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14. Phosphatidylserine receptors enhance SARS-CoV-2 infection

Author

Bohan, Dana, primary, Van Ert, Hanora, additional, Ruggio, Natalie, additional, Rogers, Kai J., additional, Badreddine, Mohammad, additional, Aguilar Briseño, José A., additional, Elliff, Jonah M., additional, Rojas Chavez, Roberth Anthony, additional, Gao, Boning, additional, Stokowy, Tomasz, additional, Christakou, Eleni, additional, Kursula, Petri, additional, Micklem, David, additional, Gausdal, Gro, additional, Haim, Hillel, additional, Minna, John, additional, Lorens, James B., additional, and Maury, Wendy, additional

Published
2021
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16. Phosphatidylserine Receptors Enhance SARS-CoV-2 Infection: AXL as a Therapeutic Target for COVID-19

Author

Bohan, Dana, primary, Van Ert, Hanora, additional, Ruggio, Natalie, additional, Rogers, Kai J., additional, Badreddine, Mohammad, additional, Aguilar Briseño, José A., additional, Chavez, Roberth Anthony Rojas, additional, Gao, Boning, additional, Stokowy, Tomasz, additional, Christakou, Eleni, additional, Micklem, David, additional, Gausdal, Gro, additional, Haim, Hillel, additional, Minna, John, additional, Lorens, James B., additional, and Maury, Wendy, additional

Published
2021
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17. Hemolysis-associated phosphatidylserine exposure promotes polyclonal plasmablast differentiation

Author

Vijay, Rahul, primary, Guthmiller, Jenna J., additional, Sturtz, Alexandria J., additional, Crooks, Sequoia, additional, Johnson, Jordan T., additional, Li, Lei, additional, Lan, Linda Yu-Ling, additional, Pope, Rosemary L., additional, Chen, Yani, additional, Rogers, Kai J., additional, Dutta, Nirmal, additional, Toombs, Jason E., additional, Wilson, Mary E., additional, Wilson, Patrick C., additional, Maury, Wendy, additional, Brekken, Rolf A., additional, and Butler, Noah S., additional

Published
2021
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19. Frontline Science: CD40 signaling restricts RNA virus replication in Mϕs, leading to rapid innate immune control of acute virus infection

Author

Rogers, Kai J, primary, Shtanko, Olena, additional, Stunz, Laura L, additional, Mallinger, Laura N, additional, Arkee, Tina, additional, Schmidt, Megan E, additional, Bohan, Dana, additional, Brunton, Bethany, additional, White, Judith M, additional, Varga, Steve M, additional, Butler, Noah S, additional, Bishop, Gail A, additional, and Maury, Wendy, additional

Published
2020
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22. Frontline Science: CD40 signaling restricts RNA virus replication in Mϕs, leading to rapid innate immune control of acute virus infection.

Author

Rogers, Kai J., Shtanko, Olena, Stunz, Laura L., Mallinger, Laura N., Arkee, Tina, Schmidt, Megan E., Bohan, Dana, Brunton, Bethany, White, Judith M., Varga, Steve M., Butler, Noah S., Bishop, Gail A., and Maury, Wendy

Subjects
VIRUS diseases, RNA viruses, VIRAL replication, EBOLA virus, VESICULAR stomatitis
Abstract

Many acute viral infections target tissue Mϕs, yet the mechanisms of Mϕ‐mediated control of viruses are poorly understood. Here, we report that CD40 expressed by peritoneal Mϕs restricts early infection of a broad range of RNA viruses. Loss of CD40 expression enhanced virus replication as early as 12–24 h of infection and, conversely, stimulation of CD40 signaling with an agonistic Ab blocked infection. With peritoneal cell populations infected with the filovirus, wild‐type (WT) Ebola virus (EBOV), or a BSL2 model virus, recombinant vesicular stomatitis virus encoding Ebola virus glycoprotein (rVSV/EBOV GP), we examined the mechanism conferring protection. Here, we demonstrate that restricted virus replication in Mϕs required CD154/CD40 interactions that stimulated IL‐12 production through TRAF6‐dependent signaling. In turn, IL‐12 production resulted in IFN‐γ production, which induced proinflammatory polarization of Mϕs, protecting the cells from infection. These CD40‐dependent events protected mice against virus challenge. CD40−/− mice were exquisitely sensitive to intraperitoneal challenge with a dose of rVSV/EBOV GP that was sublethal to CD40+/+ mice, exhibiting viremia within 12 h of infection and rapidly succumbing to infection. This study identifies a previously unappreciated role for Mϕ‐intrinsic CD40 signaling in controlling acute virus infection. [ABSTRACT FROM AUTHOR]

Published
2021
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23. Human RECQ Helicase Pathogenic Variants, Population Variation and 'Missing' Diseases

Author

Fu, Wenqing, Ligabue, Alessio, Rogers, Kai J., Akey, Joshua M., and Monnat, Raymond J.

Subjects
congenital, hereditary, and neonatal diseases and abnormalities, Genotype, RecQ Helicases, DNA Mutational Analysis, nutritional and metabolic diseases, Computational Biology, Web Browser, Article, Genetics, Population, Gene Frequency, ROC Curve, Mutation, Humans, Genetic Predisposition to Disease, Databases, Nucleic Acid, Genetic Association Studies, Software
Abstract

Heritable loss of function mutations in the human RECQ helicase genes BLM, WRN, and RECQL4 cause Bloom, Werner, and Rothmund-Thomson syndromes, cancer predispositions with additional developmental or progeroid features. In order to better understand RECQ pathogenic and population variation, we systematically analyzed genetic variation in all five human RECQ helicase genes. A total of 3,741 unique base pair-level variants were identified, across 17,605 potential mutation sites. Direct counting of BLM, RECQL4, and WRN pathogenic variants was used to determine aggregate and disease-specific carrier frequencies. The use of biochemical and model organism data, together with computational prediction, identified over 300 potentially pathogenic population variants in RECQL and RECQL5, the two RECQ helicases that are not yet linked to a heritable deficiency syndrome. Despite the presence of these predicted pathogenic variants in the human population, we identified no individuals homozygous for any biochemically verified or predicted pathogenic RECQL or RECQL5 variant. Nor did we find any individual heterozygous for known pathogenic variants in two or more of the disease-associated RECQ helicase genes BLM, RECQL4, or WRN. Several postulated RECQ helicase deficiency syndromes-RECQL or RECQL5 loss of function, or compound haploinsufficiency for the disease-associated RECQ helicases-may remain missing, as they likely incompatible with life.

Published
2016

24. TIM-1 Mediates Dystroglycan-Independent Entry of Lassa Virus

Author

Brouillette, Rachel B., primary, Phillips, Elisabeth K., additional, Patel, Radhika, additional, Mahauad-Fernandez, Wadie, additional, Moller-Tank, Sven, additional, Rogers, Kai J., additional, Dillard, Jacob A., additional, Cooney, Ashley L., additional, Martinez-Sobrido, Luis, additional, Okeoma, Chioma, additional, and Maury, Wendy, additional

Published
2018
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28. Acute PlasmodiumInfection Promotes Interferon-Gamma-Dependent Resistance to Ebola Virus Infection

Author

Rogers, Kai J., Shtanko, Olena, Vijay, Rahul, Mallinger, Laura N., Joyner, Chester J., Galinski, Mary R., Butler, Noah S., and Maury, Wendy

Abstract

During the 2013–2016 Ebola virus (EBOV) epidemic, a significant number of patients admitted to Ebola treatment units were co-infected with Plasmodium falciparum,a predominant agent of malaria. However, there is no consensus on how malaria impacts EBOV infection. The effect of acute Plasmodiuminfection on EBOV challenge was investigated using mouse-adapted EBOV and a biosafety level 2 (BSL-2) model virus. We demonstrate that acute Plasmodiuminfection protects from lethal viral challenge, dependent upon interferon gamma (IFN-γ) elicited as a result of parasite infection. Plasmodium-infected mice lacking the IFN-γ receptor are not protected. Ex vivoincubation of naive human or mouse macrophages with sera from acutely parasitemic rodents or macaques programs a proinflammatory phenotype dependent on IFN-γ and renders cells resistant to EBOV infection. We conclude that acute Plasmodiuminfection can safeguard against EBOV by the production of protective IFN-γ. These findings have implications for anti-malaria therapies administered during episodic EBOV outbreaks in Africa.

Published
2020
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29. Phosphatidylserine Receptors Enhance SARS-CoV-2 Infection: AXL as a Therapeutic Target for COVID-19.

Author

Bohan D, Ert HV, Ruggio N, Rogers KJ, Badreddine M, Aguilar Briseño JA, Rojas Chavez RA, Gao B, Stokowy T, Christakou E, Micklem D, Gausdal G, Haim H, Minna J, Lorens JB, and Maury W

Abstract

Phosphatidylserine (PS) receptors are PS binding proteins that mediate uptake of apoptotic bodies. Many enveloped viruses utilize this PS/PS receptor mechanism to adhere to and internalize into the endosomal compartment of cells and this is termed apoptotic mimicry. For viruses that have a mechanism(s) of endosomal escape, apoptotic mimicry is a productive route of virus entry. We evaluated if PS receptors serve as cell surface receptors for SARS-CoV-2 and found that the PS receptors, AXL, TIM-1 and TIM-4, facilitated virus infection when low concentrations of the SARS-CoV-2 cognate receptor, ACE2, was present. Consistent with the established mechanism of PS receptor utilization by other viruses, PS liposomes competed with SARS-CoV-2 for binding and entry. We demonstrated that this PS receptor enhances SARS-CoV-2 binding to and infection of an array of human lung cell lines and is an under-appreciated but potentially important host factor facilitating SARS-CoV-2 entry.

Published
2021
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