scholarly journals Herpes simplex encephalitis

2022 ◽  
Author(s):  
Irvine Sihlahla
1996 ◽  
Vol 76 (02) ◽  
pp. 184-186 ◽  
Author(s):  
Kenji lijima ◽  
Fumiyo Murakami ◽  
Yasushi Horie ◽  
Katsumi Nakamura ◽  
Shiro Ikawa ◽  
...  

SummaryA 74-year-old female developed pneumonia following herpes simplex encephalitis. Her white blood cell counts reached 28,400/μl, about 90% of which consisted of granulocytes. The polymorphonuclear (PMN) elastase/α1-arantitrypsin complex levels increased and reached the maximum of 5,019 ng/ml, indicating the release of a large amount of elastase derived from the granulocytes. The mechanism of PMN elastase release was most likely to be granulocyte destruction associated with phagocytosis. The cleavage of fibrinogen and fibrin by PMN elastase, independent of plasmin, was indicated by the presence of the fragments in immunoprecipitated plasma from the patient corresponding to elastase-induced FDP D and DD fragments and the absence of fragments corresponding to plasmin-induced FDP D and DD fragments on SDS-PAGE. These findings suggested that the large amount of PMN elastase released from the excessive numbers of granulocytes in this patient with herpes simplex encephalitis and pneumonia, induced the cleavage of fibrinogen and fibrin without the participation of plasmin.


1983 ◽  
Vol 1 (2) ◽  
pp. 79-81 ◽  
Author(s):  
Victor J. Ojeda ◽  
Michael Archer ◽  
Terry A. Robertson ◽  
Marion R. Bucens

2020 ◽  
Vol 2 (1) ◽  
Author(s):  
Wanhui Lin ◽  
Shenggen Chen ◽  
Hanbin Lin ◽  
Changyun Liu ◽  
Huapin Huang

Author(s):  
Maria Silvia Gurgel Assis ◽  
Taciane Cristina Fernandes Pedrosa ◽  
Fernanda Segurasse de Moraes ◽  
Tamires Guedes Caldeira ◽  
Gislaine Ribeiro Pereira ◽  
...  

2015 ◽  
Vol 212 (9) ◽  
pp. 1371-1379 ◽  
Author(s):  
Line Lykke Andersen ◽  
Nanna Mørk ◽  
Line S. Reinert ◽  
Emil Kofod-Olsen ◽  
Ryo Narita ◽  
...  

Herpes simplex encephalitis (HSE) in children has previously been linked to defects in type I interferon (IFN) production downstream of Toll-like receptor 3. Here, we describe a novel genetic etiology of HSE by identifying a heterozygous loss-of-function mutation in the IFN regulatory factor 3 (IRF3) gene, leading to autosomal dominant (AD) IRF3 deficiency by haploinsufficiency, in an adolescent female patient with HSE. IRF3 is activated by most pattern recognition receptors recognizing viral infections and plays an essential role in induction of type I IFN. The identified IRF3 R285Q amino acid substitution results in impaired IFN responses to HSV-1 infection and particularly impairs signaling through the TLR3–TRIF pathway. In addition, the R285Q mutant of IRF3 fails to become phosphorylated at S386 and undergo dimerization, and thus has impaired ability to activate transcription. Finally, transduction with WT IRF3 rescues the ability of patient fibroblasts to express IFN in response to HSV-1 infection. The identification of IRF3 deficiency in HSE provides the first description of a defect in an IFN-regulating transcription factor conferring increased susceptibility to a viral infection in the CNS in humans.


Radiology ◽  
1978 ◽  
Vol 129 (2) ◽  
pp. 419-425 ◽  
Author(s):  
Dieter R. Enzmann ◽  
B. Ranson ◽  
D. Norman ◽  
E. Talberth

The Lancet ◽  
1971 ◽  
Vol 297 (7704) ◽  
pp. 861 ◽  
Author(s):  
A.R.M. Upton ◽  
J.B. Foster ◽  
D.D. Barwick

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