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Article ; Online: Neuroinflammation and COVID-19.

Vanderheiden, Abigail / Klein, Robyn S

2022 Volume 76, Page(s) 102608

Abstract: Coronavirus disease 2019 (COVID-19) has caused a historic pandemic of respiratory disease. COVID-19 also causes acute and post-acute neurological symptoms, which range from mild, such as headaches, to severe, including hemorrhages. Current evidence ... ...

Abstract	Coronavirus disease 2019 (COVID-19) has caused a historic pandemic of respiratory disease. COVID-19 also causes acute and post-acute neurological symptoms, which range from mild, such as headaches, to severe, including hemorrhages. Current evidence suggests that there is no widespread infection of the central nervous system (CNS) by SARS-CoV-2, thus what is causing COVID-19 neurological disease? Here, we review potential immunological mechanisms driving neurological disease in COVID-19 patients. We begin by discussing the implications of imbalanced peripheral immunity on CNS function. Next, we examine the evidence for dysregulation of the blood-brain barrier during SARS-CoV-2 infection. Last, we discuss the role myeloid cells may play in promoting COVID-19 neurological disease. Combined, we highlight the role of innate immunity in COVID-19 neuroinflammation and suggest areas for future research.
MeSH term(s)	COVID-19/complications ; Humans ; Nervous System Diseases ; Neuroinflammatory Diseases ; Pandemics ; SARS-CoV-2
Language	English
Publishing date	2022-06-29
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	1078046-4
ISSN	1873-6882 ; 0959-4388
ISSN (online)	1873-6882
ISSN	0959-4388
DOI	10.1016/j.conb.2022.102608
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Vaccination prevents IL-1β-mediated cognitive deficits after COVID-19.

Vanderheiden, Abigail / Hill, Jeremy / Jiang, Xiaoping / Deppen, Ben / Bamunuarachchi, Gayan / Soudani, Nadia / Joshi, Astha / Cain, Matthew D / Boon, Adrianus C M / Klein, Robyn S

Research square

2023

Abstract: Up to 25% of SARS-CoV-2 patients exhibit post-acute cognitive sequelae. Although millions of cases of COVID-19-mediated memory dysfunction are accumulating worldwide, the underlying mechanisms and how vaccination lowers risk are unknown. Interleukin-1, a ...

Abstract	Up to 25% of SARS-CoV-2 patients exhibit post-acute cognitive sequelae. Although millions of cases of COVID-19-mediated memory dysfunction are accumulating worldwide, the underlying mechanisms and how vaccination lowers risk are unknown. Interleukin-1, a key component of innate immune defense against SARS-CoV-2 infection, is elevated in the hippocampi of COVID-19 patients. Here we show that intranasal infection of C57BL/6J mice with SARS-CoV-2 beta variant, leads to CNS infiltration of Ly6C
Language	English
Publishing date	2023-09-15
Publishing country	United States
Document type	Preprint
DOI	10.21203/rs.3.rs-3353171/v1
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: CD4+ and CD8+ T cells are required to prevent SARS-CoV-2 persistence in the nasal compartment.

Kar, Meenakshi / Johnson, Katherine E E / Vanderheiden, Abigail / Elrod, Elizabeth J / Floyd, Katharine / Geerling, Elizabeth / Stone, E Taylor / Salinas, Eduardo / Banakis, Stephanie / Wang, Wei / Sathish, Shruti / Shrihari, Swathi / Davis-Gardner, Meredith E / Kohlmeier, Jacob / Pinto, Amelia / Klein, Robyn / Grakoui, Arash / Ghedin, Elodie / Suthar, Mehul S

bioRxiv : the preprint server for biology

2024

Abstract: SARS-CoV-2 is the causative agent of COVID-19 and continues to pose a significant public health threat throughout the world. Following SARS-CoV-2 infection, virus-specific CD4+ and CD8+ T cells are rapidly generated to form effector and memory cells and ... ...

Abstract	SARS-CoV-2 is the causative agent of COVID-19 and continues to pose a significant public health threat throughout the world. Following SARS-CoV-2 infection, virus-specific CD4+ and CD8+ T cells are rapidly generated to form effector and memory cells and persist in the blood for several months. However, the contribution of T cells in controlling SARS-CoV-2 infection within the respiratory tract are not well understood. Using C57BL/6 mice infected with a naturally occurring SARS-CoV-2 variant (B.1.351), we evaluated the role of T cells in the upper and lower respiratory tract. Following infection, SARS-CoV-2-specific CD4+ and CD8+ T cells are recruited to the respiratory tract and a vast proportion secrete the cytotoxic molecule Granzyme B. Using antibodies to deplete T cells prior to infection, we found that CD4+ and CD8+ T cells play distinct roles in the upper and lower respiratory tract. In the lungs, T cells play a minimal role in viral control with viral clearance occurring in the absence of both CD4+ and CD8+ T cells through 28 days post-infection. In the nasal compartment, depletion of both CD4+ and CD8+ T cells, but not individually, results in persistent and culturable virus replicating in the nasal compartment through 28 days post-infection. Using
Language	English
Publishing date	2024-01-24
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.01.23.576505
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Article ; Online: A wild boar cathelicidin peptide derivative inhibits severe acute respiratory syndrome coronavirus-2 and its drifted variants.

von Beck, Troy / Navarrete, Karla / Arce, Nicholas A / Gao, Mu / Dale, Gordon A / Davis-Gardner, Meredith E / Floyd, Katharine / Mena Hernandez, Luis / Mullick, Nikita / Vanderheiden, Abigail / Skountzou, Ioanna / Kuchipudi, Suresh V / Saravanan, Rathi / Li, Renhao / Skolnick, Jeffrey / Suthar, Mehul S / Jacob, Joshy

Scientific reports

2023 Volume 13, Issue 1, Page(s) 14650

Abstract: The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) poses a clear threat to humanity. It has infected over 200 million and killed 4 million people worldwide, and infections continue with no end in sight. To control the pandemic, multiple ... ...

Abstract	The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) poses a clear threat to humanity. It has infected over 200 million and killed 4 million people worldwide, and infections continue with no end in sight. To control the pandemic, multiple effective vaccines have been developed, and global vaccinations are in progress. However, the virus continues to mutate. Even when full vaccine coverage is achieved, vaccine-resistant mutants will likely emerge, thus requiring new annual vaccines against drifted variants analogous to influenza. A complimentary solution to this problem could be developing antiviral drugs that inhibit SARS CoV-2 and its drifted variants. Host defense peptides represent a potential source for such an antiviral as they possess broad antimicrobial activity and significant diversity across species. We screened the cathelicidin family of peptides from 16 different species for antiviral activity and identified a wild boar peptide derivative that inhibits SARS CoV-2. This peptide, which we named Yongshi and means warrior in Mandarin, acts as a viral entry inhibitor. Following the binding of SARS-CoV-2 to its receptor, the spike protein is cleaved, and heptad repeats 1 and 2 multimerize to form the fusion complex that enables the virion to enter the cell. A deep learning-based protein sequence comparison algorithm and molecular modeling suggest that Yongshi acts as a mimetic to the heptad repeats of the virus, thereby disrupting the fusion process. Experimental data confirm the binding of Yongshi to the heptad repeat 1 with a fourfold higher affinity than heptad repeat 2 of SARS-CoV-2. Yongshi also binds to the heptad repeat 1 of SARS-CoV-1 and MERS-CoV. Interestingly, it inhibits all drifted variants of SARS CoV-2 that we tested, including the alpha, beta, gamma, delta, kappa and omicron variants.
MeSH term(s)	Humans ; Cathelicidins ; SARS-CoV-2 ; COVID-19 ; Antiviral Agents
Chemical Substances	Cathelicidins ; Antiviral Agents
Language	English
Publishing date	2023-09-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-41850-7
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Article ; Online: Erratum for Vanderheiden et al., "CCR2 Signaling Restricts SARS-CoV-2 Infection".

Vanderheiden, Abigail / Thomas, Jeronay / Soung, Allison L / Davis-Gardner, Meredith E / Floyd, Katharine / Jin, Fengzhi / Cowan, David A / Pellegrini, Kathryn / Creanga, Adrian / Pegu, Amarendra / Derrien-Colemyn, Alexandrine / Shi, Pei-Yong / Grakoui, Arash / Klein, Robyn S / Bosinger, Steven E / Kohlmeier, Jacob E / Menachery, Vineet D / Suthar, Mehul S

mBio

2022 Volume 13, Issue 3, Page(s) e0025922

Language	English
Publishing date	2022-04-14
Publishing country	United States
Document type	Journal Article ; Published Erratum
ZDB-ID	2557172-2
ISSN	2150-7511 ; 2161-2129
ISSN (online)	2150-7511
ISSN	2161-2129
DOI	10.1128/mbio.00259-22
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Article ; Online: COVID-19 induces CNS cytokine expression and loss of hippocampal neurogenesis.

Soung, Allison L / Vanderheiden, Abigail / Nordvig, Anna S / Sissoko, Cheick A / Canoll, Peter / Mariani, Madeline B / Jiang, Xiaoping / Bricker, Traci / Rosoklija, Gorazd B / Arango, Victoria / Underwood, Mark / Mann, J John / Dwork, Andrew J / Goldman, James E / Boon, Adrianus C M / Boldrini, Maura / Klein, Robyn S

Brain : a journal of neurology

2022 Volume 145, Issue 12, Page(s) 4193–4201

Abstract: Infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is associated with acute and postacute cognitive and neuropsychiatric symptoms including impaired memory, concentration, attention, sleep and affect. Mechanisms underlying ... ...

Abstract	Infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is associated with acute and postacute cognitive and neuropsychiatric symptoms including impaired memory, concentration, attention, sleep and affect. Mechanisms underlying these brain symptoms remain understudied. Here we report that SARS-CoV-2-infected hamsters exhibit a lack of viral neuroinvasion despite aberrant blood-brain barrier permeability. Hamsters and patients deceased from coronavirus disease 2019 (COVID-19) also exhibit microglial activation and expression of interleukin (IL)-1β and IL-6, especially within the hippocampus and the medulla oblongata, when compared with non-COVID control hamsters and humans who died from other infections, cardiovascular disease, uraemia or trauma. In the hippocampal dentate gyrus of both COVID-19 hamsters and humans, we observed fewer neuroblasts and immature neurons. Protracted inflammation, blood-brain barrier disruption and microglia activation may result in altered neurotransmission, neurogenesis and neuronal damage, explaining neuropsychiatric presentations of COVID-19. The involvement of the hippocampus may explain learning, memory and executive dysfunctions in COVID-19 patients.
MeSH term(s)	Humans ; COVID-19 ; Cytokines ; SARS-CoV-2 ; Hippocampus ; Neurogenesis/physiology
Chemical Substances	Cytokines
Language	English
Publishing date	2022-08-18
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80072-7
ISSN	1460-2156 ; 0006-8950
ISSN (online)	1460-2156
ISSN	0006-8950
DOI	10.1093/brain/awac270
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Article: Plasmacytoid dendritic cells produce type I interferon and reduce viral replication in airway epithelial cells after SARS-CoV-2 infection.

Cervantes-Barragan, Luisa / Vanderheiden, Abigail / Royer, Charlotte J / Davis-Gardner, Meredith E / Ralfs, Philipp / Chirkova, Tatiana / Anderson, Larry J / Grakoui, Arash / Suthar, Mehul S

bioRxiv : the preprint server for biology

2021

Abstract: Infection with SARS-CoV-2 has caused a pandemic of unprecedented dimensions. SARS-CoV-2 infects airway and lung cells causing viral pneumonia. The importance of type I interferon (IFN) production for the control of SARS-CoV-2 infection is highlighted by ... ...

Abstract	Infection with SARS-CoV-2 has caused a pandemic of unprecedented dimensions. SARS-CoV-2 infects airway and lung cells causing viral pneumonia. The importance of type I interferon (IFN) production for the control of SARS-CoV-2 infection is highlighted by the increased severity of COVID-19 in patients with inborn errors of type I IFN response or auto-antibodies against IFN-α. Plasmacytoid dendritic cells (pDCs) are a unique immune cell population specialized in recognizing and controlling viral infections through the production of high concentrations of type I IFN. In this study, we isolated pDCs from healthy donors and showed that pDCs are able to recognize SARS-CoV-2 and rapidly produce large amounts of type I IFN. Sensing of SARS-CoV-2 by pDCs was independent of viral replication since pDCs were also able to recognize UV-inactivated SARS-CoV-2 and produce type I IFN. Transcriptional profiling of SARS-CoV-2 and UV-SARS-CoV-2 stimulated pDCs also showed a rapid type I and III IFN response as well as induction of several chemokines, and the induction of apoptosis in pDCs. Moreover, we modeled SARS-CoV-2 infection in the lung using primary human airway epithelial cells (pHAEs) and showed that co-culture of pDCs with SARS-CoV-2 infected pHAEs induces an antiviral response and upregulation of antigen presentation in pHAE cells. Importantly, the presence of pDCs in the co-culture results in control of SARS-CoV-2 replication in pHAEs. Our study identifies pDCs as one of the key cells that can recognize SARS-CoV-2 infection, produce type I and III IFN and control viral replication in infected cells. Importance: Type I interferons (IFNs) are a major part of the innate immune defense against viral infections. The importance of type I interferon (IFN) production for the control of SARS-CoV-2 infection is highlighted by the increased severity of COVID-19 in patients with defects in the type I IFN response. Interestingly, many cells are not able to produce type I IFN after being infected with SARS-CoV-2 and cannot control viral infection. In this study we show that plasmacytoid dendritic cells are able to recognize SARS-CoV-2 and produce type I IFN, and that pDCs are able to help control viral infection in SARS-CoV-2 infected airway epithelial cells.
Language	English
Publishing date	2021-05-13
Publishing country	United States
Document type	Preprint
DOI	10.1101/2021.05.12.443948
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: CD4+ and CD8+ T cells are required to prevent SARS-CoV-2 persistence in the nasal compartment

Kar, Meenakshi / Johnson, Katherine E.E. / Vanderheiden, Abigail / Elrod, Elizabeth J. / Floyd, Katharine / Geerling, Elizabeth / Stone, E. Taylor / Salinas, Eduardo / Banakis, Stephanie / Wang, Wei / Sathish, Shruti / Shrihari, Swathi / Davis-Gardner, Meredith E. / Kohlmeier, Jacob / Pinto, Amelia / Klein, Robyn / Grakoui, Arash / Ghedin, Elodie / Suthar, Mehul S.

bioRxiv

Abstract	SARS-CoV-2 is the causative agent of COVID-19 and continues to pose a significant public health threat throughout the world. Following SARS-CoV-2 infection, virus-specific CD4+ and CD8+ T cells are rapidly generated to form effector and memory cells and persist in the blood for several months. However, the contribution of T cells in controlling SARS-CoV-2 infection within the respiratory tract are not well understood. Using C57BL/6 mice infected with a naturally occurring SARS-CoV-2 variant (B.1.351), we evaluated the role of T cells in the upper and lower respiratory tract. Following infection, SARS-CoV-2-specific CD4+ and CD8+ T cells are recruited to the respiratory tract and a vast proportion secrete the cytotoxic molecule Granzyme B. Using antibodies to deplete T cells prior to infection, we found that CD4+ and CD8+ T cells play distinct roles in the upper and lower respiratory tract. In the lungs, T cells play a minimal role in viral control with viral clearance occurring in the absence of both CD4+ and CD8+ T cells through 28 days post-infection. In the nasal compartment, depletion of both CD4+ and CD8+ T cells, but not individually, results in persistent and culturable virus replicating in the nasal compartment through 28 days post-infection. Using in situ hybridization, we found that SARS-CoV-2 infection persisted in the nasal epithelial layer of tandem CD4+ and CD8+ T cell-depleted mice. Sequence analysis of virus isolates from persistently infected mice revealed mutations spanning across the genome, including a deletion in ORF6. Overall, our findings highlight the importance of T cells in controlling virus replication within the respiratory tract during SARS-CoV-2 infection.
Keywords	covid19
Language	English
Publishing date	2024-01-24
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2024.01.23.576505
Database	COVID19

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Article ; Online: SARS-CoV-2 spike-protein D614G mutation increases virion spike density and infectivity.

Zhang, Lizhou / Jackson, Cody B / Mou, Huihui / Ojha, Amrita / Peng, Haiyong / Quinlan, Brian D / Rangarajan, Erumbi S / Pan, Andi / Vanderheiden, Abigail / Suthar, Mehul S / Li, Wenhui / Izard, Tina / Rader, Christoph / Farzan, Michael / Choe, Hyeryun

Nature communications

2020 Volume 11, Issue 1, Page(s) 6013

Abstract: SARS-CoV-2 variants with spike (S)-protein D614G mutations now predominate globally. We therefore compare the properties of the mutated S protein ( ... ...

Abstract	SARS-CoV-2 variants with spike (S)-protein D614G mutations now predominate globally. We therefore compare the properties of the mutated S protein (S
MeSH term(s)	Amino Acid Substitution ; Angiotensin-Converting Enzyme 2/metabolism ; COVID-19/epidemiology ; COVID-19/virology ; HEK293 Cells ; Humans ; Mutation ; Pandemics ; SARS-CoV-2/genetics ; SARS-CoV-2/pathogenicity ; Spike Glycoprotein, Coronavirus/genetics ; Spike Glycoprotein, Coronavirus/metabolism ; Virion/metabolism ; Virus Assembly/genetics ; Virus Internalization
Chemical Substances	Spike Glycoprotein, Coronavirus ; spike protein, SARS-CoV-2 ; ACE2 protein, human (EC 3.4.17.23) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
Language	English
Publishing date	2020-11-26
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-020-19808-4
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Article ; Online: CCR2 Signaling Restricts SARS-CoV-2 Infection.

Vanderheiden, Abigail / Thomas, Jeronay / Soung, Allison L / Davis-Gardner, Meredith E / Floyd, Katharine / Jin, Fengzhi / Cowan, David A / Pellegrini, Kathryn / Shi, Pei-Yong / Grakoui, Arash / Klein, Robyn S / Bosinger, Steven E / Kohlmeier, Jacob E / Menachery, Vineet D / Suthar, Mehul S

mBio

2021 Volume 12, Issue 6, Page(s) e0274921

Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused a historic pandemic of respiratory disease (coronavirus disease 2019 [COVID-19]), and current evidence suggests that severe disease is associated with dysregulated immunity within ... ...

Abstract	Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused a historic pandemic of respiratory disease (coronavirus disease 2019 [COVID-19]), and current evidence suggests that severe disease is associated with dysregulated immunity within the respiratory tract. However, the innate immune mechanisms that mediate protection during COVID-19 are not well defined. Here, we characterize a mouse model of SARS-CoV-2 infection and find that early CCR2 signaling restricts the viral burden in the lung. We find that a recently developed mouse-adapted SARS-CoV-2 (MA-SARS-CoV-2) strain as well as the emerging B.1.351 variant trigger an inflammatory response in the lung characterized by the expression of proinflammatory cytokines and interferon-stimulated genes. Using intravital antibody labeling, we demonstrate that MA-SARS-CoV-2 infection leads to increases in circulating monocytes and an influx of CD45
MeSH term(s)	Animals ; COVID-19 ; Cytokines/immunology ; Disease Models, Animal ; Female ; Immunity, Innate ; Inflammation ; Lung/cytology ; Lung/immunology ; Lung/virology ; Mice ; Mice, Inbred C57BL ; Monocytes/immunology ; Pneumonia, Viral/immunology ; Pneumonia, Viral/prevention & control ; Pneumonia, Viral/virology ; Receptors, CCR2/genetics ; Receptors, CCR2/immunology ; Receptors, CCR2/metabolism ; SARS-CoV-2/genetics ; SARS-CoV-2/immunology ; Signal Transduction/immunology ; Viral Load ; Virus Replication/immunology
Chemical Substances	Ccr2 protein, mouse ; Cytokines ; Receptors, CCR2
Language	English
Publishing date	2021-11-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2557172-2
ISSN	2150-7511 ; 2161-2129
ISSN (online)	2150-7511
ISSN	2161-2129
DOI	10.1128/mBio.02749-21
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