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Article ; Online: Autoantibodies against complement components and functional consequences.

Dragon-Durey, Marie-Agnès / Blanc, Caroline / Marinozzi, Maria Chiara / van Schaarenburg, Rosanne A / Trouw, Leendert A

2013 Volume 56, Issue 3, Page(s) 213–221

Abstract: The complement system represents a major component of our innate immune defense. Although the physiological contribution of the complement system is beneficial, it can cause tissue damage when inappropriately activated or when it is a target of an ... ...

Abstract	The complement system represents a major component of our innate immune defense. Although the physiological contribution of the complement system is beneficial, it can cause tissue damage when inappropriately activated or when it is a target of an autoantibody response. Autoantibodies directed against a variety of individual complement components, convertases, regulators and receptors have been described. For several autoantibodies the functional consequences are well documented and clear associations exist with clinical presentation, whereas for other autoantibodies targeting complement components this relation is currently insufficiently clear. Several anti-complement autoantibodies can also be detected in healthy controls, indicating that a second hit is required for such autoantibodies to induce or participate in pathology or alternatively that these antibodies are part of the natural antibody repertoire. In the present review, we describe autoantibodies against complement components and their functional consequences and discuss about their clinical relevance.
MeSH term(s)	Animals ; Autoantibodies/immunology ; Complement C3-C5 Convertases/immunology ; Complement Factor H/immunology ; Complement Pathway, Alternative/immunology ; Complement Pathway, Classical/immunology ; Complement Pathway, Mannose-Binding Lectin/immunology ; Complement System Proteins/immunology ; Humans ; Receptors, Complement/immunology
Chemical Substances	Autoantibodies ; Receptors, Complement ; Complement Factor H (80295-65-4) ; Complement System Proteins (9007-36-7) ; Complement C3-C5 Convertases (EC 3.4.21.-)
Language	English
Publishing date	2013-12-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	424427-8
ISSN	1872-9142 ; 0161-5890
ISSN (online)	1872-9142
ISSN	0161-5890
DOI	10.1016/j.molimm.2013.05.009
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Article ; Online: Detection of Autoantibodies to Complement Components by Surface Plasmon Resonance-Based Technology.

Noe, Remi / Chauvet, Sophie / Togarsimalemath, Shambhuprasad K / Marinozzi, Maria Chiara / Radanova, Maria / Vasilev, Vasil V / Fremeaux-Bacchi, Veronique / Dragon-Durey, Marie-Agnes / Roumenina, Lubka T

Methods in molecular biology (Clifton, N.J.)

2018 Volume 1901, Page(s) 271–280

Abstract: The innate immune complement system is a powerful defense cascade against pathogens, but can induce host tissue damage when overactivated. In pathological conditions, mainly but not restricted to renal diseases, such as lupus nephritis, atypical ... ...

Abstract	The innate immune complement system is a powerful defense cascade against pathogens, but can induce host tissue damage when overactivated. In pathological conditions, mainly but not restricted to renal diseases, such as lupus nephritis, atypical hemolytic uremic syndrome, and C3 glomerulopathies, complement is overactivated or dysregulated by autoantibodies directed against its components and regulators. Among the key autoantibody targets are the initiator of the classical complement pathway C1q, the alternative pathway regulator Factor H, the components of the alternative pathway C3 convertase complex C3 and Factor B and the convertase complex itself. This methodological article describes our experience with a method for detection of anti-complement autoantibodies in real time using surface plasmon resonance-based technology. It allows label-free evaluation of the binding efficacy and stability of the formed antigen-antibody complexes.
MeSH term(s)	Antigens/metabolism ; Autoantibodies/analysis ; Complement System Proteins/immunology ; Dialysis ; Humans ; Immunoglobulin G/isolation & purification ; Surface Plasmon Resonance/methods
Chemical Substances	Antigens ; Autoantibodies ; Immunoglobulin G ; Complement System Proteins (9007-36-7)
Language	English
Publishing date	2018-12-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-8949-2_24
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Article: Autoantibodies against complement components and functional consequences

Dragon-Durey, Marie-Agnès / Blanc, Caroline / Marinozzi, Maria Chiara / van Schaarenburg, Rosanne A / Trouw, Leendert A

Molecular immunology. 2013 Dec. 15, v. 56, no. 3

2013

Abstract	The complement system represents a major component of our innate immune defense. Although the physiological contribution of the complement system is beneficial, it can cause tissue damage when inappropriately activated or when it is a target of an autoantibody response. Autoantibodies directed against a variety of individual complement components, convertases, regulators and receptors have been described. For several autoantibodies the functional consequences are well documented and clear associations exist with clinical presentation, whereas for other autoantibodies targeting complement components this relation is currently insufficiently clear. Several anti-complement autoantibodies can also be detected in healthy controls, indicating that a second hit is required for such autoantibodies to induce or participate in pathology or alternatively that these antibodies are part of the natural antibody repertoire. In the present review, we describe autoantibodies against complement components and their functional consequences and discuss about their clinical relevance.
Keywords	autoantibodies ; complement ; immune response ; receptors
Language	English
Dates of publication	2013-1215
Size	p. 213-221.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	424427-8
ISSN	1872-9142 ; 0161-5890
ISSN (online)	1872-9142
ISSN	0161-5890
DOI	10.1016/j.molimm.2013.05.009
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Article ; Online: Heterogeneous histologic and clinical evolution in 3 cases of dense deposit disease with long-term follow-up.

Figuères, Marie-Lucile / Frémeaux-Bacchi, Véronique / Rabant, Marion / Galmiche, Louise / Marinozzi, Maria Chiara / Grünfeld, Jean-Pierre / Noël, Laure-Hélène / Servais, Aude

Human pathology

2014 Volume 45, Issue 11, Page(s) 2326–2333

Abstract: Dense deposit disease is characterized by dense deposits in the glomerular and tubular basement membranes. We report 3 cases with long-term follow-up differing in histologic pattern and clinical evolution. Clinical and histologic data were collected ... ...

Abstract	Dense deposit disease is characterized by dense deposits in the glomerular and tubular basement membranes. We report 3 cases with long-term follow-up differing in histologic pattern and clinical evolution. Clinical and histologic data were collected between 1976 and 2012. Age at the first manifestations was 6, 11, and 23 years, respectively. They included proteinuria (patient 1) and nephrotic syndrome (patients 2 and 3); renal function was normal in all cases. Two patients (1 and 3) had low complement component 3 (C3) levels. All patients had C3 nephritic factor. Genetic analysis revealed a rare variant of the factor I gene (patient 1) and a heterozygous mutation in complement factor H-related 5 gene (patient 2). Patient 1 underwent 3 biopsies during her 38 years of follow-up. Thickening of the capillary walls of the glomerular and tubular basement membranes was observed, with mild mesangial proliferation and progressive C3 and complement membrane attack complex mesangial deposits. However, renal function remained normal. Patient 2 also underwent 3 biopsies (22 years of follow-up), revealing a gradual decrease in C3 deposition and mesangial cell proliferation. He presented mild renal insufficiency. Patient 3 underwent 2 biopsies, which displayed unusual bulky membranous deposits, confirmed by electron microscopy, with no mesangial cell proliferation and little C3 and complement membrane attack complex deposits. Kidney function remained normal. These 3 cases of dense deposit disease differed in histologic pattern evolution: accumulation of C3 deposits, decrease in C3 deposits and proliferation, and isolated dense deposits. The histologic factors involved in clinical progression remain to be identified.
MeSH term(s)	Adolescent ; Adult ; Child ; Disease Progression ; Female ; Follow-Up Studies ; Glomerulonephritis/pathology ; Glomerulonephritis, Membranoproliferative/pathology ; Humans ; Kidney Glomerulus/pathology ; Male ; Nephrotic Syndrome/pathology ; Renal Insufficiency/pathology ; Young Adult
Language	English
Publishing date	2014-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	207657-3
ISSN	1532-8392 ; 0046-8177
ISSN (online)	1532-8392
ISSN	0046-8177
DOI	10.1016/j.humpath.2014.07.021
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Zs.A 722: Show issues

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Article ; Online: Both Monoclonal and Polyclonal Immunoglobulin Contingents Mediate Complement Activation in Monoclonal Gammopathy Associated-C3 Glomerulopathy.

Chauvet, Sophie / Roumenina, Lubka T / Aucouturier, Pierre / Marinozzi, Maria-Chiara / Dragon-Durey, Marie-Agnès / Karras, Alexandre / Delmas, Yahsou / Le Quintrec, Moglie / Guerrot, Dominique / Jourde-Chiche, Noémie / Ribes, David / Ronco, Pierre / Bridoux, Frank / Fremeaux-Bacchi, Véronique

Frontiers in immunology

2018 Volume 9, Page(s) 2260

Abstract: C3 glomerulopathy (C3G) results from acquired or genetic abnormalities in the complement alternative pathway (AP). C3G with monoclonal immunoglobulin (MIg-C3G) was recently included in the spectrum of "monoclonal gammopathy of renal significance." ... ...

Abstract	C3 glomerulopathy (C3G) results from acquired or genetic abnormalities in the complement alternative pathway (AP). C3G with monoclonal immunoglobulin (MIg-C3G) was recently included in the spectrum of "monoclonal gammopathy of renal significance." However, mechanisms of complement dysregulation in MIg-C3G are not described and the pathogenic effect of the monoclonal immunoglobulin is not understood. The purpose of this study was to investigate the mechanisms of complement dysregulation in a cohort of 41 patients with MIg-C3G. Low C3 level and elevated sC5b-9, both biomarkers of C3 and C5 convertase activation, were present in 44 and 78% of patients, respectively. Rare pathogenic variants were identified in 2/28 (7%) tested patients suggesting that the disease is acquired in a large majority of patients. Anti-complement auto-antibodies were found in 20/41 (49%) patients, including anti-FH (17%), anti-CR1 (27%), anti-FI (5%) auto-antibodies, and C3 Nephritic Factor (7%) and were polyclonal in 77% of patients. Using cofactor assay, the regulation of the AP was altered in presence of purified IgG from 3/9 and 4/7 patients with anti-FH or anti-CR1 antibodies respectively. By using fluid and solid phase AP activation, we showed that total purified IgG of 22/34 (65%) MIg-C3G patients were able to enhance C3 convertase activity. In five documented cases, we showed that the C3 convertase enhancement was mostly due to the monoclonal immunoglobulin, thus paving the way for a new mechanism of complement dysregulation in C3G. All together the results highlight the contribution of both polyclonal and monoclonal Ig in MIg-C3G. They provide direct insights to treatment approaches and opened up a potential way to a personalized therapeutic strategy based on chemotherapy adapted to the B cell clone or immunosuppressive therapy.
MeSH term(s)	Adult ; Complement C3/immunology ; Complement C3/metabolism ; Complement C5/immunology ; Complement C5/metabolism ; Complement Pathway, Alternative/immunology ; Female ; Glomerulonephritis/blood ; Glomerulonephritis/immunology ; Glomerulonephritis/pathology ; Humans ; Immunoglobulin G/blood ; Immunoglobulin G/immunology ; Male ; Middle Aged ; Paraproteinemias/blood ; Paraproteinemias/immunology ; Paraproteinemias/pathology
Chemical Substances	Complement C3 ; Complement C5 ; Immunoglobulin G
Language	English
Publishing date	2018-10-02
Publishing country	Switzerland
Document type	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.2018.02260
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Article ; Online: Anti-Factor B and Anti-C3b Autoantibodies in C3 Glomerulopathy and Ig-Associated Membranoproliferative GN.

Marinozzi, Maria Chiara / Roumenina, Lubka T / Chauvet, Sophie / Hertig, Alexandre / Bertrand, Dominique / Olagne, Jérome / Frimat, Marie / Ulinski, Tim / Deschênes, Georges / Burtey, Stephane / Delahousse, Michel / Moulin, Bruno / Legendre, Christophe / Frémeaux-Bacchi, Véronique / Le Quintrec, Moglie

Journal of the American Society of Nephrology : JASN

2017 Volume 28, Issue 5, Page(s) 1603–1613

Abstract: In C3 glomerulopathy (C3G), the alternative pathway of complement is frequently overactivated by autoantibodies that stabilize the C3 convertase C3bBb. Anti-C3b and anti-factor B (anti-FB) IgG have been reported in three patients with C3G. We screened a ... ...

Abstract	In C3 glomerulopathy (C3G), the alternative pathway of complement is frequently overactivated by autoantibodies that stabilize the C3 convertase C3bBb. Anti-C3b and anti-factor B (anti-FB) IgG have been reported in three patients with C3G. We screened a cohort of 141 patients with C3G and Ig-associated membranoproliferative GN (Ig-MPGN) for anti-FB and anti-C3b autoantibodies using ELISA. We identified seven patients with anti-FB IgG, three patients with anti-C3b IgG, and five patients with anti-FB and anti-C3b IgG. Of these 15 patients, ten were diagnosed with Ig-MPGN. Among those patients with available data, 92% had a nephrotic syndrome, 64% had AKI, and 67% had a documented infection. Patients negative for anti-C3b and anti-FB IgG had much lower rates of infection (17 [25%] patients with C3G and one [10%] patient with Ig-MPGN). After 48 months, four of 15 (26%) positive patients had developed ESRD or died. All 15 patients had high plasma Bb levels, six (40%) patients had low levels of C3, and nine (60%) patients had high levels of soluble C5b9.
MeSH term(s)	Adolescent ; Adult ; Autoantibodies/immunology ; Child ; Complement C3b/immunology ; Complement Factor B/immunology ; Female ; Glomerulonephritis, Membranoproliferative/immunology ; Humans ; Immunoglobulin G/immunology ; Male ; Middle Aged ; Retrospective Studies ; Young Adult
Chemical Substances	Autoantibodies ; Immunoglobulin G ; Complement C3b (80295-43-8) ; Complement Factor B (EC 3.4.21.47)
Language	English
Publishing date	2017-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.2016030343
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Article ; Online: C5 nephritic factors drive the biological phenotype of C3 glomerulopathies.

Marinozzi, Maria-Chiara / Chauvet, Sophie / Le Quintrec, Moglie / Mignotet, Morgane / Petitprez, Florent / Legendre, Christophe / Cailliez, Mathilde / Deschenes, Georges / Fischbach, Michel / Karras, Alexandre / Nobili, Francois / Pietrement, Christine / Dragon-Durey, Marie-Agnes / Fakhouri, Fadi / Roumenina, Lubka T / Fremeaux-Bacchi, Veronique

Kidney international

2017 Volume 92, Issue 5, Page(s) 1232–1241

Abstract: C3 Glomerulopathies, which include Dense Deposit Disease and C3 Glomerulonephritis, are associated with genetic and acquired dysregulation of the C3 convertase alternative pathway of complement. The potential role of the activation of the C5 convertase ... ...

Abstract	C3 Glomerulopathies, which include Dense Deposit Disease and C3 Glomerulonephritis, are associated with genetic and acquired dysregulation of the C3 convertase alternative pathway of complement. The potential role of the activation of the C5 convertase has not been studied extensively. Here we analyzed IgG samples from patients with C3 Glomerulopathies to identify circulating autoantibodies that stabilize the C3 alternative pathway (C3 Nephritic Factors) as well as C5 convertases (C5 Nephritic Factors), thus preventing decay of these enzyme complexes. Rare variants in alternative pathway genes were found in 28 of 120 tested patients. C3 and C5 Nephritic Factors were found in 76 of 101 (75%) and 29 of 59 (49%) of the patients, respectively. Therefore, we compared the results of the assays for the C3 and C5 nephritic factors functional activity: 29% were positive for C3 Nephritic Factors alone, 39% were positive for both C3 and C5 Nephritic Factors, and 10% were positive for C5 Nephritic Factors alone. We found that the addition of properdin-enhanced stabilization of C3 convertase in the presence of IgG doubly positive for both Nephritic Factors, while it did not modify the stabilization mediated by IgG solely positive for C3 Nephritic Factors. Both C3 and C5 Nephritic Factors correlated with C3 consumption, while only C5 Nephritic Factors correlated with sC5b9 levels. C5 Nephritic Factors-positive patients were more likely to have C3 Glomerulonephritis than Dense Deposit Disease. Thus, dysregulation of the C5 convertase contributes to C3 Glomerulopathies inter-disease differences and may have direct therapeutic implications.
MeSH term(s)	Adolescent ; Adult ; Child ; Complement C3 Convertase, Alternative Pathway/immunology ; Complement C3 Nephritic Factor/analysis ; Complement C3 Nephritic Factor/genetics ; Complement C3 Nephritic Factor/immunology ; Complement C3-C5 Convertases/immunology ; Complement C3-C5 Convertases/metabolism ; Complement Membrane Attack Complex/analysis ; Complement Pathway, Alternative/immunology ; Female ; Follow-Up Studies ; Glomerulonephritis, Membranoproliferative/blood ; Glomerulonephritis, Membranoproliferative/genetics ; Glomerulonephritis, Membranoproliferative/immunology ; Glomerulonephritis, Membranoproliferative/mortality ; Humans ; Kaplan-Meier Estimate ; Male ; Middle Aged ; Phenotype ; Properdin/metabolism ; Serologic Tests ; Young Adult
Chemical Substances	Complement C3 Nephritic Factor ; Complement Membrane Attack Complex ; SC5b-9 protein complex ; Properdin (11016-39-0) ; Complement C3-C5 Convertases (EC 3.4.21.-) ; Complement C3 Convertase, Alternative Pathway (EC 3.4.21.47)
Language	English
Publishing date	2017-07-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2017.04.017
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Article ; Online: A Familial C3GN Secondary to Defective C3 Regulation by Complement Receptor 1 and Complement Factor H.

Chauvet, Sophie / Roumenina, Lubka T / Bruneau, Sarah / Marinozzi, Maria Chiara / Rybkine, Tania / Schramm, Elizabeth C / Java, Anuja / Atkinson, John P / Aldigier, Jean Claude / Bridoux, Frank / Touchard, Guy / Fremeaux-Bacchi, Veronique

Journal of the American Society of Nephrology : JASN

2015 Volume 27, Issue 6, Page(s) 1665–1677

Abstract: C3 glomerulopathy is a recently described form of CKD. C3GN is a subtype of C3 glomerulopathy characterized by predominant C3 deposits in the glomeruli and is commonly the result of acquired or genetic abnormalities in the alternative pathway (AP) of the ...

Abstract	C3 glomerulopathy is a recently described form of CKD. C3GN is a subtype of C3 glomerulopathy characterized by predominant C3 deposits in the glomeruli and is commonly the result of acquired or genetic abnormalities in the alternative pathway (AP) of the complement system. We identified and characterized the first mutation of the C3 gene (p. I734T) in two related individuals diagnosed with C3GN. Immunofluorescence and electron microscopy studies showed C3 deposits in the subendothelial space, associated with unusual deposits located near the complement receptor 1 (CR1)-expressing podocytes. In vitro, this C3 mutation exhibited decreased binding to CR1, resulting in less CR1-dependent cleavage of C3b by factor 1. Both patients had normal plasma C3 levels, and the mutant C3 interacted with factor B comparably to wild-type (WT) C3 to form a C3 convertase. Binding of mutant C3 to factor H was normal, but mutant C3 was less efficiently cleaved by factor I in the presence of factor H, leading to enhanced C3 fragment deposition on glomerular cells. In conclusion, our results reveal that a CR1 functional deficiency is a mechanism of intraglomerular AP dysregulation and could influence the localization of the glomerular C3 deposits.
MeSH term(s)	Adult ; Complement C3/genetics ; Complement Factor H/genetics ; Gene Expression Regulation ; Glomerulonephritis, Membranoproliferative/genetics ; Humans ; Male ; Middle Aged ; Pedigree ; Receptors, Complement 3b/genetics
Chemical Substances	CFH protein, human ; Complement C3 ; Receptors, Complement 3b ; Complement Factor H (80295-65-4)
Language	English
Publishing date	2015-10-15
Publishing country	United States
Document type	Case Reports ; Journal Article
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.2015040348
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Article: Molecular epidemiology of KI and WU polyomaviruses in infants with acute respiratory disease and in adult hematopoietic stem cell transplant recipients

Debiaggi, Maurizia / Canducci, Filippo / Brerra, Roberto / Sampaolo, Michela / Marinozzi, Maria Chiara / Parea, Maurizio / Arghittu, Milena / Alessandrino, Emilio Paolo / Nava, Stefano / Nucleo, Elisabetta / Romero, Egidio / Clementi, Massimo

Journal of medical virology. 2010 Jan., v. 82, no. 1

2010

Abstract: Polyomaviruses KI (KIPyV) and WU (WUPyV) were described recently in children with acute respiratory disease. The pathogenic potential of these human viruses has not been determined completely, but a correlation between immunosuppression and virus ... ...

Abstract	Polyomaviruses KI (KIPyV) and WU (WUPyV) were described recently in children with acute respiratory disease. The pathogenic potential of these human viruses has not been determined completely, but a correlation between immunosuppression and virus reactivation has been suggested. In the present study, the association between KI/WUPyV infection and immunosuppression was investigated using sequential nasopharyngeal aspirates from asymptomatic adult hematopoietic stem cell transplant recipients. In parallel, an investigation on the WU/KIPyV prevalence in children with acute respiratory disease was also carried out. Two of the 126 samples obtained from the 31 hematopoietic transplant recipients were positive for KIPyV (1 sample, 0.79%) and WUPyV (1 sample, 0.79%). Both samples were obtained 15 days after allogeneic transplantation and virus persistence was not observed in subsequent samples. In symptomatic children, 7 of the 486 nasopharyngeal aspirates were positive for WUPyV (1.4%) and 1 for KIPyV (0.2%). Single polyomavirus infection was detected in four patients, whereas the remaining patients were co-infected with respiratory syncityal virus (three patients) or adenovirus (one patient). The results suggest that WU/KIPyVs have a limited circulation in Italy and a low pathogenic potential in young children. Brief and asymptomatic infection can occur in hematopoietic transplant recipients. J. Med. Virol. 82:153-156, 2010.
Keywords	covid19
Language	English
Dates of publication	2010-01
Size	p. 153-156.
Publishing place	Wiley Subscription Services, Inc., A Wiley Company
Document type	Article
ZDB-ID	752392-0
ISSN	1096-9071 ; 0146-6615
ISSN (online)	1096-9071
ISSN	0146-6615
DOI	10.1002/jmv.21659
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Article: Two-year prospective study of single infections and co-infections by respiratory syncytial virus and viruses identified recently in infants with acute respiratory disease

Canducci, Filippo / Debiaggi, Maurizia / Sampaolo, Michela / Marinozzi, Maria Chiara / Berrè, Stefano / Terulla, Cristina / Gargantini, Gianluigi / Cambieri, Patrizia / Romero, Egidio / Clementi, Massimo

Journal of medical virology. 2008 Apr., v. 80, no. 4

2008

Abstract: A prospective 2-year analysis including 322 infant patients with acute respiratory disease (ARD) hospitalized in a pediatric department in northern Italy was carried out to evaluate the role as respiratory pathogens or co-pathogens of recently identified ...

Abstract	A prospective 2-year analysis including 322 infant patients with acute respiratory disease (ARD) hospitalized in a pediatric department in northern Italy was carried out to evaluate the role as respiratory pathogens or co-pathogens of recently identified viruses. The presence of respiratory syncitial virus (RSV), human Metapneumoviruses (hMPVs), human Bocaviruses (hBoVs), and human Coronaviruses (hCoVs) was assayed by molecular detection and clinical symptoms evaluated. Nasopharyngeal aspirates from 150 of the 322 infants (46.6%) tested positive for at least one pathogen. Ninety samples (28.0%) tested positive for RSV RNA (61.5% genotype A and 38.5% genotype B), 46 (14.3%) for hMPV RNA (71.7% subtype A and 28.3% subtype B), 28 (8.7%) for hCoV RNA (39.3% hCoV-OC43, 35.7% hCoV-NL63, 21.4% hCoV-HKU1, and 3.6% hCoV-229E), and 7 (2.2%) for hBoV DNA (of the 6 typed, 50% subtype 1 and 50% subtype 2); 21/150 samples revealed the presence of 2 or more viruses. Co-infection rates were higher for hMPVs, hCoVs, and hBoV (38.3%, 46.4%, and 57.1%,) and lower for RSV (23.3%). RSV was associated with the presence of complications (P < 0.001) and hypoxia (P < 0.015). When the presence of RSV alone and the RSV-hMPV co-infections were considered, RSV mono-infected patients resulted to have longer hospitalization and higher hypoxia (P < 0.001). The data highlight that (i) RSV has a central role as a respiratory pathogen of infants, (ii) the wide circulation of recently identified viruses does not reduce the clinical and epidemiological importance of RSV, and that (iii) recently identified agents (hMPVs, hBoVs, and hCoVs) act as primary pathogens or co-pathogens. J. Med. Virol. 80:716-723, 2008.
Keywords	covid19
Language	English
Dates of publication	2008-04
Size	p. 716-723.
Publishing place	Wiley Subscription Services, Inc., A Wiley Company
Document type	Article
ZDB-ID	752392-0
ISSN	1096-9071 ; 0146-6615
ISSN (online)	1096-9071
ISSN	0146-6615
DOI	10.1002/jmv.21108
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