Corey A. Balinsky

Naval Medical Research Command

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Kathryn C. Zoon

National Institute of Allergy and Infectious Diseases

Hana Schmeisser

National Institute of Allergy and Infectious Diseases

Peifang Sun

Naval Medical Research Command

Andrew G. Letizia

Naval Medical Research Command

Vihasi Jani

Naval Medical Research Command

Megan A. Schilling

Naval Medical Research Command

Daniel L. Rock

University of Illinois Urbana-Champaign

Joseph Bekisz

National Institute of Allergy and Infectious Diseases

Samuel Fey

National Institute of Allergy and Infectious Diseases

Victor A. Sugiharto

Naval Medical Research Command

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Naval Medical Research Command

National Institutes of Health

National Institute of Allergy and Infectious Diseases

Icahn School of Medicine at Mount Sinai

Plum Island Animal Disease Center

Naval Medical Research Unit Six

Henry M. Jackson Foundation

United States Department of Agriculture

United States Department of the Navy

Agricultural Research Service

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Memory B-Cell Development After Asymptomatic or Mild Symptomatic SARS-CoV-2 Infection

The Journal of Infectious Diseases (2022)

Yu Kato Nathaniel I. Bloom Peifang Sun Corey A. Balinsky Qi Qiu

The development of memory B cells after asymptomatic severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is not well understood.

Memory B cell

Antibody titer

10.1093/infdis/jiac319

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Citations (8)

Antibodies to S2 domain of SARS-CoV-2 spike protein in Moderna mRNA vaccinated subjects sustain antibody-dependent NK cell-mediated cell cytotoxicity against Omicron BA.1

Frontiers in Immunology (2023)

Corey A. Balinsky Le Jiang Vihasi Jani Ying Cheng Zhiwen Zhang

Vaccination with the primary two-dose series of SARS-CoV-2 mRNA protects against infection with the ancestral strain, and limits the presentation of severe disease after re-infection by multiple variants of concern (VOC), including Omicron, despite the lack of a strong neutralizing response to these variants. We compared antibody responses in serum samples collected from mRNA-1273 (Moderna) vaccinated subjects to identify mechanisms of immune escape and cross-protection. Using pseudovirus constructs containing domain-specific amino acid changes representative of Omicron BA.1, combined with domain competition and RBD-antibody depletion, we showed that RBD antibodies were primarily responsible for virus neutralization and variant escape. Antibodies to NTD played a less significant role in antibody neutralization but acted along with RBD to enhance neutralization. S2 of Omicron BA.1 had no impact on neutralization escape, suggesting it is a less critical domain for antibody neutralization; however, it was as capable as S1 at eliciting IgG3 responses and NK-cell mediated, antibody-dependent cell cytotoxicity (ADCC). Antibody neutralization and ADCC activities to RBD, NTD, and S1 were all prone to BA.1 escape. In contrast, ADCC activities to S2 resisted BA.1 escape. In conclusion, S2 antibodies showed potent ADCC function and resisted Omicron BA.1 escape, suggesting that S2 contributes to cross-protection against Omicron BA.1. In line with its conserved nature, S2 may hold promise as a vaccine target against future variants of SARS-CoV-2.

Immune escape

10.3389/fimmu.2023.1266829

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Antiproliferative Properties of Type I and Type II Interferon

Pharmaceuticals (2010)

Joseph Bekisz Samuel Baron Corey A. Balinsky Angel Morrow Kathryn C. Zoon

The clinical possibilities of interferon (IFN) became apparent with early studies demonstrating that it was capable of inhibiting tumor cells in culture and in vivo using animal models. IFN gained the distinction of being the first recombinant cytokine to be licensed in the USA for the treatment of a malignancy in 1986, with the approval of IFN-α2a (Hoffman-La Roche) and IFN-α2b (Schering-Plough) for the treatment of Hairy Cell Leukemia. In addition to this application, other approved antitumor applications for IFN-α2a are AIDS-related Kaposi's Sarcoma and Chronic Myelogenous Leukemia (CML) and other approved antitumor applications for IFN-α2b are Malignant Melanoma, Follicular Lymphoma, and AIDS-related Kapoisi's Sarcoma. In the ensuing years, a considerable number of studies have been conducted to establish the mechanisms of the induction and action of IFN's anti-tumor activity. These include identifying the role of Interferon Regulatory Factor 9 (IRF9) as a key factor in eliciting the antiproliferative effects of IFN-α as well as identifying genes induced by IFN that are involved in recognition of tumor cells. Recent studies also show that IFN-activated human monocytes can be used to achieve >95% eradication of select tumor cells. The signaling pathways by which IFN induces apoptosis can vary. IFN treatment induces the tumor suppressor gene p53, which plays a role in apoptosis for some tumors, but it is not essential for the apoptotic response. IFN-α also activates phosphatidylinositol 3-kinase (PI3K), which is associated with cell survival. Downstream of PI3K is the mammalian target of rapamycin (mTOR) which, in conjunction with PI3K, may act in signaling induced by growth factors after IFN treatment. This paper will explore the mechanisms by which IFN acts to elicit its antiproliferative effects and more closely examine the clinical applications for the anti-tumor potential of IFN.

Chronic myelogenous leukemia

10.3390/ph3040994

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Citations (135)

Dengue virus core protein mediates reduction of antiviral activity in Huh7 cells

Cytokine (2009)

Corey A. Balinsky Hana Schmeisser Kathryn C. Zoon

Core protein

Antibody-dependent enhancement

10.1016/j.cyto.2009.07.220

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African Swine Fever Virus Multigene Family 360 and 530 Genes Affect Host Interferon Response

Journal of Virology (2004)

Claudio L. Afonso M E Piccone K. M. Zaffuto John G. Neilan G. F. Kutish

African swine fever virus (ASFV) multigene family 360 and 530 (MGF360/530) genes affect viral growth in macrophage cell cultures and virulence in pigs (L. Zsak, Z. Lu, T. G. Burrage, J. G. Neilan, G. F. Kutish, D. M. Moore, and D. L. Rock, J. Virol. 75:3066-3076, 2001). The mechanism by which these novel genes affect virus-host interactions is unknown. To define MGF360/530 gene function, we compared macrophage transcriptional responses following infection with parental ASFV (Pr4) and an MGF360/530 deletion mutant (Pr4 Delta 35). A swine cDNA microarray containing 7,712 macrophage cDNA clones was used to compare the transcriptional profiles of swine macrophages infected with Pr4 and Pr4 Delta 35 at 3 and 6 h postinfection (hpi). While at 3 hpi most (7,564) of the genes had similar expression levels in cells infected with either virus, 38 genes had significantly increased (>2.0-fold, P < 0.05) mRNA levels in Pr4 Delta 35-infected macrophages. Similar up-regulation of these genes was observed at 6 hpi. Viral infection was required for this induced transcriptional response. Most Pr Delta 35 up-regulated genes were part of a type I interferon (IFN) response or were genes that are normally induced by double-stranded RNA and/or viral infection. These included monocyte chemoattractant protein, transmembrane protein 3, tetratricopeptide repeat protein 1, a ubiquitin-like 17-kDa protein, ubiquitin-specific protease ISG43, an RNA helicase DEAD box protein, GTP-binding MX protein, the cytokine IP-10, and the PKR activator PACT. Differential expression of IFN early-response genes in Pr4 Delta 35 relative to Pr4 was confirmed by Northern blot analysis and real-time PCR. Analysis of IFN-alpha mRNA and secreted IFN-alpha levels at 3, 8, and 24 hpi revealed undetectable IFN-alpha in mock- and Pr4-infected macrophages but significant IFN-alpha levels at 24 hpi in Pr4 Delta 35-infected macrophages. The absence of IFN-alpha in Pr4-infected macrophages suggests that MGF360/530 genes either directly or indirectly suppress a type I IFN response. An inability to suppress host type I IFN responses may account for the growth defect of Pr4 Delta 35 in macrophages and its attenuation in swine.

ISG15

Protein kinase R

10.1128/jvi.78.4.1858-1864.2004

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Citations (188)

PS1-023. Human interferon-alpha2c induces autophagy in Daudi Burkitt’s lymphoma cells

Cytokine (2011)

Hana Schmeisser Samuel Fey Julie Horowitz Elizabeth R. Fischer Kotaro Miyake

Burkitt's lymphoma

10.1016/j.cyto.2011.07.042

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Pseudovirus-Based Assays for the Measurement of Antibody-Mediated Neutralization of SARS-CoV-2

Methods in molecular biology (2022)

Corey A. Balinsky Vihasi Jani Peifang Sun Maya Williams Gabriel Defang

10.1007/978-1-0716-2111-0_21

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Citations (3)

Sheeppox Virus Kelch-Like Gene SPPV-019 Affects Virus Virulence

Journal of Virology (2007)

Corey A. Balinsky Gustavo Delhon Claudio L. Afonso Guillermo R. Risatti Manuel V. Borca

ABSTRACT Sheeppox virus (SPPV), a member of the Capripoxvirus genus of the Poxviridae , is the etiologic agent of a significant disease of sheep in the developing world. Genomic analysis of pathogenic and vaccine capripoxviruses identified genes with potential roles in virulence and host range, including three genes with similarity to kelch-like genes of other poxviruses and eukaryotes. Here, a mutant SPPV with a deletion in the SPPV-019 kelch-like gene, ΔKLP, was derived from the pathogenic strain SPPV-SA. ΔKLP exhibited in vitro growth characteristics similar to those of SPPV-SA and revertant virus (RvKLP). ΔKLP-infected cells exhibited a reduction in Ca 2+ -independent cell adhesion, suggesting that SPPV-019 may modulate cellular adhesion. When inoculated in sheep by the intranasal or intradermal routes, ΔKLP was markedly attenuated, since all ΔKLP-infected lambs survived infection. In contrast, SPPV-SA and RvKLP induced mortality approaching 100%. Lambs inoculated with ΔKLP exhibited marked reduction or delay in fever response, gross lesions, viremia, and virus shedding compared to parental and revertant viruses. Together, these findings indicate that SPPV-019 is a significant SPPV virulence determinant in sheep.

Viremia

10.1128/jvi.01093-07

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Citations (53)

PS2-57 Characterization of IFIT3 as a novel antiviral protein

Cytokine (2010)

Christopher Clark Hana Schmeisser Josef Mejido Corey A. Balinsky Angel Morrow

Transferrin receptor

Internalization

Cell surface receptor

10.1016/j.cyto.2010.07.262

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Asymptomatic or Symptomatic SARS-CoV-2 Infection Plus Vaccination Confers Increased Adaptive Immunity to Variants of Concern of SARS-CoV-2 Including Omicron

SSRN Electronic Journal (2022)

Peifang Sun Irene Ramos Camila H. Coelho Alba Grifoni Corey A. Balinsky

The ongoing evolution of SARS-CoV-2 requires monitoring the capability of immune responses to cross-recognize Variants of Concern (VOC). In this cross-sectional study, we examined serological and cell-mediated immune memory to SARS-CoV-2 variants, including Omicron, among a cohort of 18-21-year-old Marines with a history of either asymptomatic or mild SARS-CoV-2 infection 6 to 14 months earlier. Among the 210 participants in the study, 169 were unvaccinated while 41 received 2 doses of mRNA-based COVID-19 vaccines. Vaccination of previously infected participants strongly boosted neutralizing and binding activity and memory B and T cell responses including recognition of Omicron, compared to infected but unvaccinated participants. Additionally, no measurable differences were observed in immune memory in healthy young adults with previous symptomatic or asymptomatic infections, for ancestral or variant strains. These results provide mechanistic immunological insights into population-based differences observed in immunity against Omicron and other variants among individuals with different clinical histories.â€‹Funding Information: Work was supported by a grant (9700130) from the Defense Health Agency through the Naval Medical Research Center (AGL) and by the Defense Advanced Research Projects Agency (contract number N6600119C4022 (SCS), as well as LJI Institutional funds (SC). SV is supported by a grant from the Swedish Research Council (2021-06713).Declaration of Interests: SC has consulted for GSK, JP Morgan, Citi, Morgan Stanley, Avalia NZ, Nutcracker Therapeutics, University of California, California State Universities, United Airlines, Adagio, and Roche. AS is a consultant for Gritstone Bio, Flow Pharma, Arcturus Therapeutics, ImmunoScape, CellCarta, Avalia, Moderna, Fortress and Repertoire. LJI has filed for patent protection for various aspects of T cell epitope and vaccine design work. PS, IR, CHC, AG, CAB, SV, AT, NIB, VJ, SJJ, DAB, EC, CWG, JM, AM, EN, LW, CKP, VAS, MS, ASM, CB, SCS, and AGL have no competing interests to declare.Ethics Approval Statement: The study protocols were approved by the Naval Medical Research Center Institutional Review Board (protocol numbers NMRC.2020.0006 and NMRC.2021.0004) in compliance with all applicable federal regulations governing the protection of human subjects. All participants provided written informed consent for participation.

2019-20 coronavirus outbreak

Pandemic

Betacoronavirus

10.2139/ssrn.4137687

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