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Julia K Hilliard - One of the best experts on this subject based on the ideXlab platform.
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LONG-TERM SURVEILLANCE OF LANGUR ALPHAHERPESVIRUS IN A ZOO POPULATION OF SILVERED LANGURS (TRACHYPITHECUS CRISTATUS)
Journal of zoo and wildlife medicine : official publication of the American Association of Zoo Veterinarians, 2018Co-Authors: Kate A. Gustavsen, Julia K Hilliard, Martin J. Wildes, Bonnie L. Raphael, Denise Mcaloose, Colleen Mccann, Paul P. CalleAbstract:Abstract: Langur alphaherpesvirus (HVL), a provisionally named alphaherpesvirus in the Simplexvirus genus, was first identified in 1991 at the Bronx Zoo in wild-origin silvered langurs (Trachypithecus cristatus) and their descendants. HVL is closely related to B virus (Macacine alphaherpesvirus 1) based on serologic and genetic data, but its natural history and zoonotic potential remain unknown. A cohort study was undertaken to describe the epidemiology, clinical impact, and potential management implications of this virus in a naturally infected, zoo-based population of silvered langurs. Opportunistic surveillance sampling from 1991 through 2015 resulted in 235 serum samples and 225 mucosal swabs from 75 individuals. A total of 43 individuals (57.3%) were seropositive for HVL within this period. Seroprevalence increased significantly with age, and indirect evidence suggested a peak in transmission at the onset of sexual maturity. These findings were similar to the behavior of other Simplexviruses in thei...
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Identification of unique B virus (Macacine Herpesvirus 1) epitopes of zoonotic and macaque isolates using monoclonal antibodies.
PloS one, 2017Co-Authors: David Katz, Irina Patrusheva, Mugdha Vasireddi, Wei Shi, Manjunath S. Gowda, Hyuk-kyu Seoh, Martin J. Wildes, Chadi Filfili, Julia K HilliardAbstract:Our overall aim is to develop epitope-based assays for accurate differential diagnosis of B virus zoonotic infections in humans. Antibodies to cross-reacting epitopes on human-Simplexviruses continue to confound the interpretation of current assays where abundant antibodies exist from previous infections with HSV types 1 and 2. To find B virus-specific epitopes we cloned ten monoclonal antibodies (mAbs) from the hybridomas we produced. Our unique collection of rare human sera from symptomatic and asymptomatic patients infected with B virus was key to the evaluation and identification of the mAbs as reagents in competition ELISAs (mAb-CE). The analysis of the ten mAbs revealed that the target proteins for six mAbs was glycoprotein B of which two are reactive to simian Simplexviruses and not to human Simplexviruses. Two mAbs reacted specifically with B virus glycoprotein D, and two other mAbs were specific to VP13/14 and gE-gI complex respectively. The mAbs specific to VP13/14 and gE-gI are strain specific reacting with B virus isolates from rhesus and Japanese macaques and not with isolates from cynomolgus and pigtail macaques. The mAb-CE revealed that a high proportion of naturally B virus infected rhesus macaques and two symptomatic humans possess antibodies to epitopes of VP13/14 protein and on the gE-gI complex. The majority of sera from B virus infected macaques and Simplexvirus-infected humans competed with the less specific mAbs. These experiments produced a novel panel of mAbs that enabled B virus strain identification and confirmation of B virus infected macaques by the mAb-CE. For human sera the mAb-CE could be used only for selected cases due to the selective B virus strain-specificity of the mAbs against VP13/14 and gE/gI. To fully accomplish our aim to provide reagents for unequivocal differential diagnosis of zoonotic B virus infections, additional mAbs with a broader range of specificities is critical.
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The relative reactivity of mAbs to viruses of the Simplexvirus group was tested by tELISA.
2017Co-Authors: David Katz, Irina Patrusheva, Mugdha Vasireddi, Wei Shi, Manjunath S. Gowda, Hyuk-kyu Seoh, Chadi N. Filfili, Martin J. Wildes, Julia K HilliardAbstract:The relative reactivity of mAbs to viruses of the Simplexvirus group was tested by tELISA.
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B Virus (Macacine herpesvirus 1) Glycoprotein D Is Functional but Dispensable for Virus Entry into Macaque and Human Skin Cells
Journal of Virology, 2015Co-Authors: Ludmila Perelygina, Irina Patrusheva, Mugdha Vasireddi, Nicole Brock, Julia K HilliardAbstract:Glycoprotein D (gD) plays an essential role in cell entry of many Simplexviruses. B virus (Macacine herpesvirus 1) is closely related to herpes simplex virus 1 (HSV-1) and encodes gD, which shares more than 70% amino acid similarity with HSV-1 gD. Previously, we have demonstrated that B virus gD polyclonal antibodies were unable to neutralize B virus infectivity on epithelial cell lines, suggesting gD is not required for B virus entry into these cells. In the present study, we confirmed this finding by producing a B virus mutant, BV-ΔgDZ, in which the gD gene was replaced with a lacZ expression cassette. Recombinant plaques were selected on complementing VD60 cells expressing HSV-1 gD. Virions lacking gD were produced in Vero cells infected with BV-ΔgDZ. In contrast to HSV-1, B virus lacking gD was able to infect and form plaques on noncomplementing cell lines, including Vero, HEp-2, LLC-MK2, primary human and macaque dermal fibroblasts, and U373 human glioblastoma cells. The gD-negative BV-ΔgDZ also failed to enter entry-resistant murine B78H1 cells bearing a single gD receptor, human nectin-1, but gained the ability to enter when phenotypically supplemented with HSV-1 gD. Cell attachment and penetration rates, as well as the replication characteristics of BV-ΔgDZ in Vero cells, were almost identical to those of wild-type (wt) B virus. These observations indicate that B virus can utilize gD-independent cell entry and transmission mechanisms, in addition to generally used gD-dependent mechanisms. IMPORTANCE B virus is the only known Simplexvirus that causes zoonotic infection, resulting in approximately 80% mortality in untreated humans or in lifelong persistence with the constant threat of reactivation in survivors. Here, we report that B virus lacking the gD envelope glycoprotein infects both human and monkey cells as efficiently as wild-type B virus. These data provide evidence for a novel mechanism(s) utilized by B virus to gain access to target cells. This mechanism is different from those used by its close relatives, HSV-1 and -2, where gD is a pivotal protein in the virus entry process. The possibility remains that unidentified receptors, specific for B virus, permit virus entry into target cells through gD-independent pathways. Understanding the molecular mechanisms of B virus entry may help in developing rational therapeutic strategies for the prevention and treatment of B virus infection in both macaques and humans.
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Identification of a herpes B virus-specific glycoprotein d immunodominant epitope recognized by natural and foreign hosts.
The Journal of infectious diseases, 2002Co-Authors: Ludmila Perelygina, Irina Patrusheva, Holley Zurkuhlen, Julia K HilliardAbstract:The mapping of linear epitopes of B virus (Cercopithecine herpesvirus 1 and herpes B virus) glycoprotein D (gD) was accomplished by screening the constructed gD epitope library with serum from B virus–infected macaques. The immunodominant epitope, gD (362–370), was identified within the C-terminal region of B virus gD that was highly conserved among 19 B virus clinical isolates but was not present in either herpes simplex virus (HSV)–1 or HSV-2 gD. A substantial percentage of serum samples from macaques (95%) and humans (80%) infected with B virus contained antibodies to this epitope. Antibodies against HSV types 1 or 2 did not react with this epitope; thus, gD (362–370) has unique potential to detect B virus–specific antibody responses in human serum, even in the presence of antibodies to HSV1 and HSV-2. B virus (Cercopithecine herpesvirus 1 and herpes B virus) can cause a deadly zoonosis when transmitted to humans by a macaque actively shedding virus. A member of the genus Simplexvirus from the subfamily Alphaherpesvirinae, B virus establishes a life-long latency in the sensory ganglia of infected monkeys [1, 2]. Since the B virus shedding by seropositive macaques is sporadic [3–5], identification of infected animals is usually accomplished by detection of B virus–specific antibodies [6]. Because of the extensive serologic cross-reactivity between the closely related herpes simplex virus (HSV) types 1 and 2 and B virus antigens, detection of B virus infections in humans with preexisting HSV-1/HSV-2 antibodies is technically challenging [7, 8]. B virus serodiagnosis currently relies on competition ELISA and immunoblotting strategies [9–11], but both techniques require complex analysis and B virus propagation in a biosafety level–4 laboratory. Initiation of antiviral therapies as early as possible after infection in humans is vital in preventing fatal disease; thus, there is a clinical need for early diagnostic capabilities [12–15]. A highly specific diagnostic method for early detection of B
Irina Patrusheva - One of the best experts on this subject based on the ideXlab platform.
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Identification of unique B virus (Macacine Herpesvirus 1) epitopes of zoonotic and macaque isolates using monoclonal antibodies.
PloS one, 2017Co-Authors: David Katz, Irina Patrusheva, Mugdha Vasireddi, Wei Shi, Manjunath S. Gowda, Hyuk-kyu Seoh, Martin J. Wildes, Chadi Filfili, Julia K HilliardAbstract:Our overall aim is to develop epitope-based assays for accurate differential diagnosis of B virus zoonotic infections in humans. Antibodies to cross-reacting epitopes on human-Simplexviruses continue to confound the interpretation of current assays where abundant antibodies exist from previous infections with HSV types 1 and 2. To find B virus-specific epitopes we cloned ten monoclonal antibodies (mAbs) from the hybridomas we produced. Our unique collection of rare human sera from symptomatic and asymptomatic patients infected with B virus was key to the evaluation and identification of the mAbs as reagents in competition ELISAs (mAb-CE). The analysis of the ten mAbs revealed that the target proteins for six mAbs was glycoprotein B of which two are reactive to simian Simplexviruses and not to human Simplexviruses. Two mAbs reacted specifically with B virus glycoprotein D, and two other mAbs were specific to VP13/14 and gE-gI complex respectively. The mAbs specific to VP13/14 and gE-gI are strain specific reacting with B virus isolates from rhesus and Japanese macaques and not with isolates from cynomolgus and pigtail macaques. The mAb-CE revealed that a high proportion of naturally B virus infected rhesus macaques and two symptomatic humans possess antibodies to epitopes of VP13/14 protein and on the gE-gI complex. The majority of sera from B virus infected macaques and Simplexvirus-infected humans competed with the less specific mAbs. These experiments produced a novel panel of mAbs that enabled B virus strain identification and confirmation of B virus infected macaques by the mAb-CE. For human sera the mAb-CE could be used only for selected cases due to the selective B virus strain-specificity of the mAbs against VP13/14 and gE/gI. To fully accomplish our aim to provide reagents for unequivocal differential diagnosis of zoonotic B virus infections, additional mAbs with a broader range of specificities is critical.
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The relative reactivity of mAbs to viruses of the Simplexvirus group was tested by tELISA.
2017Co-Authors: David Katz, Irina Patrusheva, Mugdha Vasireddi, Wei Shi, Manjunath S. Gowda, Hyuk-kyu Seoh, Chadi N. Filfili, Martin J. Wildes, Julia K HilliardAbstract:The relative reactivity of mAbs to viruses of the Simplexvirus group was tested by tELISA.
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B Virus (Macacine herpesvirus 1) Glycoprotein D Is Functional but Dispensable for Virus Entry into Macaque and Human Skin Cells
Journal of Virology, 2015Co-Authors: Ludmila Perelygina, Irina Patrusheva, Mugdha Vasireddi, Nicole Brock, Julia K HilliardAbstract:Glycoprotein D (gD) plays an essential role in cell entry of many Simplexviruses. B virus (Macacine herpesvirus 1) is closely related to herpes simplex virus 1 (HSV-1) and encodes gD, which shares more than 70% amino acid similarity with HSV-1 gD. Previously, we have demonstrated that B virus gD polyclonal antibodies were unable to neutralize B virus infectivity on epithelial cell lines, suggesting gD is not required for B virus entry into these cells. In the present study, we confirmed this finding by producing a B virus mutant, BV-ΔgDZ, in which the gD gene was replaced with a lacZ expression cassette. Recombinant plaques were selected on complementing VD60 cells expressing HSV-1 gD. Virions lacking gD were produced in Vero cells infected with BV-ΔgDZ. In contrast to HSV-1, B virus lacking gD was able to infect and form plaques on noncomplementing cell lines, including Vero, HEp-2, LLC-MK2, primary human and macaque dermal fibroblasts, and U373 human glioblastoma cells. The gD-negative BV-ΔgDZ also failed to enter entry-resistant murine B78H1 cells bearing a single gD receptor, human nectin-1, but gained the ability to enter when phenotypically supplemented with HSV-1 gD. Cell attachment and penetration rates, as well as the replication characteristics of BV-ΔgDZ in Vero cells, were almost identical to those of wild-type (wt) B virus. These observations indicate that B virus can utilize gD-independent cell entry and transmission mechanisms, in addition to generally used gD-dependent mechanisms. IMPORTANCE B virus is the only known Simplexvirus that causes zoonotic infection, resulting in approximately 80% mortality in untreated humans or in lifelong persistence with the constant threat of reactivation in survivors. Here, we report that B virus lacking the gD envelope glycoprotein infects both human and monkey cells as efficiently as wild-type B virus. These data provide evidence for a novel mechanism(s) utilized by B virus to gain access to target cells. This mechanism is different from those used by its close relatives, HSV-1 and -2, where gD is a pivotal protein in the virus entry process. The possibility remains that unidentified receptors, specific for B virus, permit virus entry into target cells through gD-independent pathways. Understanding the molecular mechanisms of B virus entry may help in developing rational therapeutic strategies for the prevention and treatment of B virus infection in both macaques and humans.
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Identification of a herpes B virus-specific glycoprotein d immunodominant epitope recognized by natural and foreign hosts.
The Journal of infectious diseases, 2002Co-Authors: Ludmila Perelygina, Irina Patrusheva, Holley Zurkuhlen, Julia K HilliardAbstract:The mapping of linear epitopes of B virus (Cercopithecine herpesvirus 1 and herpes B virus) glycoprotein D (gD) was accomplished by screening the constructed gD epitope library with serum from B virus–infected macaques. The immunodominant epitope, gD (362–370), was identified within the C-terminal region of B virus gD that was highly conserved among 19 B virus clinical isolates but was not present in either herpes simplex virus (HSV)–1 or HSV-2 gD. A substantial percentage of serum samples from macaques (95%) and humans (80%) infected with B virus contained antibodies to this epitope. Antibodies against HSV types 1 or 2 did not react with this epitope; thus, gD (362–370) has unique potential to detect B virus–specific antibody responses in human serum, even in the presence of antibodies to HSV1 and HSV-2. B virus (Cercopithecine herpesvirus 1 and herpes B virus) can cause a deadly zoonosis when transmitted to humans by a macaque actively shedding virus. A member of the genus Simplexvirus from the subfamily Alphaherpesvirinae, B virus establishes a life-long latency in the sensory ganglia of infected monkeys [1, 2]. Since the B virus shedding by seropositive macaques is sporadic [3–5], identification of infected animals is usually accomplished by detection of B virus–specific antibodies [6]. Because of the extensive serologic cross-reactivity between the closely related herpes simplex virus (HSV) types 1 and 2 and B virus antigens, detection of B virus infections in humans with preexisting HSV-1/HSV-2 antibodies is technically challenging [7, 8]. B virus serodiagnosis currently relies on competition ELISA and immunoblotting strategies [9–11], but both techniques require complex analysis and B virus propagation in a biosafety level–4 laboratory. Initiation of antiviral therapies as early as possible after infection in humans is vital in preventing fatal disease; thus, there is a clinical need for early diagnostic capabilities [12–15]. A highly specific diagnostic method for early detection of B
Ludmila Perelygina - One of the best experts on this subject based on the ideXlab platform.
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B Virus (Macacine herpesvirus 1) Glycoprotein D Is Functional but Dispensable for Virus Entry into Macaque and Human Skin Cells
Journal of Virology, 2015Co-Authors: Ludmila Perelygina, Irina Patrusheva, Mugdha Vasireddi, Nicole Brock, Julia K HilliardAbstract:Glycoprotein D (gD) plays an essential role in cell entry of many Simplexviruses. B virus (Macacine herpesvirus 1) is closely related to herpes simplex virus 1 (HSV-1) and encodes gD, which shares more than 70% amino acid similarity with HSV-1 gD. Previously, we have demonstrated that B virus gD polyclonal antibodies were unable to neutralize B virus infectivity on epithelial cell lines, suggesting gD is not required for B virus entry into these cells. In the present study, we confirmed this finding by producing a B virus mutant, BV-ΔgDZ, in which the gD gene was replaced with a lacZ expression cassette. Recombinant plaques were selected on complementing VD60 cells expressing HSV-1 gD. Virions lacking gD were produced in Vero cells infected with BV-ΔgDZ. In contrast to HSV-1, B virus lacking gD was able to infect and form plaques on noncomplementing cell lines, including Vero, HEp-2, LLC-MK2, primary human and macaque dermal fibroblasts, and U373 human glioblastoma cells. The gD-negative BV-ΔgDZ also failed to enter entry-resistant murine B78H1 cells bearing a single gD receptor, human nectin-1, but gained the ability to enter when phenotypically supplemented with HSV-1 gD. Cell attachment and penetration rates, as well as the replication characteristics of BV-ΔgDZ in Vero cells, were almost identical to those of wild-type (wt) B virus. These observations indicate that B virus can utilize gD-independent cell entry and transmission mechanisms, in addition to generally used gD-dependent mechanisms. IMPORTANCE B virus is the only known Simplexvirus that causes zoonotic infection, resulting in approximately 80% mortality in untreated humans or in lifelong persistence with the constant threat of reactivation in survivors. Here, we report that B virus lacking the gD envelope glycoprotein infects both human and monkey cells as efficiently as wild-type B virus. These data provide evidence for a novel mechanism(s) utilized by B virus to gain access to target cells. This mechanism is different from those used by its close relatives, HSV-1 and -2, where gD is a pivotal protein in the virus entry process. The possibility remains that unidentified receptors, specific for B virus, permit virus entry into target cells through gD-independent pathways. Understanding the molecular mechanisms of B virus entry may help in developing rational therapeutic strategies for the prevention and treatment of B virus infection in both macaques and humans.
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Identification of a herpes B virus-specific glycoprotein d immunodominant epitope recognized by natural and foreign hosts.
The Journal of infectious diseases, 2002Co-Authors: Ludmila Perelygina, Irina Patrusheva, Holley Zurkuhlen, Julia K HilliardAbstract:The mapping of linear epitopes of B virus (Cercopithecine herpesvirus 1 and herpes B virus) glycoprotein D (gD) was accomplished by screening the constructed gD epitope library with serum from B virus–infected macaques. The immunodominant epitope, gD (362–370), was identified within the C-terminal region of B virus gD that was highly conserved among 19 B virus clinical isolates but was not present in either herpes simplex virus (HSV)–1 or HSV-2 gD. A substantial percentage of serum samples from macaques (95%) and humans (80%) infected with B virus contained antibodies to this epitope. Antibodies against HSV types 1 or 2 did not react with this epitope; thus, gD (362–370) has unique potential to detect B virus–specific antibody responses in human serum, even in the presence of antibodies to HSV1 and HSV-2. B virus (Cercopithecine herpesvirus 1 and herpes B virus) can cause a deadly zoonosis when transmitted to humans by a macaque actively shedding virus. A member of the genus Simplexvirus from the subfamily Alphaherpesvirinae, B virus establishes a life-long latency in the sensory ganglia of infected monkeys [1, 2]. Since the B virus shedding by seropositive macaques is sporadic [3–5], identification of infected animals is usually accomplished by detection of B virus–specific antibodies [6]. Because of the extensive serologic cross-reactivity between the closely related herpes simplex virus (HSV) types 1 and 2 and B virus antigens, detection of B virus infections in humans with preexisting HSV-1/HSV-2 antibodies is technically challenging [7, 8]. B virus serodiagnosis currently relies on competition ELISA and immunoblotting strategies [9–11], but both techniques require complex analysis and B virus propagation in a biosafety level–4 laboratory. Initiation of antiviral therapies as early as possible after infection in humans is vital in preventing fatal disease; thus, there is a clinical need for early diagnostic capabilities [12–15]. A highly specific diagnostic method for early detection of B
Mugdha Vasireddi - One of the best experts on this subject based on the ideXlab platform.
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Identification of unique B virus (Macacine Herpesvirus 1) epitopes of zoonotic and macaque isolates using monoclonal antibodies.
PloS one, 2017Co-Authors: David Katz, Irina Patrusheva, Mugdha Vasireddi, Wei Shi, Manjunath S. Gowda, Hyuk-kyu Seoh, Martin J. Wildes, Chadi Filfili, Julia K HilliardAbstract:Our overall aim is to develop epitope-based assays for accurate differential diagnosis of B virus zoonotic infections in humans. Antibodies to cross-reacting epitopes on human-Simplexviruses continue to confound the interpretation of current assays where abundant antibodies exist from previous infections with HSV types 1 and 2. To find B virus-specific epitopes we cloned ten monoclonal antibodies (mAbs) from the hybridomas we produced. Our unique collection of rare human sera from symptomatic and asymptomatic patients infected with B virus was key to the evaluation and identification of the mAbs as reagents in competition ELISAs (mAb-CE). The analysis of the ten mAbs revealed that the target proteins for six mAbs was glycoprotein B of which two are reactive to simian Simplexviruses and not to human Simplexviruses. Two mAbs reacted specifically with B virus glycoprotein D, and two other mAbs were specific to VP13/14 and gE-gI complex respectively. The mAbs specific to VP13/14 and gE-gI are strain specific reacting with B virus isolates from rhesus and Japanese macaques and not with isolates from cynomolgus and pigtail macaques. The mAb-CE revealed that a high proportion of naturally B virus infected rhesus macaques and two symptomatic humans possess antibodies to epitopes of VP13/14 protein and on the gE-gI complex. The majority of sera from B virus infected macaques and Simplexvirus-infected humans competed with the less specific mAbs. These experiments produced a novel panel of mAbs that enabled B virus strain identification and confirmation of B virus infected macaques by the mAb-CE. For human sera the mAb-CE could be used only for selected cases due to the selective B virus strain-specificity of the mAbs against VP13/14 and gE/gI. To fully accomplish our aim to provide reagents for unequivocal differential diagnosis of zoonotic B virus infections, additional mAbs with a broader range of specificities is critical.
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The relative reactivity of mAbs to viruses of the Simplexvirus group was tested by tELISA.
2017Co-Authors: David Katz, Irina Patrusheva, Mugdha Vasireddi, Wei Shi, Manjunath S. Gowda, Hyuk-kyu Seoh, Chadi N. Filfili, Martin J. Wildes, Julia K HilliardAbstract:The relative reactivity of mAbs to viruses of the Simplexvirus group was tested by tELISA.
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B Virus (Macacine herpesvirus 1) Glycoprotein D Is Functional but Dispensable for Virus Entry into Macaque and Human Skin Cells
Journal of Virology, 2015Co-Authors: Ludmila Perelygina, Irina Patrusheva, Mugdha Vasireddi, Nicole Brock, Julia K HilliardAbstract:Glycoprotein D (gD) plays an essential role in cell entry of many Simplexviruses. B virus (Macacine herpesvirus 1) is closely related to herpes simplex virus 1 (HSV-1) and encodes gD, which shares more than 70% amino acid similarity with HSV-1 gD. Previously, we have demonstrated that B virus gD polyclonal antibodies were unable to neutralize B virus infectivity on epithelial cell lines, suggesting gD is not required for B virus entry into these cells. In the present study, we confirmed this finding by producing a B virus mutant, BV-ΔgDZ, in which the gD gene was replaced with a lacZ expression cassette. Recombinant plaques were selected on complementing VD60 cells expressing HSV-1 gD. Virions lacking gD were produced in Vero cells infected with BV-ΔgDZ. In contrast to HSV-1, B virus lacking gD was able to infect and form plaques on noncomplementing cell lines, including Vero, HEp-2, LLC-MK2, primary human and macaque dermal fibroblasts, and U373 human glioblastoma cells. The gD-negative BV-ΔgDZ also failed to enter entry-resistant murine B78H1 cells bearing a single gD receptor, human nectin-1, but gained the ability to enter when phenotypically supplemented with HSV-1 gD. Cell attachment and penetration rates, as well as the replication characteristics of BV-ΔgDZ in Vero cells, were almost identical to those of wild-type (wt) B virus. These observations indicate that B virus can utilize gD-independent cell entry and transmission mechanisms, in addition to generally used gD-dependent mechanisms. IMPORTANCE B virus is the only known Simplexvirus that causes zoonotic infection, resulting in approximately 80% mortality in untreated humans or in lifelong persistence with the constant threat of reactivation in survivors. Here, we report that B virus lacking the gD envelope glycoprotein infects both human and monkey cells as efficiently as wild-type B virus. These data provide evidence for a novel mechanism(s) utilized by B virus to gain access to target cells. This mechanism is different from those used by its close relatives, HSV-1 and -2, where gD is a pivotal protein in the virus entry process. The possibility remains that unidentified receptors, specific for B virus, permit virus entry into target cells through gD-independent pathways. Understanding the molecular mechanisms of B virus entry may help in developing rational therapeutic strategies for the prevention and treatment of B virus infection in both macaques and humans.
Alberto Severini - One of the best experts on this subject based on the ideXlab platform.
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Structure and sequence of the saimiriine herpesvirus 1 genome.
Virology, 2010Co-Authors: Shaun Tyler, Alberto Severini, Darla H. Black, Matthew Walker, Richard EberleAbstract:We report here the complete genome sequence of the squirrel monkey α-herpesvirus saimiriine herpesvirus 1 (HVS1). Unlike the Simplexviruses of other primate species, only the unique short region of the HVS1 genome is bounded by inverted repeats. While all Old World simian Simplexviruses characterized to date lack the herpes simplex virus RL1 (γ34.5) gene, HVS1 has an RL1 gene. HVS1 lacks several genes that are present in other primate Simplexviruses (US8.5, US10–12, UL43/43.5 and UL49A). Although the overall genome structure appears more like that of varicelloviruses, the encoded HVS1 proteins are most closely related to homologous proteins of the primate Simplexviruses. Phylogenetic analyses confirm that HVS1 is a Simplexvirus. Limited comparison of two HVS1 strains revealed a very low degree of sequence variation more typical of varicelloviruses. HVS1 is thus unique among the primate α-herpesviruses in that its genome has properties of both Simplexviruses and varicelloviruses.
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The Complete Genome Sequence of Herpesvirus Papio 2 (Cercopithecine Herpesvirus 16) Shows Evidence of Recombination Events among Various Progenitor Herpesviruses
Journal of virology, 2006Co-Authors: Shaun Tyler, Alberto SeveriniAbstract:We have sequenced the entire genome of herpesvirus papio 2 (HVP-2; Cercopithecine herpesvirus 16) strain X313, a baboon herpesvirus with close homology to other primate alphaherpesviruses, such as SA8, monkey B virus, and herpes simplex virus (HSV) type 1 and type 2. The genome of HVP-2 is 156,487 bp in length, with an overall GC content of 76.5%. The genome organization is identical to that of the other members of the genus Simplexvirus, with a long and a short unique region, each bordered by inverted repeats which end with an “a” sequence. All of the open reading frames detected in this genome were homologous and colinear with those of SA8 and B virus. The HSV gene RL1 (γ134.5; neurovirulence factor) is not present in HVP-2, as is the case for SA8 and B virus. The HVP-2 genome is 85% homologous to its closest relative, SA8. However, segment-by-segment bootstrap analysis of the genome revealed at least two regions that display closer homology to the corresponding sequences of B virus. The first region comprises the UL41 to UL44 genes, and the second region is located within the UL36 gene. We hypothesize that this localized and defined shift in homology is due to recombination events between an SA8-like progenitor of HVP-2 and a herpesvirus species more closely related to the B virus. Since some of the genes involved in these putative recombination events are determinants of virulence, a comparative analysis of their function may provide insight into the pathogenic mechanism of Simplexviruses.
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Complete genome sequence of cercopithecine herpesvirus 2 (SA8) and comparison with other Simplexviruses
Virology, 2005Co-Authors: Shaun Tyler, Geoffrey A. Peters, Alberto SeveriniAbstract:We have obtained the complete sequence of the herpesvirus simian agent 8 (SA8; cercopithecine herpesvirus 2) a baboon Simplexvirus closely related to the monkey B virus and herpes simplex virus types 1 and 2. The genome of SA8 is 150,715 bp long, with an overall G/C content of 76%, the highest among the Simplexviruses sequenced so far. The sequencing has confirmed that the genomic arrangement of SA8 is similar to that of other Simplexviruses: unique long and unique short regions bordered by two sets of inverted repeats. All genes identified in SA8 are homologous and collinear with those of the monkey B virus, including the lack of the RL1 open reading frame, a gene responsible for neurovirulence in human herpes simplex viruses. This latter finding supports the hypothesis that a different pathogenetic mechanism may have developed in human Simplexviruses, after their divergence from monkey Simplexviruses.
