Resistance and Susceptibility of Bovine Cells Expressing Herpesviral Glycoprotein D Homologs to Herpesviral Infections

Chase, Christopher; Lohff, Cortland; Letchworth, Geoffrey J.

doi:10.1006/viro.1993.1269

Virology

1993

DOI: 10.1006/viro.1993.1269

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Resistance and Susceptibility of Bovine Cells Expressing Herpesviral Glycoprotein D Homologs to Herpesviral Infections

Christopher Chase

Cortland Lohff

Geoffrey J. Letchworth

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Cited by 26 publications

(24 citation statements)

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“…After initial attachment to heparan sulfate glycosaminoglycans, entry occurs through the concerted action of four essential glycoproteins, gD, gB, and the heterodimer gH͞gL (1). Their specific roles are not precisely known, except for gD, which represents the glycoprotein with receptor-binding activity (2)(3)(4)(5).Thus, cells expressing the gD of HSV, as well as of PrV or BHV-1, become resistant to infection with homologous and heterologous ␣herpesviruses, by sequestering a cellular molecule that interacts with gD (2,(6)(7)(8). This phenomenon has been designated as gD-mediated restriction, or interference, to infection.…”

mentioning

confidence: 99%

The murine homolog of human Nectin1δ serves as a species nonspecific mediator for entry of human and animal αherpesviruses in a pathway independent of a detectable binding to gD

Menotti

Lopez

Avitabile

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

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The full-length cDNA of the murine homolog of human nectin1␦ (mNectin1␦), also known as human poliovirus receptor related 1 (PRR1) or herpesvirus entry mediator C, was cloned and showed a >90% identity with its human counterpart. mNectin1␦ is expressed in some murine cell lines, exemplified by NIH 3T3 and L cells, and in murine tissues. It mediates entry of an extended range of herpes simplex virus (HSV) strains, porcine pseudorabies virus (PrV), and bovine herpesvirus 1. A soluble form of the mediator blocked infectivity in mNectin1␦ and human nectin1␦ (hNectin1␦)-expressing cells, suggesting a physical interaction of the mediator with virions. The higher concentrations of soluble mNectin1 required to block infectivity relative to soluble hNectin1 suggest that the target of the two molecules is not identical. Entry of HSV, but not PrV, was blocked by soluble mNectin1␦ in NIH 3T3 and L cells. Two features were unexpected. First, soluble mNectin1␦ failed to physically interact with HSV glycoprotein D (gD) at a detectable level, although it interacted physically with virions. Second, coexpression of mNectin1␦ and HSV gD did not restrict HSV or PrV infection, whereas coexpression of hNectin and gD did restrict infection, suggesting that mNectin1␦ fails to be sequestered by HSV gD. We conclude that mNectin1␦ serves as a species-nonspecific mediator for entry of the human and animal ␣herpesviruses. This activity, at least for HSV, is independent of a detectable binding to gD. H erpes simplex virus (HSV) has a broad host range and can infect animals and cultured cells from species other than the natural host. Mouse is the commonly used small animal model in HSV research, including studies on latency, prototypic vaccines, antiviral compounds, and HSV-based vectors. The mouse can be infected by inoculation at peripheral sites, e.g., skin, vagina, or directly into the central nervous system. Infection mimics the infection in humans. Thus, following peripheral inoculation, the virus spreads to nerve endings of the sensory neurons, is transported in anterograde direction to the nuclei of sensitive neurons, where it establishes latency. Virus can be reactivated by exogenous stimuli, and after replication, moves in retrograde direction to peripheral tissues, where it induces lesions. This pattern of infection underscores the existence in mice of receptors for HSV entry into cells, and cell-to-cell spread, with pathways of transmission to tissues analogous to those in humans. Similar to HSV, the porcine ␣herpesvirus pseudorabies virus (PrV) has a very broad host range in cultured cells, and can infect and cause disease in animal species other than the natural host. Mice have been used for experimental infections and to trace the pattern of virus spread to the nervous system. In contrast, the host range of bovine herpesvirus 1 (BHV-1) appears to be narrower, probably reflecting limited availability also of cellular functions involved in postentry steps. A key question in the validation of the mouse animal model is to what exte...

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mentioning

confidence: 99%

The murine homolog of human Nectin1δ serves as a species nonspecific mediator for entry of human and animal αherpesviruses in a pathway independent of a detectable binding to gD

Menotti

Lopez

Avitabile

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

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“…This gD-mediated interference with HSV infection is at the level of viral penetration into cells, not viral binding or postpenetration steps (3,8,11).The phenomenon of gD-mediated interference is common to several of the alphaherpesviruses. Cells expressing pseudorabies virus (PRV) or bovine herpesvirus type 1 (BHV-1) gD are also resistant to infection by homologous virus (5,6,28). In addition, cross-interference among different alphaherpesviruses has been noted (5,6,12,22).…”

mentioning

confidence: 99%

“…Cells expressing pseudorabies virus (PRV) or bovine herpesvirus type 1 (BHV-1) gD are also resistant to infection by homologous virus (5,6,28). In addition, cross-interference among different alphaherpesviruses has been noted (5,6,12,22). For example, cells expressing BHV-1 gD are at least partially resistant to infection by BHV-1, PRV, and HSV-1 (5).…”

mentioning

confidence: 99%

Viral determinants of the variable sensitivity of herpes simplex virus strains to gD-mediated interference

Dean

Warner

Terhune

et al. 1995

J Virol

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Cells that express glycoprotein D (gD) of herpes simplex virus type 1 (HSV-1) resist infection by HSV-1 and HSV-2 because of interference with viral penetration. The results presented here show that both HSV-1 and HSV-2 gD can mediate interference and that various HSV-1 and HSV-2 strains differ in sensitivity to this interference. The relative degree of sensitivity was not necessarily dependent on whether the cell expressed the heterologous or homologous form of gD but rather on the properties of the virus. Marker transfer experiments revealed that the allele of gD expressed by the virus was a major determinant of sensitivity to interference. Amino acid substitutions in the most distal part of the gD ectodomain had a major effect, but substitutions solely in the cytoplasmic domain also influenced sensitivity to interference. In addition, evidence was obtained that another viral gene(s) in addition to the one encoding gD can influence sensitivity to interference. The results indicate that HSV-1 and HSV-2 gD share determinants required to mediate interference with infection by HSV of either serotype and that the pathway of HSV entry that is blocked by expression of cell-associated gD can be cleared or bypassed through subtle alterations in virion-associated proteins, particularly gD.Cells expressing gD of herpes simplex virus type 1 (HSV-1) can be resistant to infection by HSV-1 or HSV-2 (3, 11). This has been shown for several cell types, including human Hep-2 cells, mouse L cells, and baby hamster kidney (BHK) cells. This gD-mediated interference with HSV infection is at the level of viral penetration into cells, not viral binding or postpenetration steps (3,8,11).The phenomenon of gD-mediated interference is common to several of the alphaherpesviruses. Cells expressing pseudorabies virus (PRV) or bovine herpesvirus type 1 (BHV-1) gD are also resistant to infection by homologous virus (5,6,28). In addition, cross-interference among different alphaherpesviruses has been noted (5,6,12,22). For example, cells expressing BHV-1 gD are at least partially resistant to infection by BHV-1, PRV, and HSV-1 (5). Cross-interference is not always reciprocal (5,6). The patterns of cross-interference observed indicate that both homologous and heterologous forms of gD have determinants capable of blocking the entry of a single virus and that different alphaherpesviruses may have common requirements for entry that can be blocked by a single form of gD. This is despite limited conservation of primary amino acid sequence among the gD homologs (10 to 35% identity), the absence of cross-neutralizing epitopes, and differences in host range among the alphaherpesviruses.The entry of HSV, PRV, and BHV-1 into cells depends on binding of the virus to cell surface glycosaminoglycans via gC, followed by fusion of the virion envelope with a cell membrane. The available evidence indicates that at least four envelope glycoproteins, designated gB, gD, gH, and gL, are required for the fusion or penetration step. These glycoproteins are present

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“…The most investigated mechanism of interference with superinfection relates to the interaction of the viral surface protein with its receptor on the cell surface, with blockage of the receptor to the superinfecting virus. It was demonstrated for example, that expression of HSV-1 glycoprotein gD efficiently blocks superinfection by HSV-1 but not by HSV-2, which appear to use a different receptor (Chase et al, 1993). Interference with superinfection may also occur through an intracellular mechanism, independent of receptor occupancy.…”

mentioning

confidence: 96%

The Latency-Associated Gene of Herpes Simplex Virus Type 1 (HSV-1) Interferes with Superinfection by HSV-1

Mador¹,

Panet

Steiner³

2002

J. of Neurovirology

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During herpes simplex virus type 1 (HSV-1) lifelong latency in human peripheral sensory ganglia (PSG), only the viral latency-associated transcript (LAT) gene is expressed. This raises the possibility that this gene is involved in establishment of latency of the virus, its maintenance, or reactivation. Here we present data that indicate yet another independent function of the LAT gene: interference with HSV-1 superinfection of latently infected neurons. Neuronal cells stably expressing the LATs are protected from infection with HSV-1, but not from infection by other RNA and DNA viruses, including HSV-2. These unexpected findings may explain the observation that human PSG are latently infected with just a single strain of HSV-1, despite repeated exposure during life to multiple viral strains. Thus, the LATs may protect the latent HSV-1 reservoir from cytopathic superinfections, and at the same time the host is protected at the viral entry site from HSV-1 insults that may eventually cause viral encephalitis.

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Resistance and Susceptibility of Bovine Cells Expressing Herpesviral Glycoprotein D Homologs to Herpesviral Infections

Cited by 26 publications

References 0 publications

The murine homolog of human Nectin1δ serves as a species nonspecific mediator for entry of human and animal αherpesviruses in a pathway independent of a detectable binding to gD

The murine homolog of human Nectin1δ serves as a species nonspecific mediator for entry of human and animal αherpesviruses in a pathway independent of a detectable binding to gD

Viral determinants of the variable sensitivity of herpes simplex virus strains to gD-mediated interference

The Latency-Associated Gene of Herpes Simplex Virus Type 1 (HSV-1) Interferes with Superinfection by HSV-1

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