Compartment-specific immunolocalization of conserved epitopes of the glycoprotein gB of herpes simplex virus type 1 and bovine herpes virus type 2 in infected cells

1989 ◽  
Vol 108 (1-2) ◽  
pp. 1-17 ◽  
Author(s):  
Sylvia M. Pietschmann ◽  
H. R. Gelderblom ◽  
G. Pauli
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Herpes Virus ◽  
Infected Cells ◽  
Herpès Virus ◽  
Simplex Virus

scholarly journals Pathological processes of immunological decontamination of herpes simplex virus type 1 from the cornea

2020 ◽  
pp. 4-11
Author(s):  
Т.З. Керимов ◽  
В.П. Соболев ◽  
М.А. Соболева ◽  
Н.А. Гаврилова ◽  
С.А. Борзенок
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Herpes Virus ◽  
Toll Like Receptors ◽  
Herpès Virus ◽  
Simplex Virus ◽  
Hsv 1

В обзоре представлено описание патофизиологических механизмов герпесвирусной инфекции. Согласно данным медицинской статистики, вирусом простого герпеса 1 типа инфицировано большинство населения планеты. В развивающихся странах данный вирус является ведущей инфекционной причиной поражения роговицы. Также вирусу простого герпеса 1 типа отводится роль одного из факторов, приводящих к отторжению трансплантата роговицы. Вышеописанные патологические явления сопряжены с перестройкой клеточных систем в ответ на вирусное воздействие. Недавние открытия в данной области обнаружили значительный вклад трансмембранных и эндосомальных Toll-подобных рецепторов во врожденный противовирусный клеточный ответ. Показано, что эндосомальные Toll-подобные рецепторы 3 типа экспрессируются в кератоцитах только после их фенотипического перехода в фибробласты. Данная трансформация обычно происходит в результате механических и патогенных воздействий на роговицу. Изменение рецепторного состава клеток в ответ на герпесвирусную инвазию вызывает выработку интерферонов 1 типа - интерферона-альфа, интерферона-бета, и синтезу провоспалительных цитокинов, что приводит к вирусной деконтаминации. This review describes pathophysiological mechanisms of herpes virus infection in cornea cells. It has been previously reported that herpes simplex virus type 1 (HSV-1) infects most of the world’s population. In developing countries, HSV-1 is the leading infectious cause of corneal damage. Also, herpes simplex virus type 1 was assigned the role of one of the factors leading to rejection of the corneal transplant. These pathological phenomena are associated with restructuring of cellular systems in response to viral exposure. Recent discoveries have revealed a significant contribution of transmembrane and endosomal Toll-like receptors to the innate antiviral cell response. It is well known that endosomal Toll-like receptors-3 are expressed in keratocytes only after their phenotypic transformation to fibroblasts. This transformation usually occurs as a result of mechanical or infectious impact on the cornea. Changes in the receptor composition of cells as a response to herpes virus invasion is the main cause of type 1 interferons (interferon-alpha and interferon-beta) production and expression of proinflammatory cytokines, which leads to viral decontamination.

scholarly journals Differential feulgen-deoxyribonucleic acid hydrolysis patterns of Herpes simplex virus type 1 and type 2 infected cells.

1975 ◽  
Vol 23 (4) ◽  
pp. 283-288 ◽  
Author(s):  
L R Trusal ◽  
A Anthony ◽  
J J Docherty
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Deoxyribonucleic Acid ◽  
Human Embryonic Lung ◽  
Infected Cells ◽  
Simplex Virus

Infection of human embryonic lung cells with herpes simplex virus type 1 (HSV-1) and herpes simplex type 1 (HSV-2) resulted in: (a) qualitative (nuclear cytopathologic) alterations and quantitative (nuclear area) differences in infected compared to control nuclei; (b) increased Feulgen-deoxyribonucleic acid (F-DNA) amounts in infected cells, probably due to viral DNA; (c) higher F-DNA levels in HSV-2 infected cells; and (d) increased rates of F-DNA hydrolysis in viral-infected as compared to uninfected nuclei.

scholarly journals Glycoprotein D Homologs in Herpes Simplex Virus Type 1, Pseudorabies Virus, and Bovine Herpes Virus Type 1 Bind Directly to Human HveC (Nectin-1) with Different Affinities

Virology ◽  
2001 ◽  
Vol 280 (1) ◽  
pp. 7-18 ◽  
Author(s):  
Sarah A. Connolly ◽  
J.Charles Whitbeck ◽  
Ann H. Rux ◽  
Claude Krummenacher ◽  
Sylvia van Drunen Littel-van den Hurk ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Herpes Virus ◽  
Pseudorabies Virus ◽  
Glycoprotein D ◽  
Herpès Virus ◽  
Simplex Virus

scholarly journals Binding of surfactant protein A (SP-A) to herpes simplex virus type 1-infected cells is mediated by the carbohydrate moiety of SP-A.

1992 ◽  
Vol 267 (35) ◽  
pp. 25039-25043 ◽  
Author(s):  
J.F. van Iwaarden ◽  
J.A. van Strijp ◽  
H Visser ◽  
H.P. Haagsman ◽  
J Verhoef ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Protein A ◽  
Surfactant Protein ◽  
Surfactant Protein A ◽  
Infected Cells ◽  
Simplex Virus

scholarly journals Herpes Simplex Virus Type 2 Mucin-Like Glycoprotein mgG Promotes Virus Release from the Surface of Infected Cells

Viruses ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 887
Author(s):  
Edward Trybala ◽  
Nadia Peerboom ◽  
Beata Adamiak ◽  
Malgorzata Krzyzowska ◽  
Jan-Åke Liljeqvist ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Culture Medium ◽  
Glycoprotein G ◽  
Infected Cells ◽  
Virus Interaction ◽  
Simplex Virus

The contribution of virus components to liberation of herpes simplex virus type 2 (HSV-2) progeny virions from the surface of infected cells is poorly understood. We report that the HSV-2 mutant deficient in the expression of a mucin-like membrane-associated glycoprotein G (mgG) exhibited defect in the release of progeny virions from infected cells manifested by ~2 orders of magnitude decreased amount of infectious virus in a culture medium as compared to native HSV-2. Electron microscopy revealed that the mgG deficient virions were produced in infected cells and present at the cell surface. These virions could be forcibly liberated to a nearly native HSV-2 level by the treatment of cells with glycosaminoglycan (GAG)-mimicking oligosaccharides. Comparative assessment of the interaction of mutant and native virions with surface-immobilized chondroitin sulfate GAG chains revealed that while the mutant virions associated with GAGs ~fourfold more extensively, the lateral mobility of bound virions was much poorer than that of native virions. These data indicate that the mgG of HSV-2 balances the virus interaction with GAG chains, a feature critical to prevent trapping of the progeny virions at the surface of infected cells.

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