Transient naming deficits associated with insular lesions in a patient with encephalitis.
We describe a patient with acute herpes simplex encephalitis with left-hemispheric hippocampal, parahippocampal and insular lesions. Although prototypic language areas were unaffected, the patient suffered from an inability to name objects or animals displayed on pictures. This deficit was transient and gradually disappeared 8 weeks after the initial diagnosis. Our findings are in line with a previous report showing similar deficits in a patient with a comparable lesion pattern and support the hypothesis that left insular lesions can produce severe naming deficits. Using FDG-PET we ruled out that functional deactivation in classical language areas account for the observed naming deficits. PMID: 31532322 [PubMed - as supplied by publisher]
Anti-NMDA receptor (NMDAR) encephalitis is characterized by mood and behavior changes, seizures, abnormal movements, autonomic instability, and encephalopathy. It occurs most commonly in young adults. A paraneoplastic association has been made with ovarian teratoma, though this is rare in children1. More recently, cases of anti-NMDAR encephalitis following viral infections have been reported, including herpes simplex virus (HSV), Japanese encephalitis virus (JEV), and now the 2019 novel coronavirus (SARS-CoV-2)2-5.
Discussion Herpes simplex virus (HSV) infections are common with an estimated 50% of the US population being infected by age 30, and with latent infection harboring in the trigeminal nerve in 100% of people by age 60 years. HSV infections can cause a vesicular or pustular skin rash that is painful, burning or pruritic and also flu-like symptoms with fever, chills, headache, and fatigue. HSV can also be asymptomatic. To laymen, herpes simplex viruses cause “cold sores,” but to health care personnel, herpes causes many systemic infections including eczema herpeticum, folliculitis, herpes gladiatorum, whitlow, e...
Conclusion: Our results revealed that restraint stress/CORT increased HSV-1 susceptibility by delivering PML into autolysosomes for degradation. The results obtained from in vitro and in vivo models not only demonstrated the adverse effects of stress on HSV-1 infection, but also systematically investigated the underlying molecular mechanisms. These discoveries broaden our understanding of the interplay between host and viruses, and a comprehensive understanding of the role of autophagy in viral infection will provide information for future development of innovative drugs against viral infection.
An association between herpes simplex virus (HSV) encephalitis and NDMA receptor (NMDAR) encephalitis has been well described. Here, we report a rare case of HSV encephalitis occurring alongside autoimmune encephalitis with leucine-rich glioma inactivated 1 (LGI-1) and NMDAR antibodies.
We report a child homozygous for a genomic deletion of the entire coding sequence and part of the 3’U TR of the last exon of IFNAR1, who died from HSE at the age of two years. An older cousin died following vaccination against measles, mumps and rubella at 12 months of age, and another 17-year-old cousin homozygous for the same variant has had other viral illnesses. The encoded IFNAR1 protein is exp ressed on the cell surface but is truncated and cannot interact with the tyrosine kinase TYK2. The patient’s fibroblasts and EBV-B cells did not respond to IFN-α2b or IFN-β, in terms of STAT1, STAT2 and S...
(University of Liverpool) Researchers at the University of Liverpool have identified the specific type of immune cell that induces brain inflammation in herpes simplex virus (HSV) encephalitis. Crucially, they have also determined the signalling protein that calls this immune cell into the brain from the bloodstream. The findings, published in Cell Reports, could aid the development of targeted treatments for the brain infection, which is the most common cause of viral encephalitis worldwide.
Infections of the brain with herpes simplex virus type 1 (HSV-1) cause life-threatening Herpes simplex encephalitis (HSE) characterized by viral replication in neurons and neuro-inflammation including an infiltration of peripheral immune cells. HSV-1 reprograms host cells to foster its own replication and for immune evasion, but eventually the immune responses clear the infection in most patients. However, many survivors suffer from long-term neuronal damage and cannot regenerate all brain functions. HSV-1 influences the physiology of neurons, astrocytes, oligodendrocytes and microglia, and significantly changes their prot...
CONCLUSIONS: Our series demonstrated the dramatic efficacy of systematic ACV prophylaxis during all cranial surgeries. Moreover, our results on epilepsy, together with those of the literature, encourage more consideration regarding epilepsy surgery in this specific etiology. All types of surgical procedures (curative or palliative) can be offered to the patients, but in the case of focal surgery, due to the poor anatomical limits, invasive recordings are highly recommended. PMID: 32868196 [PubMed - as supplied by publisher]
Conclusion: Our identification of the 22 novel motifs shed light on HSV gB biology and provide new options for gB engineering to improve the efficiency and safety of oHSVs.
Authors: Kapadia RK, Tyler KL, Pastula DM PMID: 32778604 [PubMed - in process]