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Article ; Online: Persistent CD8

LaVergne, Stephanie M / Dutt, Taru S / McFann, Kim / Baxter, Bridget A / Webb, Tracy L / Berry, Kailey / Tipton, Maddy / Stromberg, Sophia / Sullivan, Brian M / Dunn, Julie / Henao-Tamayo, Marcela / Ryan, Elizabeth P

Frontiers in immunology

2024 Volume 14, Page(s) 1303971

Abstract: Introduction: Post-acute sequelae of COVID-19 affects the quality of life of many COVID-19 survivors, yet the etiology of post-acute sequelae of COVID-19 remains unknown. We aimed to determine if persistent inflammation and ongoing T-cell activation ... ...

Abstract	Introduction: Post-acute sequelae of COVID-19 affects the quality of life of many COVID-19 survivors, yet the etiology of post-acute sequelae of COVID-19 remains unknown. We aimed to determine if persistent inflammation and ongoing T-cell activation during convalescence were a contributing factor to the pathogenesis of post-acute sequelae of COVID-19. Methods: We evaluated 67 individuals diagnosed with COVID-19 by nasopharyngeal polymerase chain reaction for persistent symptoms during convalescence at separate time points occurring up to 180 days post-diagnosis. Fifty-two of these individuals were evaluated longitudinally. We obtained whole blood samples at each study visit, isolated peripheral blood mononuclear cells, and stained for multiple T cell activation markers for flow cytometry analysis. The activation states of participants' CD4 Results: Overall, we found that participants with persistent symptoms had significantly higher levels of inflammation at multiple time points during convalescence when compared to those who fully recovered from COVID-19. Participants with persistent dyspnea, forgetfulness, confusion, and chest pain had significantly higher levels of proliferating effector T-cells (CD8 Discussion: These findings suggest continued CD8+ T-cell activation following SARS-CoV-2 infection in adults experiencing post-acute sequelae of COVID-19 and that the increase in T regulatory cells for a subset of these patients represents the ongoing attempt by the host to reduce inflammation.
MeSH term(s)	Humans ; Adult ; COVID-19/complications ; CD8-Positive T-Lymphocytes ; Retrospective Studies ; Convalescence ; Leukocytes, Mononuclear ; Ki-67 Antigen ; Post-Acute COVID-19 Syndrome ; Quality of Life ; SARS-CoV-2 ; CD4-Positive T-Lymphocytes ; Cohort Studies ; CD3 Complex ; Disease Progression ; Inflammation ; Cell Proliferation ; Survivors ; Dyspnea ; Chest Pain
Chemical Substances	Ki-67 Antigen ; CD3 Complex
Language	English
Publishing date	2024-01-23
Publishing country	Switzerland
Document type	Observational Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1303971
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Article ; Online: Expansion of CD8+ T cell population in Lassa virus survivors with low T cell precursor frequency reveals durable immune response in most survivors.

LaVergne, Stephanie M / Sakabe, Saori / Momoh, Mambu / Kanneh, Lansana / Bond, Nell / Garry, Robert F / Grant, Donald S / de la Torre, Juan Carlos / Oldstone, Michael B A / Schieffelin, John S / Sullivan, Brian M

PLoS neglected tropical diseases

2022 Volume 16, Issue 11, Page(s) e0010882

Abstract: Introduction: Lassa virus is a priority pathogen for vaccine research and development, however the duration of cellular immunity and protection in Lassa fever (LF) survivors remains unclear.: Methods: We investigated Lassa virus specific CD8+ T cell ... ...

Abstract	Introduction: Lassa virus is a priority pathogen for vaccine research and development, however the duration of cellular immunity and protection in Lassa fever (LF) survivors remains unclear. Methods: We investigated Lassa virus specific CD8+ T cell responses in 93 LF survivors. Peripheral blood mononuclear cells from these individuals were infected with recombinant vesicular stomatitis virus encoding Lassa virus antigens and virus specific T cell responses were measured after 18-hour incubation. Participants who had undetectable CD8+ T cell response underwent further analysis using a 10-day T cell proliferation assays to evaluate for low T cell precursor frequency. Results: Forty-five of the 93 LF survivors did not have a Lassa virus specific CD8+ T cell response. Of those with responses and a known date of onset of LF (N = 11), 9 had LF within the last ten years. Most participants without a measurable CD8+ T cell response were more than 10 years removed from a clinical history of LF (N = 14/16). Fourteen of 21 patients (67%) with undetectable CD8+ T cell response had a measurable Lassa virus specific CD8+ T cell response with the 10-day assay. Discussion: Despite reports of strong CD8+ T cell responses during acute Lassa virus infection, circulating Lassa virus-specific CD8+ T cells declined to undetectable levels in most Lassa fever survivors after ten years when evaluated with an 18-hour T cell stimulation. However, when Lassa virus-specific T cells were expanded prior to restimulation, a Lassa virus-specific CD8+ T cell response could be detected in many if the samples that were negative in the 18-hour stimulation assay, suggesting that prolonged cellular immunity does exist in Lassa fever survivors at low frequencies.
MeSH term(s)	Humans ; Lassa virus ; Lassa Fever ; Leukocytes, Mononuclear ; Precursor Cells, T-Lymphoid ; Immunity ; CD8-Positive T-Lymphocytes
Language	English
Publishing date	2022-11-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2429704-5
ISSN	1935-2735 ; 1935-2735
ISSN (online)	1935-2735
ISSN	1935-2735
DOI	10.1371/journal.pntd.0010882
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Article ; Online: Inflammatory platelet production stimulated by tyrosyl-tRNA synthetase mimicking viral infection.

Morodomi, Yosuke / Kanaji, Sachiko / Sullivan, Brian M / Zarpellon, Alessandro / Orje, Jennifer N / Won, Eric / Shapiro, Ryan / Yang, Xiang-Lei / Ruf, Wolfram / Schimmel, Paul / Ruggeri, Zaverio M / Kanaji, Taisuke

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

2022 Volume 119, Issue 48, Page(s) e2212659119

Abstract: Platelets play a role not only in hemostasis and thrombosis, but also in inflammation and innate immunity. We previously reported that an activated form of tyrosyl-tRNA synthetase ( ... ...

Abstract	Platelets play a role not only in hemostasis and thrombosis, but also in inflammation and innate immunity. We previously reported that an activated form of tyrosyl-tRNA synthetase (YRS
MeSH term(s)	Mice ; Animals ; Thrombopoiesis ; Tyrosine-tRNA Ligase ; Thrombocytopenia ; Virus Diseases ; Thrombosis ; Mice, Transgenic ; Spinocerebellar Ataxias
Chemical Substances	Tyrosine-tRNA Ligase (EC 6.1.1.1)
Language	English
Publishing date	2022-11-21
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.2212659119
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Article ; Online: The U24 protein from human herpesvirus 6 and 7 affects endocytic recycling.

Sullivan, Brian M / Coscoy, Laurent

Journal of virology

2009 Volume 84, Issue 3, Page(s) 1265–1275

Abstract: Modulation of T-cell receptor expression and signaling is essential to the survival of many viruses. The U24 protein expressed by human herpesvirus 6A, a ubiquitous human pathogen, has been previously shown to downregulate the T-cell receptor. Here, we ... ...

Abstract	Modulation of T-cell receptor expression and signaling is essential to the survival of many viruses. The U24 protein expressed by human herpesvirus 6A, a ubiquitous human pathogen, has been previously shown to downregulate the T-cell receptor. Here, we show that U24 also mediates cell surface downregulation of a canonical early endosomal recycling receptor, the transferrin receptor, indicating that this viral protein acts by blocking early endosomal recycling. We present evidence that U24 is a C-tail-anchored protein that is dependent for its function on TRC40/Asna-1, a component of a posttranslational membrane insertion pathway. Finally, we find that U24 proteins from other roseoloviruses have a similar genetic organization and a conserved function that is dependent on a proline-rich motif. Inhibition of a basic cellular process by U24 has interesting implications not only for the pathogenicity of roseoloviruses but also for our understanding of the biology of endosomal transport.
MeSH term(s)	Amino Acid Sequence ; Blotting, Western ; Cell Line ; Down-Regulation ; Electrophoresis, Polyacrylamide Gel ; Endocytosis/physiology ; Herpesvirus 6, Human/metabolism ; Herpesvirus 7, Human/metabolism ; Humans ; Molecular Sequence Data ; Receptors, Transferrin/metabolism ; Sequence Homology, Amino Acid ; Viral Proteins/chemistry ; Viral Proteins/physiology
Chemical Substances	Receptors, Transferrin ; Viral Proteins
Language	English
Publishing date	2009-11-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/JVI.01775-09
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Article ; Online: A unique variant of lymphocytic choriomeningitis virus that induces pheromone binding protein MUP: Critical role for CTL.

Ware, Brian C / Sullivan, Brian M / LaVergne, Stephanie / Marro, Brett S / Egashira, Toru / Campbell, Kevin P / Elder, John / Oldstone, Michael B A

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

2019 Volume 116, Issue 36, Page(s) 18001–18008

Abstract: Lymphocytic choriomeningitis virus (LCMV) WE variant 2.2 (v2.2) generated a high level of the major mouse urinary protein: MUP. Mice infected with LCMV WE v54, which differed from v2.2 by a single amino acid in the viral glycoprotein, failed to generate ... ...

Abstract	Lymphocytic choriomeningitis virus (LCMV) WE variant 2.2 (v2.2) generated a high level of the major mouse urinary protein: MUP. Mice infected with LCMV WE v54, which differed from v2.2 by a single amino acid in the viral glycoprotein, failed to generate MUP above baseline levels found in uninfected controls. Variant 54 bound at 2.5 logs higher affinity to the LCMV receptor α-dystroglycan (α-DG) than v2.2 and entered α-DG-expressing but not α-DG-null cells. Variant 2.2 infected both α-DG-null or -expressing cells. Variant 54 infected more dendritic cells, generated a negligible CD8 T cell response, and caused a persistent infection, while v2.2 generated cytotoxic T lymphocytes (CTLs) and cleared virus within 10 days. By 20 days postinfection and through the 80-day observation period, significantly higher amounts of MUP were found in v2.2-infected mice. Production of MUP was dependent on virus-specific CTL as deletion of such cells aborted MUP production. Furthermore, MUP production was not elevated in v2.2 persistently infected mice unless virus was cleared following transfer of virus-specific CTL.
MeSH term(s)	Animals ; CD8-Positive T-Lymphocytes/immunology ; Dystroglycans/immunology ; Gene Expression Regulation/immunology ; Lymphocytic Choriomeningitis/immunology ; Lymphocytic Choriomeningitis/pathology ; Lymphocytic choriomeningitis virus/immunology ; Mice ; Proteins/immunology
Chemical Substances	Dag1 protein, mouse ; Proteins ; major urinary proteins ; Dystroglycans (146888-27-9)
Language	English
Publishing date	2019-08-19
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.1907070116
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Article ; Online: Endotheliopathy and Platelet Dysfunction as Hallmarks of Fatal Lassa Fever.

Horton, Lucy E / Cross, Robert W / Hartnett, Jessica N / Engel, Emily J / Sakabe, Saori / Goba, Augustine / Momoh, Mambu / Sandi, John Demby / Geisbert, Thomas W / Garry, Robert F / Schieffelin, John S / Grant, Donald S / Sullivan, Brian M

Emerging infectious diseases

2021 Volume 26, Issue 11, Page(s) 2625–2637

Abstract: Lassa fever (LF) causes multisystem disease and has a fatality rate <70%. Severe cases exhibit abnormal coagulation, endothelial barrier disruption, and dysfunctional platelet aggregation but the underlying mechanisms remain poorly understood. In Sierra ... ...

Abstract	Lassa fever (LF) causes multisystem disease and has a fatality rate <70%. Severe cases exhibit abnormal coagulation, endothelial barrier disruption, and dysfunctional platelet aggregation but the underlying mechanisms remain poorly understood. In Sierra Leone during 2015-2018, we assessed LF patients' day-of-admission plasma samples for levels of proteins necessary for coagulation, fibrinolysis, and platelet function. P-selectin, soluble endothelial protein C receptor, soluble thrombomodulin, plasminogen activator inhibitor 1, ADAMTS-13, von Willebrand factor, tissue factor, soluble intercellular adhesion molecule 1, and vascular cell adhesion molecule 1 were more elevated in LF patients than in controls. Endothelial protein C receptor, thrombomodulin, intercellular adhesion molecule 1, plasminogen activator inhibitor 1, D-dimer, and hepatocyte growth factor were higher in fatal than nonfatal LF cases. Platelet disaggregation occurred only in samples from fatal LF cases. The impaired homeostasis and platelet dysfunction implicate alterations in the protein C pathway, which might contribute to the loss of endothelial barrier function in fatal infections.
MeSH term(s)	Adolescent ; Adult ; Aged ; Blood Coagulation ; Blood Platelets/pathology ; Child ; Child, Preschool ; Endothelium/physiopathology ; Female ; Fibrinolysis ; Humans ; Infant ; Lassa Fever/diagnosis ; Lassa Fever/epidemiology ; Male ; Middle Aged ; Sierra Leone ; Young Adult
Language	English
Publishing date	2021-02-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1380686-5
ISSN	1080-6059 ; 1080-6040
ISSN (online)	1080-6059
ISSN	1080-6040
DOI	10.3201/eid2611.191694
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Article ; Online: The High Degree of Sequence Plasticity of the Arenavirus Noncoding Intergenic Region (IGR) Enables the Use of a Nonviral Universal Synthetic IGR To Attenuate Arenaviruses.

Iwasaki, Masaharu / Cubitt, Beatrice / Sullivan, Brian M / de la Torre, Juan C

Journal of virology

2016 Volume 90, Issue 6, Page(s) 3187–3197

Abstract: Unlabelled: Hemorrhagic fever arenaviruses (HFAs) pose important public health problems in regions where they are endemic. Concerns about human-pathogenic arenaviruses are exacerbated because of the lack of FDA-licensed arenavirus vaccines and because ... ...

Abstract	Unlabelled: Hemorrhagic fever arenaviruses (HFAs) pose important public health problems in regions where they are endemic. Concerns about human-pathogenic arenaviruses are exacerbated because of the lack of FDA-licensed arenavirus vaccines and because current antiarenaviral therapy is limited to an off-label use of ribavirin that is only partially effective. We have recently shown that the noncoding intergenic region (IGR) present in each arenavirus genome segment, the S and L segments (S-IGR and L-IGR, respectively), plays important roles in the control of virus protein expression and that this knowledge could be harnessed for the development of live-attenuated vaccine strains to combat HFAs. In this study, we further investigated the sequence plasticity of the arenavirus IGR. We demonstrate that recombinants of the prototypic arenavirus lymphocytic choriomeningitis virus (rLCMVs), whose S-IGRs were replaced by the S-IGR of Lassa virus (LASV) or an entirely nonviral S-IGR-like sequence (Ssyn), are viable, indicating that the function of S-IGR tolerates a high degree of sequence plasticity. In addition, rLCMVs whose L-IGRs were replaced by Ssyn or S-IGRs of the very distantly related reptarenavirus Golden Gate virus (GGV) were viable and severely attenuated in vivo but able to elicit protective immunity against a lethal challenge with wild-type LCMV. Our findings indicate that replacement of L-IGR by a nonviral Ssyn could serve as a universal molecular determinant of arenavirus attenuation. Importance: Hemorrhagic fever arenaviruses (HFAs) cause high rates of morbidity and mortality and pose important public health problems in regions where they are endemic. Implementation of live-attenuated vaccines (LAVs) will represent a major step to combat HFAs. Here we document that the arenavirus noncoding intergenic region (IGR) has a high degree of plasticity compatible with virus viability. This observation led us to generate recombinant LCMVs containing nonviral synthetic IGRs. These rLCMVs were severely attenuated in vivo but able to elicit protective immunity against a lethal challenge with wild-type LCMV. These nonviral synthetic IGRs can be used as universal molecular determinants of arenavirus attenuation for the rapid development of safe and effective, as well as stable, LAVs to combat HFA.
MeSH term(s)	Animals ; Arenaviridae Infections/pathology ; Arenaviridae Infections/prevention & control ; DNA, Intergenic ; Disease Models, Animal ; Lassa virus/genetics ; Lymphocytic choriomeningitis virus/genetics ; Lymphocytic choriomeningitis virus/pathogenicity ; Lymphocytic choriomeningitis virus/physiology ; Mice, Inbred C57BL ; Microbial Viability ; Mutagenesis, Insertional ; Recombination, Genetic ; Survival Analysis ; Vaccines, Attenuated/administration & dosage ; Vaccines, Attenuated/genetics ; Vaccines, Attenuated/immunology ; Viral Vaccines/administration & dosage ; Viral Vaccines/genetics ; Viral Vaccines/immunology
Chemical Substances	DNA, Intergenic ; Vaccines, Attenuated ; Viral Vaccines
Language	English
Publishing date	2016-01-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/JVI.03145-15
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Article ; Online: Downregulation of the T-cell receptor complex and impairment of T-cell activation by human herpesvirus 6 u24 protein.

Sullivan, Brian M / Coscoy, Laurent

Journal of virology

2007 Volume 82, Issue 2, Page(s) 602–608

Abstract: We have performed a screen aimed at identifying human herpesvirus 6 (HHV-6)-encoded proteins that modulate immune recognition. Here we show that the U24 protein encoded by HHV-6 variant A downregulates cell surface expression of the T-cell receptor (TCR)/ ...

Abstract	We have performed a screen aimed at identifying human herpesvirus 6 (HHV-6)-encoded proteins that modulate immune recognition. Here we show that the U24 protein encoded by HHV-6 variant A downregulates cell surface expression of the T-cell receptor (TCR)/CD3 complex, a complex essential to T-cell activation and the generation of an immune adaptive response. In the presence of U24, the TCR/CD3 complex is endocytosed but is not recycled back to the plasma membrane. Instead, it accumulates in early and late endosomes. Interestingly, whereas CD3 downregulation from the cell surface is normally associated with T-cell activation, U24 downregulates CD3 independently of T-cell activation. Moreover, we found that U24-expressing T cells are resistant to activation by antigen-presenting cells. HHV-6 has evolved a unique mechanism of inhibition of T-cell activation that may impair the establishment of an adaptive immune response. Furthermore, lymphocyte activation creates an environment favorable to the reactivation and replication of lymphotropic herpesviruses. Thus, by inhibiting T-cell activation, HHV-6 might limit its reactivation and thus minimize immune recognition.
MeSH term(s)	Antigen-Presenting Cells/immunology ; Cell Membrane/chemistry ; Down-Regulation ; Endoplasmic Reticulum/chemistry ; Herpesvirus 6, Human/immunology ; Humans ; Lymphocyte Activation ; Receptors, Antigen, T-Cell/metabolism ; T-Lymphocytes/immunology ; Viral Proteins/immunology
Chemical Substances	Receptors, Antigen, T-Cell ; Viral Proteins
Language	English
Publishing date	2007-10-31
Publishing country	United States
Document type	Journal Article
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/JVI.01571-07
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Article ; Online: Lymphocytic choriomeningitis virus Clone 13 infection causes either persistence or acute death dependent on IFN-1, cytotoxic T lymphocytes (CTLs), and host genetics.

Oldstone, Michael B A / Ware, Brian C / Horton, Lucy E / Welch, Megan J / Aiolfi, Roberto / Zarpellon, Alessandro / Ruggeri, Zaverio M / Sullivan, Brian M

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

2018 Volume 115, Issue 33, Page(s) E7814–E7823

Abstract: Understanding of T cell exhaustion and successful therapy to restore T cell function was first described using Clone (Cl) 13 variant selected from the lymphocytic choriomeningitis virus (LCMV) Armstrong (ARM) 53b parental strain. T cell exhaustion plays ... ...

Abstract	Understanding of T cell exhaustion and successful therapy to restore T cell function was first described using Clone (Cl) 13 variant selected from the lymphocytic choriomeningitis virus (LCMV) Armstrong (ARM) 53b parental strain. T cell exhaustion plays a pivotal role in both persistent infections and cancers of mice and humans. C57BL/6, BALB, SWR/J, A/J, 129, C3H, and all but one collaborative cross (CC) mouse strain following Cl 13 infection have immunosuppressed T cell responses, high PD-1, and viral titers leading to persistent infection and normal life spans. In contrast, the profile of FVB/N, NZB, PL/J, SL/J, and CC NZO mice challenged with Cl 13 is a robust T cell response, high titers of virus, PD-1, and Lag3 markers on T cells. These mice all die 7 to 9 d after Cl 13 infection. Death is due to enhanced pulmonary endothelial vascular permeability, pulmonary edema, collapse of alveolar air spaces, and respiratory failure. Pathogenesis involves abundant levels of Cl 13 receptor alpha-dystroglycan on endothelial cells, with high viral replication in such cells leading to immunopathologic injury. Death is aborted by blockade of interferon-1 (IFN-1) signaling or deletion of CD8 T cells.
MeSH term(s)	Animals ; Antigens, CD/genetics ; Antigens, CD/metabolism ; CD8-Positive T-Lymphocytes/metabolism ; CD8-Positive T-Lymphocytes/pathology ; Humans ; Interferon Type I/genetics ; Interferon Type I/metabolism ; Lymphocytic Choriomeningitis/genetics ; Lymphocytic Choriomeningitis/metabolism ; Lymphocytic Choriomeningitis/pathology ; Lymphocytic choriomeningitis virus/physiology ; Mice ; Programmed Cell Death 1 Receptor/genetics ; Programmed Cell Death 1 Receptor/metabolism ; Virus Replication/genetics
Chemical Substances	Antigens, CD ; CD223 antigen ; Interferon Type I ; Pdcd1 protein, mouse ; Programmed Cell Death 1 Receptor
Language	English
Publishing date	2018-07-30
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.1804674115
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Article ; Online: The role of dendritic cells in viral persistence.

Ng, Cherie T / Sullivan, Brian M / Oldstone, Michael B A

Current opinion in virology

2011 Volume 1, Issue 3, Page(s) 160–166

Abstract: Viruses must modulate or suppress their host's immune system in order to persist. In this review, we discuss the means in which the lympocytic choriomenengitis virus targets and infects an essential component of the immune system, the dendritic cell, ... ...

Abstract	Viruses must modulate or suppress their host's immune system in order to persist. In this review, we discuss the means in which the lympocytic choriomenengitis virus targets and infects an essential component of the immune system, the dendritic cell, essential to bridging the innate and adaptive immune response. Infection of these cells results in pleiotropic effects that serve to deregulate the host immune response.
MeSH term(s)	Animals ; Dendritic Cells/immunology ; Humans ; Lymphocytic Choriomeningitis/immunology ; Lymphocytic choriomeningitis virus/genetics ; Lymphocytic choriomeningitis virus/immunology ; Lymphocytic choriomeningitis virus/pathogenicity ; Lymphocytic choriomeningitis virus/physiology
Language	English
Publishing date	2011-06-28
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2611378-8
ISSN	1879-6265 ; 1879-6257
ISSN (online)	1879-6265
ISSN	1879-6257
DOI	10.1016/j.coviro.2011.05.006
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