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Article ; Online: Phosphate Toxicity in CKD: The Killer among Us.

Ritter, Cynthia S / Slatopolsky, Eduardo

Clinical journal of the American Society of Nephrology : CJASN

2016 Volume 11, Issue 6, Page(s) 1088–1100

Abstract: Maintenance of a normal serum phosphate level depends on absorption in the gut, reabsorption and excretion by the kidney, and the flux between the extracellular and skeletal pools. Phosphate homeostasis is a coordinated, complex system of crosstalk ... ...

Abstract	Maintenance of a normal serum phosphate level depends on absorption in the gut, reabsorption and excretion by the kidney, and the flux between the extracellular and skeletal pools. Phosphate homeostasis is a coordinated, complex system of crosstalk between the bone, intestine, kidney, and parathyroid gland. Dysfunction of this system has serious clinical consequences in healthy individuals and those with conditions, such as CKD, in which hyperphosphatemia is associated with increased risks of cardiovascular morbidity and mortality. The last half-century of renal research has helped define the contribution of the parathyroid hormone, calcitriol, fibroblast growth factor 23, and Klotho in the regulation of phosphate. However, despite new discoveries and insights gained during this time, what remains unchanged is the recognition that phosphate retention is the initiating factor for the development of many of the complications observed in CKD, namely secondary hyperparathyroidism and bone and cardiovascular diseases. Controlling phosphate load remains the primary goal in the treatment of CKD. This review discusses the clinical effects of dysregulated phosphate metabolism, particularly in CKD, and its association with cardiovascular disease. The importance of early control of phosphate load in the treatment of CKD is emphasized, and the latest research in the treatment of phosphate retention is discussed.
MeSH term(s)	Bone Diseases, Metabolic/etiology ; Cardiovascular Diseases/etiology ; Cardiovascular Diseases/metabolism ; Fibroblast Growth Factor-23 ; Fibroblast Growth Factors/metabolism ; Glucuronidase/metabolism ; Homeostasis ; Humans ; Hyperparathyroidism, Secondary/etiology ; Hyperphosphatemia/therapy ; Klotho Proteins ; Phosphates/blood ; Phosphates/metabolism ; Renal Insufficiency, Chronic/blood ; Renal Insufficiency, Chronic/complications ; Renal Insufficiency, Chronic/metabolism
Chemical Substances	Phosphates ; Fibroblast Growth Factors (62031-54-3) ; Fibroblast Growth Factor-23 (7Q7P4S7RRE) ; Glucuronidase (EC 3.2.1.31) ; Klotho Proteins (EC 3.2.1.31)
Language	English
Publishing date	2016-02-10
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2226665-3
ISSN	1555-905X ; 1555-9041
ISSN (online)	1555-905X
ISSN	1555-9041
DOI	10.2215/CJN.11901115
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Zs.A 6584: Show issues

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Article ; Online: Single-dose mucosal replicon-particle vaccine protects against lethal Nipah virus infection up to 3 days after vaccination.

Science advances

2023 Volume 9, Issue 31, Page(s) eadh4057

Abstract: Nipah virus (NiV) causes a highly lethal disease in humans who present with acute respiratory or neurological signs. No vaccines against NiV have been approved to date. Here, we report on the clinical impact of a novel NiV-derived nonspreading replicon ... ...

Abstract	Nipah virus (NiV) causes a highly lethal disease in humans who present with acute respiratory or neurological signs. No vaccines against NiV have been approved to date. Here, we report on the clinical impact of a novel NiV-derived nonspreading replicon particle lacking the fusion (F) protein gene (NiVΔF) as a vaccine in three small animal models of disease. A broad antibody response was detected that included immunoglobulin G (IgG) and IgA subtypes with demonstrable Fc-mediated effector function targeting multiple viral antigens. Single-dose intranasal vaccination up to 3 days before challenge prevented clinical signs and reduced virus levels in hamsters and immunocompromised mice; decreases were seen in tissues and mucosal secretions, critically decreasing potential for virus transmission. This virus replicon particle system provides a vital tool to the field and demonstrates utility as a highly efficacious and safe vaccine candidate that can be administered parenterally or mucosally to protect against lethal Nipah disease.
MeSH term(s)	Cricetinae ; Humans ; Animals ; Mice ; Viral Vaccines ; Henipavirus Infections/prevention & control ; Henipavirus Infections/genetics ; Vaccination ; Disease Models, Animal ; Nipah Virus/genetics ; Replicon
Chemical Substances	Viral Vaccines
Language	English
Publishing date	2023-08-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.adh4057
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Article ; Online: The vitamin D analog 1α,25-Dihydroxy-2β-(3-Hydroxypropyloxy) vitamin D(3) (Eldecalcitol) is a potent regulator of calcium and phosphate metabolism.

Brown, Alex J / Ritter, Cynthia S

Calcified tissue international

2011 Volume 89, Issue 5, Page(s) 372–378

Abstract: The vitamin D analog 1α,25-dihydroxy-2β-(3-hydroxypropyloxy)vitamin D(3) (ED-71 or eldecalcitol) has been developed for treatment of osteoporosis, but its effects on mineral metabolism have not been investigated in detail. In the present study, we ... ...

Abstract	The vitamin D analog 1α,25-dihydroxy-2β-(3-hydroxypropyloxy)vitamin D(3) (ED-71 or eldecalcitol) has been developed for treatment of osteoporosis, but its effects on mineral metabolism have not been investigated in detail. In the present study, we compared the effects of eldecalcitol and calcitriol on calcium (Ca) and phosphate (Pi) handling in rats. Oral administration of eldecalcitol (0, 7.5, 20, or 50 pmol) q.o.d. for 2 weeks dose-dependently increased ionized Ca, intestinal Ca absorption, and urinary Ca excretion, while these doses of calcitriol had no significant effects. The highest dose of eldecalcitol did not alter serum Pi but stimulated both intestinal Pi absorption and urinary Pi excretion; the latter was attributable, in part, to increased serum FGF-23. The effects of high-dose eldecalcitol on Ca and Pi absorption and urinary excretion and FGF-23 persisted for several days following cessation of treatment. The higher potency of eldecalcitol on Ca and Pi handling was also observed in parathyroidectomized rats infused with PTH, excluding a role for differential regulation of PTH. Direct measurement of duodenal Ca absorption by the in situ loop method confirmed the higher potency of eldecalcitol in this segment via induction of TRPV6. These studies indicated that with chronic administration eldecalcitol is more potent than calcitriol at stimulating intestinal absorption of Ca and Pi, as well as FGF-23. The mechanisms responsible for the higher potency of eldecalcitol are speculated to be its higher vitamin D-binding protein (DBP) affinity and resistance to metabolism.
MeSH term(s)	Animals ; Calcitriol/pharmacology ; Calcium/metabolism ; Dose-Response Relationship, Drug ; Duodenum/metabolism ; Female ; Fibroblast Growth Factors/blood ; Phosphates/metabolism ; Rats ; TRPV Cation Channels/metabolism ; Vitamin D/analogs & derivatives ; Vitamin D/pharmacology
Chemical Substances	Phosphates ; TRPV Cation Channels ; TRPV6 channel ; fibroblast growth factor 23 ; Vitamin D (1406-16-2) ; Fibroblast Growth Factors (62031-54-3) ; Calcitriol (FXC9231JVH) ; eldecalcitol (I2JP8UE90H) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2011-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	304266-2
ISSN	1432-0827 ; 0944-0747 ; 0008-0594 ; 0171-967X
ISSN (online)	1432-0827
ISSN	0944-0747 ; 0008-0594 ; 0171-967X
DOI	10.1007/s00223-011-9528-7
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Zs.A 317: Show issues

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Article ; Online: Direct suppression of Pth gene expression by the vitamin D prohormones doxercalciferol and calcidiol requires the vitamin D receptor.

Ritter, Cynthia S / Brown, Alex J

Journal of molecular endocrinology

2011 Volume 46, Issue 2, Page(s) 63–66

Abstract: Vitamin D compounds regulate PTH at the transcriptional level, presumably via binding to the vitamin D receptor (VDR), but the exact mechanism is presently unclear. We recently reported that the several vitamin D prohormones with low VDR affinity ... ...

Abstract	Vitamin D compounds regulate PTH at the transcriptional level, presumably via binding to the vitamin D receptor (VDR), but the exact mechanism is presently unclear. We recently reported that the several vitamin D prohormones with low VDR affinity suppressed PTH, even when their activation was inhibited, raising the possibility that their actions may be VDR independent. To test this hypothesis, we developed a novel organ culture that allowed the assessment of activities of the prohormones on PTH release from wild-type and VDR-null thyroparathyroid explants. The cultures remained viable with respect to PTH release for at least 2 weeks. Full suppression of PTH by the native vitamin D hormone, 1α,25-dihydroxyvitamin D(3) [1α,25 (OH)(2)D(3)], required 2 days, consistent with a transcriptional mechanism, and was reversible, indicating that reduced PTH was not attributable to cell death. Inhibition of PTH release by 1α,25 (OH)(2)D(3) and two prohormones, 25-hydroxyvitamin D(3) and 1α-hydroxyvitamin D(2), was observed in explants from wild-type mice but not in those from VDR-null mice. These findings 1) are the first direct demonstration of the role of the VDR in regulation of PTH by 1α,25(OH)(2)D(3), 2) confirm that the suppressive actions of the vitamin D prohormones are mediated by the VDR, and 3) introduce a novel organ culture model that allows the ex vivo study of the function of parathyroid glands from transgenic animals.
MeSH term(s)	Animals ; Calcifediol/metabolism ; Calcifediol/pharmacology ; Calcitriol/metabolism ; Calcitriol/pharmacology ; Ergocalciferols/metabolism ; Ergocalciferols/pharmacology ; Gene Expression ; Gene Expression Regulation ; Mice ; Mice, Transgenic ; Organ Culture Techniques/methods ; Parathyroid Glands/cytology ; Parathyroid Glands/drug effects ; Parathyroid Glands/metabolism ; Parathyroid Glands/secretion ; Parathyroid Hormone/antagonists & inhibitors ; Parathyroid Hormone/genetics ; Parathyroid Hormone/metabolism ; Receptors, Calcitriol/deficiency ; Receptors, Calcitriol/genetics ; Transcription, Genetic
Chemical Substances	Ergocalciferols ; Parathyroid Hormone ; Receptors, Calcitriol ; 1 alpha-hydroxyergocalciferol (3DIZ9LF5Y9) ; Calcitriol (FXC9231JVH) ; Calcifediol (P6YZ13C99Q)
Language	English
Publishing date	2011-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	645012-x
ISSN	1479-6813 ; 0952-5041
ISSN (online)	1479-6813
ISSN	0952-5041
DOI	10.1677/JME-10-0128
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Zs.A 2406: Show issues

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Article ; Online: Suppression of PTH by the vitamin D analog eldecalcitol is modulated by its high affinity for the serum vitamin D-binding protein and resistance to metabolism.

Ritter, Cynthia S / Brown, Alex J

Journal of cellular biochemistry

2011 Volume 112, Issue 5, Page(s) 1348–1352

Abstract: Eldecalcitol [1α,25-dihydroxy-2β-(3-hydroxypropyloxy)vitamin D(3) ], a vitamin D analog with enhanced efficacy for treatment of osteoporosis, has been found to be less potent than 1,25-dihydroxyvitamin D(3) (calcitriol) in suppressing PTH in vivo. To ... ...

Abstract	Eldecalcitol [1α,25-dihydroxy-2β-(3-hydroxypropyloxy)vitamin D(3) ], a vitamin D analog with enhanced efficacy for treatment of osteoporosis, has been found to be less potent than 1,25-dihydroxyvitamin D(3) (calcitriol) in suppressing PTH in vivo. To define the mechanism for the latter observation, we compared the effects of eldecalcitol and calcitriol on PTH secretion by bovine parathyroid cells. While the two compounds showed similar potency when the cells were cultured in medium containing 15% newborn calf serum, eldecalcitol was 100 times more potent than calcitriol in the absence of serum. Eldecalcitol has a higher affinity for the serum vitamin D-binding protein (DBP), and therefore binding to DBP, and possibly other serum components, appears to limit the uptake and activity of eldecalcitol in parathyroid cells, providing an explanation for the lower PTH suppressing activity in vivo (100% serum). However, the 100-fold higher activity of eldecalcitol in the absence of serum was unexpected since the VDR affinity for eldecalcitol is eightfold lower than for calcitriol. The enhanced activity was not due to preferential uptake, but to a resistance to metabolism. While 1 nM [(3) H]calcitriol was completely degraded within 24 h, [(3) H]eldecalcitol was not metabolized, despite the induction of the vitamin D catabolic enzyme, 24-hydroxylase (CYP24A). The resistance to metabolism is the likely explanation for the higher potency of eldecalcitol in suppressing PTH in cell culture lacking serum. Thus, the unique properties of eldecalcitol in vivo can be attributed, at least in part, to its high-DBP affinity which increases the half-life, but limits the uptake of eldecalcitol, and to its reduced metabolism, which prolongs the activity of this analog in target tissues.
MeSH term(s)	Animals ; Cattle ; Cells, Cultured ; Osteoporosis/drug therapy ; Parathyroid Hormone/antagonists & inhibitors ; Parathyroid Hormone/secretion ; Steroid Hydroxylases/metabolism ; Vitamin D/analogs & derivatives ; Vitamin D/metabolism ; Vitamin D/pharmacology ; Vitamin D/therapeutic use ; Vitamin D-Binding Protein/blood ; Vitamin D-Binding Protein/metabolism ; Vitamin D3 24-Hydroxylase
Chemical Substances	Parathyroid Hormone ; Vitamin D-Binding Protein ; Vitamin D (1406-16-2) ; Steroid Hydroxylases (EC 1.14.-) ; Vitamin D3 24-Hydroxylase (EC 1.14.15.16) ; eldecalcitol (I2JP8UE90H)
Language	English
Publishing date	2011-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	392402-6
ISSN	1097-4644 ; 0730-2312
ISSN (online)	1097-4644
ISSN	0730-2312
DOI	10.1002/jcb.23051
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Zs.A 1114: Show issues

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Article ; Online: Teaching a new mouse old tricks: Humanized mice as an infection model for Variola virus.

Hutson, Christina L / Kondas, Ashley V / Ritter, Jana M / Reed, Zachary / Ostergaard, Sharon Dietz / Morgan, Clint N / Gallardo-Romero, Nadia / Tansey, Cassandra / Mauldin, Matthew R / Salzer, Johanna S / Hughes, Christine M / Goldsmith, Cynthia S / Carroll, Darin / Olson, Victoria A

PLoS pathogens

2021 Volume 17, Issue 9, Page(s) e1009633

Abstract: ... While known VARV stocks are secure, smallpox remains a bioterrorist threat agent. Recent U.S ...

Abstract	Smallpox, caused by the solely human pathogen Variola virus (VARV), was declared eradicated in 1980. While known VARV stocks are secure, smallpox remains a bioterrorist threat agent. Recent U.S. Food and Drug Administration approval of the first smallpox anti-viral (tecovirimat) therapeutic was a successful step forward in smallpox preparedness; however, orthopoxviruses can become resistant to treatment, suggesting a multi-therapeutic approach is necessary. Animal models are required for testing medical countermeasures (MCMs) and ideally MCMs are tested directly against the pathogen of interest. Since VARV only infects humans, a representative animal model for testing therapeutics directly against VARV remains a challenge. Here we show that three different humanized mice strains are highly susceptible to VARV infection, establishing the first small animal model using VARV. In comparison, the non-humanized, immunosuppressed background mouse was not susceptible to systemic VARV infection. Following an intranasal VARV challenge that mimics the natural route for human smallpox transmission, the virus spread systemically within the humanized mouse before mortality (~ 13 days post infection), similar to the time from exposure to symptom onset for ordinary human smallpox. Our identification of a permissive/representative VARV animal model can facilitate testing of MCMs in a manner consistent with their intended use.
MeSH term(s)	Animals ; Disease Models, Animal ; Humans ; Mice ; Smallpox ; Variola virus
Language	English
Publishing date	2021-09-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7374
ISSN (online)	1553-7374
ISSN	1553-7374
DOI	10.1371/journal.ppat.1009633
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Article ; Online: Abrogation of MAP4K4 protein function causes congenital anomalies in humans and zebrafish.

Patterson, Victoria / Ullah, Farid / Bryant, Laura / Griffin, John N / Sidhu, Alpa / Saliganan, Sheila / Blaile, Mackenzie / Saenz, Margarita S / Smith, Rosemarie / Ellingwood, Sara / Grange, Dorothy K / Hu, Xuyun / Mireguli, Maimaiti / Luo, Yanfei / Shen, Yiping / Mulhern, Maureen / Zackai, Elaine / Ritter, Alyssa / Izumi, Kosaki /

Hoefele, Julia / Wagner, Matias / Riedhammer, Korbinian M / Seitz, Barbara / Robin, Nathaniel H / Goodloe, Dana / Mignot, Cyril / Keren, Boris / Cox, Helen / Jarvis, Joanna / Hempel, Maja / Gibson, Cynthia Forster / Tran Mau-Them, Frederic / Vitobello, Antonio / Bruel, Ange-Line / Sorlin, Arthur / Mehta, Sarju / Raymond, F Lucy / Gilmore, Kelly / Powell, Bradford C / Weck, Karen / Li, Chumei / Vulto-van Silfhout, Anneke T / Giacomini, Thea / Mancardi, Maria Margherita / Accogli, Andrea / Salpietro, Vincenzo / Zara, Federico / Vora, Neeta L / Davis, Erica E / Burdine, Rebecca / Bhoj, Elizabeth

Science advances

2023 Volume 9, Issue 17, Page(s) eade0631

Abstract: We report 21 families displaying neurodevelopmental differences and multiple congenital anomalies while bearing a series of rare variants ... ...

Abstract	We report 21 families displaying neurodevelopmental differences and multiple congenital anomalies while bearing a series of rare variants in
MeSH term(s)	Animals ; Humans ; Zebrafish ; Signal Transduction ; Protein Serine-Threonine Kinases ; Intracellular Signaling Peptides and Proteins
Chemical Substances	MAP4K4 protein, human (EC 2.7.1.11) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Intracellular Signaling Peptides and Proteins
Language	English
Publishing date	2023-04-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.ade0631
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Article ; Online: Teaching a new mouse old tricks

Christina L Hutson / Ashley V Kondas / Jana M Ritter / Zachary Reed / Sharon Dietz Ostergaard / Clint N Morgan / Nadia Gallardo-Romero / Cassandra Tansey / Matthew R Mauldin / Johanna S Salzer / Christine M Hughes / Cynthia S Goldsmith / Darin Carroll / Victoria A Olson

PLoS Pathogens, Vol 17, Iss 9, p e

Humanized mice as an infection model for Variola virus.

2021 Volume 1009633

Abstract: ... While known VARV stocks are secure, smallpox remains a bioterrorist threat agent. Recent U.S ...

Abstract	Smallpox, caused by the solely human pathogen Variola virus (VARV), was declared eradicated in 1980. While known VARV stocks are secure, smallpox remains a bioterrorist threat agent. Recent U.S. Food and Drug Administration approval of the first smallpox anti-viral (tecovirimat) therapeutic was a successful step forward in smallpox preparedness; however, orthopoxviruses can become resistant to treatment, suggesting a multi-therapeutic approach is necessary. Animal models are required for testing medical countermeasures (MCMs) and ideally MCMs are tested directly against the pathogen of interest. Since VARV only infects humans, a representative animal model for testing therapeutics directly against VARV remains a challenge. Here we show that three different humanized mice strains are highly susceptible to VARV infection, establishing the first small animal model using VARV. In comparison, the non-humanized, immunosuppressed background mouse was not susceptible to systemic VARV infection. Following an intranasal VARV challenge that mimics the natural route for human smallpox transmission, the virus spread systemically within the humanized mouse before mortality (~ 13 days post infection), similar to the time from exposure to symptom onset for ordinary human smallpox. Our identification of a permissive/representative VARV animal model can facilitate testing of MCMs in a manner consistent with their intended use.
Keywords	Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
Subject code	630
Language	English
Publishing date	2021-09-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
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Article ; Online: The vitamin D analog ED-71 is a potent regulator of intestinal phosphate absorption and NaPi-IIb.

Brown, Alex J / Zhang, Fanjie / Ritter, Cynthia S

Endocrinology

2012 Volume 153, Issue 11, Page(s) 5150–5156

Abstract: The vitamin D analog ED-71 [1α,25-dihydroxy-2β-(3-hydroxypropyloxy)vitamin D(3)] has been approved for treatment of osteoporosis in Japan, but its effects on mineral metabolism have not been fully explored. We investigated the actions of ED-71 on ... ...

Abstract	The vitamin D analog ED-71 [1α,25-dihydroxy-2β-(3-hydroxypropyloxy)vitamin D(3)] has been approved for treatment of osteoporosis in Japan, but its effects on mineral metabolism have not been fully explored. We investigated the actions of ED-71 on phosphate (Pi) absorption and induction of the intestinal sodium/phosphate cotransporters. Oral treatment of vitamin D-deficient rats with ED-71 (20 pmol every other day for 8 d) produced a maximal 8-fold increase in duodenal Pi absorption, measured by the in situ loop method, whereas 1,25-dihyroxyvitamin D(3) [1,25(OH)(2)D(3]), at doses up to 150 pmol, had no effect. This action of ED-71 was attributable to a dramatic 24-fold induction of sodium-dependent Pi transporter type IIb (NaPi-IIb) mRNA in the duodenum; Pit-1 and Pit-2 mRNA levels were not increased. In vitamin D-replete rats, ED-71 treatment (50 pmol) at 72 and 24 h before death increased NaPi-IIb mRNA in the duodenum and jejunum, but not the ileum, whereas 1,25(OH)(2)D(3) at 1000 pmol was ineffective in all segments. Single oral doses of ED-71 increased mouse intestinal NaPi-IIb mRNA and protein between 6 and 24 h. Surprisingly, rat lung NaPi-IIb was not increased by ED-71, despite its coexpression with the vitamin D receptor in alveolar type II cells. However, ED-71 did not induce intestinal NaPi-IIb in vitamin D receptor-ablated mice. The greater potency of ED-71 than 1,25(OH)(2)D(3) on NaPi-IIb appears to be due to much higher and more prolonged levels of ED-71 in the circulation. In summary, ED-71, due to its disparate pharmacokinetics, is a much more potent inducer of intestinal Pi absorption and NaPi-IIb than 1,25(OH)(2)D(3), suggesting a role for this analog in the treatment of Pi-wasting disorders.
MeSH term(s)	Absorption/drug effects ; Animals ; Calcitriol/analogs & derivatives ; Calcitriol/pharmacology ; Intestines/drug effects ; Intestines/metabolism ; Male ; Mice ; Mice, Knockout ; Phosphates/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Calcitriol/genetics ; Receptors, Calcitriol/metabolism ; Sodium-Phosphate Cotransporter Proteins, Type IIb/genetics ; Sodium-Phosphate Cotransporter Proteins, Type IIb/metabolism ; Vitamin D/analogs & derivatives ; Vitamin D Deficiency/metabolism
Chemical Substances	Phosphates ; Receptors, Calcitriol ; Slc34a2 protein, rat ; Sodium-Phosphate Cotransporter Proteins, Type IIb ; Vitamin D (1406-16-2) ; Calcitriol (FXC9231JVH) ; eldecalcitol (I2JP8UE90H)
Language	English
Publishing date	2012-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2012-1587
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Article ; Online: Pathology and Pathogenesis of SARS-CoV-2 Associated with Fatal Coronavirus Disease, United States.

Martines, Roosecelis B / Ritter, Jana M / Matkovic, Eduard / Gary, Joy / Bollweg, Brigid C / Bullock, Hannah / Goldsmith, Cynthia S / Silva-Flannery, Luciana / Seixas, Josilene N / Reagan-Steiner, Sarah / Uyeki, Timothy / Denison, Amy / Bhatnagar, Julu / Shieh, Wun-Ju / Zaki, Sherif R

Emerging infectious diseases

2020 Volume 26, Issue 9, Page(s) 2005–2015

Abstract: An ongoing pandemic of coronavirus disease (COVID-19) is caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Characterization of the histopathology and cellular localization of SARS-CoV-2 in the tissues of patients with ...

Abstract	An ongoing pandemic of coronavirus disease (COVID-19) is caused by infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Characterization of the histopathology and cellular localization of SARS-CoV-2 in the tissues of patients with fatal COVID-19 is critical to further understand its pathogenesis and transmission and for public health prevention measures. We report clinicopathologic, immunohistochemical, and electron microscopic findings in tissues from 8 fatal laboratory-confirmed cases of SARS-CoV-2 infection in the United States. All cases except 1 were in residents of long-term care facilities. In these patients, SARS-CoV-2 infected epithelium of the upper and lower airways with diffuse alveolar damage as the predominant pulmonary pathology. SARS-CoV-2 was detectable by immunohistochemistry and electron microscopy in conducting airways, pneumocytes, alveolar macrophages, and a hilar lymph node but was not identified in other extrapulmonary tissues. Respiratory viral co-infections were identified in 3 cases; 3 cases had evidence of bacterial co-infection.
MeSH term(s)	Aged ; Betacoronavirus/pathogenicity ; COVID-19 ; Coronavirus Infections/pathology ; Coronavirus Infections/virology ; Female ; Humans ; Immunohistochemistry ; Lung/pathology ; Lung/virology ; Male ; Microscopy, Electron ; Middle Aged ; Pandemics ; Pneumonia, Viral/pathology ; Pneumonia, Viral/virology ; SARS-CoV-2 ; United States/epidemiology
Keywords	covid19
Language	English
Publishing date	2020-05-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	1380686-5
ISSN	1080-6059 ; 1080-6040
ISSN (online)	1080-6059
ISSN	1080-6040
DOI	10.3201/eid2609.202095
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