering the underlying disease mechanisms that will guide effective therapies.

Etiologic diagnosis is uncertain in 35% to 50% of patients with encephalitis, despite its substantial global prevalence and disease burden. We report on 2 adult female patients with fatal leukoencephalitis associated with human pegivirus‐1 (HPgV‐1) brain infection. Neuroimaging showed inflammatory changes in cerebral white matter. Brain‐derived HPgV‐1 RNA sequences clustered phylogenetically with other pegiviruses despite an 87‐nucleotide deletion in the viral nonstructural (NS)2 gene. Neuropathology disclosed lymphocyte infiltration and gliosis predominantly in brain white matter. HPgV‐1 NS5A antigen was detected in lymphocytes as well as in astrocytes and oligodendrocytes. HPgV‐1 neuroadaptation should be considered in the differential diagnosis of progressive leukoencephalitis in humans. Ann Neurol 2018;84:789–795

No abstract

The FABP5 gene encodes a member of the fatty acid binding protein family which is also known as epidermal or cutaneous FABP. Overexpression of FABP5 is associated with a number of cancers including breast and prostate cancers, as well as psychiatric disorders and diabetes. FABP5 can bind retinoic acid as well as polyunsaturated and saturated fatty acids. Transport of FABP5 ligands such as arachidonic acid and retinoic acid to the nucleus is believed to activate the nuclear receptor peroxisome proliferator-activated receptor beta/delta (PPARβ/δ).

In the fall of 1950, eleven San Francisco residents were admitted to Berkeley Hospital with rare bacterial infections. Nearly thirty years later, a Senate subcommittee hearing revealed that the military deliberately released Serratia marcescens, a known opportunistic pathogen, from a naval ship in San Francisco Bay just days before the outbreak, which resulted in the death of Edward J. Nevin. Over the next twenty years, a court case and numerous investigations uncovered an alarming truth about the United States biological weapons program. Government and military personnel have repeatedly and publicly defended the safety and ethics of the research program, insisting that the released substances were "harmless simulants", and that their activities did not qualify as human experimentation. These claims contradict not only official project reports, but the knowledge of civilian scientists and the experiences of the exposed populations, which document the widely ignored human dimensions of the project.