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  1. Article ; Online: Influence of social determinants of health on breastfeeding intent in the United States.

    Kopp, Sarah J / Kelly, Elizabeth A / DeFranco, Emily A

    Birth (Berkeley, Calif.)

    2023  Volume 50, Issue 4, Page(s) 858–867

    Abstract: Background: Breastfeeding rates in the United States are suboptimal despite public health recommendations that infants are fed breastmilk for their first year of life. This study aimed to characterize the influence of social determinants of health on ... ...

    Abstract Background: Breastfeeding rates in the United States are suboptimal despite public health recommendations that infants are fed breastmilk for their first year of life. This study aimed to characterize the influence of social determinants of health on intended breastfeeding duration.
    Methods: This case-control study analyzed breastfeeding intent in 421 postpartum women. Data on social determinants and medical history were obtained from medical records and participant self-report. Logistic regression estimated the influence of demographic factors and social determinants on intent to breastfeed for durations of <6 months, 6-12 months, and at least 1 year.
    Results: Thirty-five percent of mothers intended to breastfeed for at least 6 months, and 15% for 1 year. Social determinants that negatively predicted breastfeeding intent included not owning transportation and living in a dangerous neighborhood (p < 0.05). Women were more likely to intend to breastfeed for 12 months if they had knowledge of breastfeeding recommendations (adjusted odds ratio [aOR] 6.19, 95% confidence interval [CI 2.67-14.34]), an identifiable medical provider (aOR 2.64 [CI 1.22-5.72]), familial support (aOR 2.80 [CI 1.01-7.80]), or were married (aOR 2.55 [CI 1.01-6.46]). Sociodemographic factors that negatively influenced breastfeeding intent included non-Hispanic Black race, no high school diploma, cigarette use, income below $20,000, fewer than five prenatal visits, and WIC or Medicaid enrollment (p < 0.05).
    Conclusions: Women who lack familial support, an identifiable healthcare provider, or knowledge of breastfeeding guidelines are less likely to intend to breastfeed. Public health initiatives should address these determinants to improve breastfeeding and infant outcomes.
    MeSH term(s) Infant ; Pregnancy ; Female ; Humans ; United States ; Breast Feeding ; Social Determinants of Health ; Case-Control Studies ; Mothers ; Prenatal Care
    Language English
    Publishing date 2023-07-03
    Publishing country United States
    Document type Journal Article
    ZDB-ID 604869-9
    ISSN 1523-536X ; 0730-7659
    ISSN (online) 1523-536X
    ISSN 0730-7659
    DOI 10.1111/birt.12740
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Age-related differences in flashbulb memories: A meta-analysis.

    Kopp, Sarah J / Sockol, Laura E / Multhaup, Kristi S

    Psychology and aging

    2020  Volume 35, Issue 4, Page(s) 459–472

    Abstract: Recent meta-analyses reveal age-related declines in short-term memory (STM), working memory, associative memory, prospective memory, face memory, recognition, and recall. The present meta-analyses extend this work beyond predominantly laboratory-based ... ...

    Abstract Recent meta-analyses reveal age-related declines in short-term memory (STM), working memory, associative memory, prospective memory, face memory, recognition, and recall. The present meta-analyses extend this work beyond predominantly laboratory-based tasks to a naturalistic phenomenon.
    MeSH term(s) Adult ; Age Factors ; Aged ; Cross-Sectional Studies ; Female ; Humans ; Male ; Memory, Short-Term/physiology ; Middle Aged
    Language English
    Publishing date 2020-04-20
    Publishing country United States
    Document type Journal Article ; Meta-Analysis
    ZDB-ID 635596-1
    ISSN 1939-1498 ; 0882-7974
    ISSN (online) 1939-1498
    ISSN 0882-7974
    DOI 10.1037/pag0000467
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Erratum for Riccio et al., "Characterization of Sex Differences in Ocular Herpes Simplex Virus 1 Infection and Herpes Stromal Keratitis Pathogenesis of Wild-Type and Herpesvirus Entry Mediator Knockout Mice".

    Riccio, Rachel E / Park, Seo J / Longnecker, Richard / Kopp, Sarah J

    mSphere

    2019  Volume 4, Issue 3

    Language English
    Publishing date 2019-05-15
    Publishing country United States
    Document type Journal Article ; Published Erratum
    ISSN 2379-5042
    ISSN (online) 2379-5042
    DOI 10.1128/mSphere.00322-19
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Characterization of Sex Differences in Ocular Herpes Simplex Virus 1 Infection and Herpes Stromal Keratitis Pathogenesis of Wild-Type and Herpesvirus Entry Mediator Knockout Mice.

    Riccio, Rachel E / Park, Seo J / Longnecker, Richard / Kopp, Sarah J

    mSphere

    2019  Volume 4, Issue 2

    Abstract: Sex differences related to immune response and inflammation play a role in the susceptibility and pathogenesis of a variety of viral infections and disease (S. L. Klein, Bioessays 34:1050-1059, 2012, https://doi.org/10.1002/bies.201200099). Herpes ... ...

    Abstract Sex differences related to immune response and inflammation play a role in the susceptibility and pathogenesis of a variety of viral infections and disease (S. L. Klein, Bioessays 34:1050-1059, 2012, https://doi.org/10.1002/bies.201200099). Herpes simplex virus 1 (HSV-1) causes chronic inflammatory disease in the cornea, an immune-privileged tissue, resulting in irreversible damage and blindness in affected individuals (A. Rowe, A. St Leger, S. Jeon, D. K. Dhaliwal, et al., Prog Retin Eye Res 32:88-101, 2013, https://doi.org/10.1016/j.preteyeres.2012.08.002). Our research focuses on the role of herpesvirus entry mediator (HVEM) as an immune regulator during ocular HSV-1 infection. Mice lacking HVEM (HVEM knockout [KO] mice) exhibit lower levels of immune cell infiltrates and less severe ocular disease in the cornea than wild-type (WT) mice. As sex differences contribute to pathogenesis in many inflammatory diseases, we tested whether sex acts as a biological variable in the immune response to HSV-1 infection and herpes stromal keratitis (HSK) pathogenesis. Adult male and female WT and HVEM KO mice were inoculated with HSV-1 via corneal scarification and monitored daily for disease course. Viral titers were determined, and immune cell infiltrates were collected and analyzed. Our results indicated no significant differences in viral titers in tear film or affected tissues, in immune cell infiltration, or in clinical symptoms between males and females of either genotype. These results suggest that sex is not a significant biological variable in this experimental model and that male and female mice of the C57BL/6 background can be used similarly in studies of ocular HSV-1 pathogenesis.
    MeSH term(s) Animals ; Eye/pathology ; Eye/virology ; Female ; Gene Knockout Techniques ; Herpesvirus 1, Human/immunology ; Inflammation ; Keratitis, Herpetic/immunology ; Keratitis, Herpetic/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Receptors, Tumor Necrosis Factor, Member 14/genetics ; Sex Factors ; Viral Load
    Chemical Substances Receptors, Tumor Necrosis Factor, Member 14
    Language English
    Publishing date 2019-03-27
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ISSN 2379-5042
    ISSN (online) 2379-5042
    DOI 10.1128/mSphere.00073-19
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Herpesvirus Entry Mediator Binding Partners Mediate Immunopathogenesis of Ocular Herpes Simplex Virus 1 Infection.

    Park, Seo J / Riccio, Rachel E / Kopp, Sarah J / Ifergan, Igal / Miller, Stephen D / Longnecker, Richard

    mBio

    2020  Volume 11, Issue 3

    Abstract: Ocular herpes simplex virus 1 (HSV-1) infection leads to an immunopathogenic disease called herpes stromal keratitis (HSK), in which ... ...

    Abstract Ocular herpes simplex virus 1 (HSV-1) infection leads to an immunopathogenic disease called herpes stromal keratitis (HSK), in which CD4
    MeSH term(s) Animals ; Cornea/immunology ; Cornea/pathology ; Cornea/virology ; Disease Models, Animal ; Female ; Herpesvirus 1, Human/immunology ; Herpesvirus 1, Human/physiology ; Host Microbial Interactions/immunology ; Inflammation ; Keratitis, Herpetic/immunology ; Keratitis, Herpetic/pathology ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Receptors, Tumor Necrosis Factor, Member 14/immunology ; Receptors, Tumor Necrosis Factor, Member 14/physiology ; Signal Transduction ; T-Lymphocytes/immunology ; Virus Internalization
    Chemical Substances Receptors, Tumor Necrosis Factor, Member 14
    Language English
    Publishing date 2020-05-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2557172-2
    ISSN 2150-7511 ; 2161-2129
    ISSN (online) 2150-7511
    ISSN 2161-2129
    DOI 10.1128/mBio.00790-20
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Structure-Based Mutations in the Herpes Simplex Virus 1 Glycoprotein B Ectodomain Arm Impart a Slow-Entry Phenotype.

    Fan, Qing / Kopp, Sarah J / Connolly, Sarah A / Longnecker, Richard

    mBio

    2017  Volume 8, Issue 3

    Abstract: Glycoprotein B (gB) is the conserved herpesvirus fusion protein, and it is required for the entry of herpesviruses. The structure of the postfusion conformation of gB has been solved for several herpesviruses; however, the gB prefusion crystal structure ... ...

    Abstract Glycoprotein B (gB) is the conserved herpesvirus fusion protein, and it is required for the entry of herpesviruses. The structure of the postfusion conformation of gB has been solved for several herpesviruses; however, the gB prefusion crystal structure and the details of how the protein refolds from a prefusion to a postfusion form to mediate fusion have not been determined. Using structure-based mutagenesis, we previously reported that three mutations (I671A, H681A, and F683A) in the C-terminal arm of the gB ectodomain greatly reduced cell-cell fusion. This fusion deficit could be rescued by the addition of a hyperfusogenic mutation, suggesting that the gB triple mutant was not misfolded. Using a bacterial artificial chromosome (BAC), we constructed two independent herpes simplex virus 1 mutant strains (gB 3A) carrying the three arm mutations. The gB 3A viruses have 200-fold smaller plaques than the wild-type virus and demonstrate remarkably delayed entry into cells. Single-step and multistep growth curves show that gB 3A viruses have delayed replication kinetics. Interestingly, incubation at 40°C promoted the entry of the gB 3A viruses. We propose that the gB 3A viruses' entry deficit is due to a loss of interactions between residues in the gB C-terminal arm and the coiled-coil core of gB. The results suggest that the triple alanine mutation may destabilize the postfusion gB conformation and/or stabilize the prefusion gB conformation and that exposure to elevated temperatures can overcome the defect in gB 3A viruses.
    MeSH term(s) Animals ; CHO Cells ; Chromosomes, Artificial, Bacterial ; Cricetulus ; Herpesvirus 1, Human/genetics ; Herpesvirus 1, Human/physiology ; Models, Molecular ; Mutagenesis ; Mutation ; Phenotype ; Protein Conformation ; Viral Envelope Proteins/chemistry ; Viral Envelope Proteins/genetics ; Viral Envelope Proteins/metabolism ; Virus Internalization
    Chemical Substances Viral Envelope Proteins ; glycoprotein B, human herpesvirus 1
    Keywords covid19
    Language English
    Publishing date 2017-05-16
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2557172-2
    ISSN 2150-7511 ; 2161-2129
    ISSN (online) 2150-7511
    ISSN 2161-2129
    DOI 10.1128/mBio.00614-17
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Natural Selection of Glycoprotein B Mutations That Rescue the Small-Plaque Phenotype of a Fusion-Impaired Herpes Simplex Virus Mutant.

    Fan, Qing / Kopp, Sarah J / Byskosh, Nina C / Connolly, Sarah A / Longnecker, Richard

    mBio

    2018  Volume 9, Issue 5

    Abstract: Glycoprotein B (gB) is a conserved viral fusion protein that is required for herpesvirus entry. To mediate fusion with the cellular membrane, gB refolds from a prefusion to a postfusion conformation. We hypothesize that an interaction between the C- ... ...

    Abstract Glycoprotein B (gB) is a conserved viral fusion protein that is required for herpesvirus entry. To mediate fusion with the cellular membrane, gB refolds from a prefusion to a postfusion conformation. We hypothesize that an interaction between the C-terminal arm and the central coiled coil of the herpes simplex virus 1 (HSV-1) gB ectodomain is critical for fusion. We previously reported that three mutations in the C-terminal arm (I671A/H681A/F683A, called gB3A) greatly reduced cell-cell fusion and that virus carrying these mutations had a small-plaque phenotype and delayed entry into cells. By serially passaging gB3A virus, we selected three revertant viruses with larger plaques. These revertant viruses acquired mutations in gB that restore the fusion function of gB3A, including gB-A683V, gB-S383F/G645R/V705I/A855V, and gB-T509M/N709H. V705I and N709H are novel mutations that map to the portion of domain V that enters domain I in the postfusion structure. S383F, G645R, and T509M are novel mutations that map to an intersection of three domains in a prefusion model of gB. We introduced these second-site mutations individually and in combination into wild-type gB and gB3A to examine the impact of the mutations on fusion and expression. V705I and A855V (a known hyperfusogenic mutation) restored the fusion function of gB3A, whereas S383F and G645R dampened fusion and T509M and N709H worked in concert to restore gB3A fusion. The results identify two regions in the gB ectodomain that modulate the fusion activity of gB, potentially by impacting intramolecular interactions and stability of the prefusion and/or postfusion gB trimer.
    MeSH term(s) Animals ; CHO Cells ; Cricetinae ; Cricetulus ; Herpesvirus 1, Human/genetics ; Herpesvirus 1, Human/physiology ; Models, Molecular ; Mutation ; Phenotype ; Protein Conformation ; Protein Refolding ; Selection, Genetic ; Viral Envelope Proteins/genetics ; Viral Envelope Proteins/metabolism ; Viral Fusion Proteins/genetics ; Virus Internalization
    Chemical Substances Viral Envelope Proteins ; Viral Fusion Proteins ; glycoprotein B, Simplexvirus
    Language English
    Publishing date 2018-10-16
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2557172-2
    ISSN 2150-7511 ; 2161-2129
    ISSN (online) 2150-7511
    ISSN 2161-2129
    DOI 10.1128/mBio.01948-18
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Herpesvirus entry mediator is a serotype specific determinant of pathogenesis in ocular herpes.

    Karaba, Andrew H / Kopp, Sarah J / Longnecker, Richard

    Proceedings of the National Academy of Sciences of the United States of America

    2012  Volume 109, Issue 50, Page(s) 20649–20654

    Abstract: Infection with herpes simplex virus type 1 (HSV-1) and HSV-2 is initiated by viral glycoprotein D (gD) binding to a receptor on the host cell. Two receptors, herpesvirus entry mediator (HVEM) and nectin-1, mediate entry in murine models of HSV-1 and HSV- ... ...

    Abstract Infection with herpes simplex virus type 1 (HSV-1) and HSV-2 is initiated by viral glycoprotein D (gD) binding to a receptor on the host cell. Two receptors, herpesvirus entry mediator (HVEM) and nectin-1, mediate entry in murine models of HSV-1 and HSV-2. HVEM is dispensable for HSV-2 infection of the vagina and brain, but is required for WT pathogenesis of HSV-1 infection of the cornea. By challenging WT and HVEM KO mice with multiple strains of HSV-1 and HSV-2, we demonstrate that without HVEM, all HSV-1 strains tested do not replicate well in the cornea and infection does not result in severe symptoms, as observed in WT mice. In contrast, all HSV-2 strains tested had no requirement for HVEM to replicate to WT levels in the cornea and still cause severe disease. These findings imply that HSV-2 does not require HVEM to cause disease regardless of route of entry, but HVEM must be present for HSV-1 to cause full pathogenesis in the eye. These findings uncover a unique role for HVEM in mediating HSV-1 infection in an area innervated by the trigeminal ganglion and may explain why the presence of HVEM can lead to severe inflammation in the cornea. Thus, the dependence on HVEM is a dividing point between HSV-1 and HSV-2 that evolved to infect areas innervated by different sensory ganglia.
    MeSH term(s) Animals ; Disease Models, Animal ; Female ; Herpes Genitalis/virology ; Herpesvirus 1, Human/classification ; Herpesvirus 1, Human/pathogenicity ; Herpesvirus 2, Human/classification ; Herpesvirus 2, Human/pathogenicity ; Herpesvirus 2, Human/physiology ; Host-Pathogen Interactions ; Keratitis, Herpetic/etiology ; Keratitis, Herpetic/virology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Receptors, Tumor Necrosis Factor, Member 14/deficiency ; Receptors, Tumor Necrosis Factor, Member 14/genetics ; Receptors, Tumor Necrosis Factor, Member 14/physiology ; Serotyping ; Species Specificity ; Virulence/physiology ; Virus Replication
    Chemical Substances Receptors, Tumor Necrosis Factor, Member 14
    Language English
    Publishing date 2012-11-26
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.1216967109
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  9. Article ; Online: Herpes simplex virus-2 glycoprotein interaction with HVEM influences virus-specific recall cellular responses at the mucosa.

    Kopp, Sarah J / Storti, Christopher S / Muller, William J

    Clinical & developmental immunology

    2012  Volume 2012, Page(s) 284104

    Abstract: Infection of susceptible cells by herpes simplex virus (HSV) requires the interaction of the HSV gD glycoprotein with one of two principal entry receptors, herpes virus entry mediator (HVEM) or nectins. HVEM naturally functions in immune signaling, and ... ...

    Abstract Infection of susceptible cells by herpes simplex virus (HSV) requires the interaction of the HSV gD glycoprotein with one of two principal entry receptors, herpes virus entry mediator (HVEM) or nectins. HVEM naturally functions in immune signaling, and the gD-HVEM interaction alters innate signaling early after mucosal infection. We investigated whether the gD-HVEM interaction during priming changes lymphocyte recall responses in the murine intravaginal model. Mice were primed with attenuated HSV-2 expressing wild-type gD or mutant gD unable to engage HVEM and challenged 32 days later with virulent HSV-2 expressing wild-type gD. HSV-specific CD8(+) T cells were decreased at the genital mucosa during the recall response after priming with virus unable to engage HVEM but did not differ in draining lymph nodes. CD4(+) T cells, which are critical for entry of HSV-specific CD8(+) T cells into mucosa in acute infection, did not differ between the two groups in either tissue. An inverse association between Foxp3(+) CD4(+) regulatory T cells and CD8(+) infiltration into the mucosa was not statistically significant. CXCR3 surface expression was not significantly different among different lymphocyte subsets. We conclude that engagement of HVEM during the acute phase of HSV infection influences the antiviral CD8(+) recall response by an unexplained mechanism.
    MeSH term(s) Animals ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/virology ; Cell Adhesion Molecules/metabolism ; Cells, Cultured ; Disease Models, Animal ; Female ; Herpes Genitalis/immunology ; Humans ; Immunity, Mucosal ; Immunologic Memory ; Mice ; Mutation/genetics ; Nectins ; Protein Binding/genetics ; Signal Transduction/immunology ; Simplexvirus/immunology ; Simplexvirus/pathogenicity ; Transgenes/genetics ; Vagina/immunology ; Vagina/virology ; Viral Envelope Proteins/genetics ; Viral Envelope Proteins/metabolism
    Chemical Substances Cell Adhesion Molecules ; Nectins ; Viral Envelope Proteins ; glycoprotein D-herpes simplex virus type 2
    Language English
    Publishing date 2012-05-14
    Publishing country Egypt
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2119646-1
    ISSN 1740-2530 ; 1740-2522
    ISSN (online) 1740-2530
    ISSN 1740-2522
    DOI 10.1155/2012/284104
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Herpesvirus entry mediator and nectin-1 mediate herpes simplex virus 1 infection of the murine cornea.

    Karaba, Andrew H / Kopp, Sarah J / Longnecker, Richard

    Journal of virology

    2011  Volume 85, Issue 19, Page(s) 10041–10047

    Abstract: Herpes simplex virus 1 (HSV-1) is a ubiquitous human pathogen that enters cells by the receptor-mediated fusion of the viral envelope with a host cell membrane. The envelope glycoprotein gD of HSV must bind to one of its receptors for entry to take place. ...

    Abstract Herpes simplex virus 1 (HSV-1) is a ubiquitous human pathogen that enters cells by the receptor-mediated fusion of the viral envelope with a host cell membrane. The envelope glycoprotein gD of HSV must bind to one of its receptors for entry to take place. Recent studies using knockout (KO) mice demonstrated that the gD receptors herpesvirus entry mediator (HVEM) and nectin-1 are the primary entry receptors for HSV-2 in the mouse vagina and brain. Nectin-1 was most crucial for the neuronal spread of HSV-2, particularly in the brain. HVEM was dispensable for infection in these models, but when both HVEM and nectin-1 were absent, infection was completely prevented. We sought to determine the receptor requirements of HSV-1 in an ocular model of infection using knockout mice. Wild-type, HVEM KO, nectin-1 KO, and HVEM/nectin-1 double-KO mice were infected via corneal scarification and monitored for clinical signs of infection and viral replication in various tissues. We report that either HVEM or nectin-1 must be present for HSV-1 infection of the cornea. Additionally, we observed that the infection was attenuated in both HVEM KO and nectin-1 KO mice. This is in contrast to what was reported for studies of HSV-2 in vagina and brain and suggests that receptor requirements for HSV vary depending on the route of inoculation and/or serotype.
    MeSH term(s) Animals ; Cell Adhesion Molecules/genetics ; Cell Adhesion Molecules/metabolism ; Cornea/virology ; Disease Models, Animal ; Eye Diseases/pathology ; Eye Diseases/virology ; Herpesviridae Infections/pathology ; Herpesviridae Infections/virology ; Herpesvirus 1, Human/pathogenicity ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Nectins ; Receptors, Tumor Necrosis Factor, Member 14/genetics ; Receptors, Tumor Necrosis Factor, Member 14/metabolism ; Receptors, Virus/genetics ; Receptors, Virus/metabolism ; Rodent Diseases/pathology ; Rodent Diseases/virology ; Virus Internalization
    Chemical Substances Cell Adhesion Molecules ; NECTIN1 protein, human ; Nectin1 protein, mouse ; Nectins ; Receptors, Tumor Necrosis Factor, Member 14 ; Receptors, Virus
    Language English
    Publishing date 2011-07-27
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 80174-4
    ISSN 1098-5514 ; 0022-538X
    ISSN (online) 1098-5514
    ISSN 0022-538X
    DOI 10.1128/JVI.05445-11
    Database MEDical Literature Analysis and Retrieval System OnLINE

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