Expression and immunogenicity of recombinant glycoprotein D of herpes simplex virus 1 in Drosophila S2

Herpes simplex virus type 1 (HSV-1) is responsible for cold sores in the general population, but also contributes to the development of other more serious diseases in some circumstances. Normal bone marrow cells from a donor positive for herpes simplex virus were transformed with Epstein-Barr virus. Glycoprotein D (gD) of herpes simplex virus contains three utilized sites (Asn-X-Ser/Thr) for addition of asparagine-linked carbohydrates (N-CHO). Four glycoproteins (gD, gB, gH, and gL) are essential for herpes simplex virus (HSV) entry into cells. Herpes simplex virus type 1 (HSV-1) glycoprotein D (gD) binds to its cellular receptor, herpesvirus entry mediator (HVEM), to enter into activated T cells. Herpes simplex virus (HSV) glycoprotein gD is a major component of the virion envelope and is thought to play an important role in the initial stages of viral infection and stimulates the production of high titers of neutralizing antibodies. Binding of herpes simplex virus (HSV) glycoprotein D (gD) to a cell surface receptor is required to trigger membrane fusion during entry into host cells.

Multiple surface envelope proteins are involved in the human herpes simplex virus type 1 entry and fusion. Herpes simplex virus (HSV) Type-1 and -2 are common infections that can cause primary and recurrent herpes labialis and genitalis, as well as gingivostomatitis, keratoconjunctivitis, encephalitis, disseminated infections in immunocompromised persons and neonatal infections. This article has been cited by other articles in PMC. The topical application of corticosteroids to the eye of man or rabbit infected with Herpes simplex virus markedly aggravates the keratitis and may lead to loss of vision. This article has been cited by other articles in PMC. Herpes simplex virus type 1 (HSV-1) acquires its final envelope by budding into cytoplasmic vesicles thought to be derived from trans-Golgi network membranes. Signals involved in protection against apoptosis by herpes simplex virus 1 (HSV-1) were investigated.

Help Black dashed lines indicate hydrogen bonds, salt bridges, and metal interactions. From the George C. Glycoprotein D (gD) of herpes simplex virus (HSV) is essential for virus entry and has four functional regions (I to IV) important for this process. Binding of herpes simplex virus (HSV) envelope glycoprotein D (gD) to a cell surface receptor is an essential step of virus entry. Department of Molecular, Genetics and Cell Biology, University of Chicago, Illinois 60637. During viral entry, herpes simplex virus (HSV) glycoprotein D (gD) interacts with a specific cellular receptor such as nectin-1 (PRR1/HveC/CD111) or the herpesvirus entry mediator A (HVEM/HveA). Please check the format of the address you have entered.

HVEM (for herpesvirus entry mediator) is a member of the tumor necrosis factor receptor superfamily and mediates entry of many strains of herpes simplex virus (HSV) into normally nonpermissive Chinese hamster ovary (CHO) cells. Herpes simplex virus type 1 (HSV-1) ocular infection in rats was blocked by treating the eyes with UV-inactivated virions containing glycoprotein D (gD) prior to ocular challenge. This is a short preview of the document. PNAS is the world’s most-cited multidisciplinary scientific serial. Highlighted regions within the gD-HveA crystal structure. PNAS is the world’s most-cited multidisciplinary scientific serial. A prerequisite for productive entry of enveloped viruses into cells is fusion between the viral envelope and a cellular membrane.

Distinct subsets of human receptors for alphaherpesviruses mediate the entry of herpes simplex virus (HSV), pseudorabies virus (PrV), or bovine herpes virus type 1 (BHV-1) into cells. PNAS is the world’s most-cited multidisciplinary scientific serial. Glycoprotein D (gD) interacts with two alternative protein receptors, nectin1 and HveA, to mediate herpes simplex virus (HSV) entry into cells. PNAS is the world’s most-cited multidisciplinary scientific serial. Studies on molecular interactions between cellular receptors of herpes simplex virus (HSV) and the viral glycoproteins showing receptor-binding activity are of great relevance for understanding the molecular basis of virus entry. Entry of herpes simplex virus into the cell requires the interaction of gD with one of its receptors, herpesvirus entry mediator or nectin 1, and the intervention of gB, gH, or gL, required to execute fusion of the virion envelope with cell membranes. Plasmid DNA encoding herpes simplex virus type-1 glycoprotein D (gD-1) was complexed with asialoorosomucoid conjugated to poly-L-lysine.

This is a short preview of the document. Viral factors responsible for HSV neurovirulence in humans are still unknown. Herpes simplex virus type 2 glycoprotein D (gD2) was cloned and expressed in the baculovirus-Spodoptera frugiperda system. In humans, herpes simplex virus causes a primary infection and then often a latent ganglionic infection that persists for life. Abstract: Background: Herpes simplex virus type 2 (HSV-2) is highly prevalent and major cause of genital herpes in humans. An antigenic determinant capable of inducing type-common herpes simplex virus (HSV)-neutralizing antibodies has been located on glycoprotein D (gD) of HSV type 1 (HSV-1). Several prokaryotic and eukaryotic expression systems have been used for in vitro production of viruses’ proteins.

Herpes simplex virus type 1 (HSV-1) entry into permissive cells involves attachment to cell-surface glycosaminoglycans (GAGs) and fusion of the virus envelope with the cell membrane triggered by the binding of glycoprotein D (gD) to cognate receptors.