Diagnosis of Herpes Simplex Encephalitis by ELISA Using Antipeptide Antibodies Against Type-Common Epitopes of Glycoprotein B of Herpes Simplex Viruses

2015 ◽  
Vol 37 (3) ◽  
pp. 217-227 ◽  
Author(s):  
Shradha S. Bhullar ◽  
Nitin H. Chandak ◽  
Neeraj N. Baheti ◽  
Hemant J. Purohit ◽  
Girdhar M. Taori ◽  
...  
Keyword(s):  
Herpes Simplex ◽  
Herpes Simplex Encephalitis ◽  
Glycoprotein B ◽  
Herpes Simplex Viruses ◽  
Antipeptide Antibodies

Variations of HSV-1 Glycoprotein B in Human Herpes Simplex Encephalitis

1998 ◽  
Vol 4 (1) ◽  
pp. 106-114 ◽  
Author(s):  
Valerie Sivadon ◽  
Pierre Lebon ◽  
Flore Rozenberg
Keyword(s):  
Herpes Simplex ◽  
Herpes Simplex Encephalitis ◽  
Glycoprotein B ◽  
Human Herpes ◽  
Hsv 1

scholarly journals Herpes Simplex Virus Mistyping due to HSV-1 × HSV-2 Interspecies Recombination in Viral Gene Encoding Glycoprotein B

Viruses ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 860
Author(s):  
Amanda M. Casto ◽  
Meei-Li W. Huang ◽  
Hong Xie ◽  
Keith R. Jerome ◽  
Anna Wald ◽  
...  
Keyword(s):  
Herpes Simplex ◽  
Recombination Event ◽  
Genomic Variation ◽  
Glycoprotein B ◽  
Viral Gene ◽  
Human Pathogens ◽  
Herpes Simplex Viruses ◽  
Single Nucleotide Change ◽  
Interspecies Recombination ◽  
Hsv 1

Human herpes simplex viruses (HSV) 1 and 2 are extremely common human pathogens with overlapping disease spectra. Infections due to HSV-1 and HSV-2 are distinguished in clinical settings using sequence-based “typing” assays. Here we describe a case of HSV mistyping caused by a previously undescribed HSV-1 × HSV-2 recombination event in UL27, the HSV gene that encodes glycoprotein B. This is the first documented case of HSV mistyping caused by an HSV-1 × HSV-2 recombination event and the first description of an HSV interspecies recombination event in UL27, which is frequently used as a target for diagnostics and experimental therapeutics. We also review the primer and probe target sequences for a commonly used HSV typing assay from nearly 700 HSV-1 and HSV-2 samples and find that about 4% of HSV-1 samples have a single nucleotide change in at least one of these loci, which could impact assay performance. Our findings illustrate how knowledge of naturally occurring genomic variation in HSV-1 and HSV-2 is essential for the design and interpretation of molecular diagnostics for these viruses.

scholarly journals Herpes Simplex Virus Mistyping due to HSV-1 x HSV-2 Interspecies Recombination in Viral Gene Encoding Glycoprotein B

2020 ◽  
Author(s):  
Amanda M. Casto ◽  
Meei-Li Huang ◽  
Hong Xie ◽  
Keith R. Jerome ◽  
Anna Wald ◽  
...  
Keyword(s):  
Herpes Simplex ◽  
Recombination Event ◽  
Glycoprotein B ◽  
Viral Gene ◽  
Human Herpes ◽  
Gene Encoding ◽  
Herpes Simplex Viruses ◽  
Simplex Virus ◽  
Interspecies Recombination ◽  
Hsv 1

AbstractHuman herpes simplex viruses (HSV) 1 and 2 are most often typed via molecular assays. Here we describe the first known case of HSV mistyping due to a previously undescribed HSV-1 x HSV-2 recombination event in UL27, the gene that encodes glycoprotein B. This is the first reported HSV interspecies recombination event impacting this gene, which is frequently used as a target for diagnostics and experimental therapeutics.

scholarly journals Identification of Functional Domains in Herpes Simplex Virus 2 Glycoprotein B

2006 ◽  
Vol 80 (8) ◽  
pp. 3792-3800 ◽  
Author(s):  
Wei Li ◽  
Tanja J. Minova-Foster ◽  
Daniel D. Norton ◽  
Martin I. Muggeridge
Keyword(s):  
Herpes Simplex ◽  
Cell Fusion ◽  
Alpha Helix ◽  
Glycoprotein B ◽  
Functional Domains ◽  
Herpes Simplex Viruses ◽  
Transfected Cells ◽  
Loop Regions ◽  
Simplex Virus ◽  
Herpes Simplex Virus 2

ABSTRACT Glycoprotein B (gB) is one of four membrane proteins that are essential for the entry of herpes simplex viruses (HSV) into cells, and coexpression of the same combination of proteins in transfected cells results in cell fusion. The latter effect is reminiscent of the ability of virus infection to cause cell fusion, particularly since the degree of fusion is greatly increased by syncytial mutations in gB. Despite intensive efforts with the gB homologs of HSV and some other herpesviruses, information about functionally important regions in the 700-amino-acid ectodomain of this protein is very limited at present. This is largely due to the misfolding of the majority of the mutants examined. It was shown previously that the percentage of correctly folded mutants could be increased by targeting only predicted loop regions (i.e., not alpha-helix or beta-strand), and by using this approach new functional domains in HSV-2 gB have now been identified.

An Alternative Elastase-mediated Degradation of Fibrinogen and Fibrin Observed in a Patient with Herpes Simplex Encephalitis and Pneumonia

1996 ◽  
Vol 76 (02) ◽  
pp. 184-186 ◽  
Author(s):  
Kenji lijima ◽  
Fumiyo Murakami ◽  
Yasushi Horie ◽  
Katsumi Nakamura ◽  
Shiro Ikawa ◽  
...  
Keyword(s):  
Herpes Simplex ◽  
Blood Cell ◽  
White Blood Cell ◽  
Herpes Simplex Encephalitis ◽  
Pmn Elastase ◽  
Cell Counts ◽  
Blood Cell Counts ◽  
Sds Page ◽  
White Blood Cell Counts ◽  
Pmn Élastase

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.

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