Acute Hepatitis as a Manifestation of Parvovirus B19 Infection

Hatakka, Aleisha; Klein, Julianne; He, Runtao; Piper, Jessica; Tam, Edward; Walkty, Andrew

doi:10.1128/jcm.00575-11

Cited by 42 publications

(28 citation statements)

References 13 publications

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“…The pathogenesis of parvoviruses is generally associated with their predilection for actively dividing cells and different parvoviruses have different organ tropism ( 32 ). Parvovirus hepatitis in other species is rare, although parvovirus B19 can be associated with acute hepatitis in humans after transfusion of contaminated blood products ( 33 , 34 ). …”

Section: Discussionmentioning

confidence: 99%

New Parvovirus Associated with Serum Hepatitis in Horses after Inoculation of Common Biological Product

Divers¹,

Tennant²,

Kumar³

et al. 2018

Emerg. Infect. Dis.

237

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Equine serum hepatitis (i.e., Theiler’s disease) is a serious and often life-threatening disease of unknown etiology that affects horses. A horse in Nebraska, USA, with serum hepatitis died 65 days after treatment with equine-origin tetanus antitoxin. We identified an unknown parvovirus in serum and liver of the dead horse and in the administered antitoxin. The equine parvovirus-hepatitis (EqPV-H) shares <50% protein identity with its phylogenetic relatives of the genus Copiparvovirus. Next, we experimentally infected 2 horses using a tetanus antitoxin contaminated with EqPV-H. Viremia developed, the horses seroconverted, and acute hepatitis developed that was confirmed by clinical, biochemical, and histopathologic testing. We also determined that EqPV-H is an endemic infection because, in a cohort of 100 clinically normal adult horses, 13 were viremic and 15 were seropositive. We identified a new virus associated with equine serum hepatitis and confirmed its pathogenicity and transmissibility through contaminated biological products.

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Section: Discussionmentioning

confidence: 99%

New Parvovirus Associated with Serum Hepatitis in Horses after Inoculation of Common Biological Product

Divers¹,

Tennant²,

Kumar³

et al. 2018

Emerg. Infect. Dis.

237

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“…The virus, provisionally named parvovirus-like hybrid virus (PHV), was detected in samples from patients with chronic seronegative (non-A-E) hepatitis and diarrhea of unknown etiology. The initial finding of a novel parvovirus-/circovirus-like agent in these patients was of great interest because these viruses are known to broadly infect insects, vertebrate animals, and humans (27)(28)(29), and specific members, such as parvovirus B19 in humans and porcine circovirus type 2 (PCV2) in pigs, have been linked to hepatitis (30)(31)(32). Furthermore, a study by Xu et al recently described the discovery of a hybrid DNA virus in serum samples from Chinese patients with seronegative hepatitis, named NIH-CQV, with a sequence nearly identical to that of PHV (33).…”

mentioning

confidence: 99%

The Perils of Pathogen Discovery: Origin of a Novel Parvovirus-Like Hybrid Genome Traced to Nucleic Acid Extraction Spin Columns

Naccache

Greninger

Lee

et al. 2013

J Virol

225

195

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f Next-generation sequencing was used for discovery and de novo assembly of a novel, highly divergent DNA virus at the interface between the Parvoviridae and Circoviridae. The virus, provisionally named parvovirus-like hybrid virus (PHV), is nearly identical by sequence to another DNA virus, NIH-CQV, previously detected in Chinese patients with seronegative (non-A-E) hepatitis. Although we initially detected PHV in a wide range of clinical samples, with all strains sharing ϳ99% nucleotide and amino acid identity with each other and with NIH-CQV, the exact origin of the virus was eventually traced to contaminated silica-binding spin columns used for nucleic acid extraction. Definitive confirmation of the origin of PHV, and presumably NIH-CQV, was obtained by in-depth analyses of water eluted through contaminated spin columns. Analysis of environmental metagenome libraries detected PHV sequences in coastal marine waters of North America, suggesting that a potential association between PHV and diatoms (algae) that generate the silica matrix used in the spin columns may have resulted in inadvertent viral contamination during manufacture. The confirmation of PHV/NIH-CQV as laboratory reagent contaminants and not bona fide infectious agents of humans underscores the rigorous approach needed to establish the validity of new viral genomes discovered by nextgeneration sequencing.

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“…Although B19 infection has been implicated in pathogenesis of liver diseases and development of SLE, the effects of B19 and its viral proteins including NS1, VP1u and VP2 on hepatic injury in SLE is still obscure [6], [9]–[16]. In the present study, we revealed the aggravated effects of B19 NS1 protein on hepatic injury in NZB/W F1 mice by significantly enhancing the expressions of iNOS and COX-2 proteins and lymphocyte infiltration.…”

Section: Discussionmentioning

confidence: 46%

“…Indeed, various studies have postulated a connection between B19 infection and liver injury. A clinical study reported the existence of B19 DNA in a liver biopsy specimen from a patient with acute hepatitis [9]. Another studies also suggested an important role of B19 infection in acute icteric hepatitis liver injury [10] and acute fulminant hepatitis with bone marrow failure [11].…”

Section: Introductionmentioning

confidence: 99%

Human Parvovirus B19 NS1 Protein Aggravates Liver Injury in NZB/W F1 Mice

et al. 2013

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Human parvovirus B19 (B19) has been associated with a variety of diseases. However, the influence of B19 viral proteins on hepatic injury in SLE is still obscure. To elucidate the effects of B19 viral proteins on livers in SLE, recombinant B19 NS1, VP1u or VP2 proteins were injected subcutaneously into NZB/W F1 mice, respectively. Significant expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were detected in NZB/W F1 mice receiving B19 NS1 as compared to those mice receiving PBS. Markedly hepatocyte disarray and lymphocyte infiltration were observed in livers from NZB/WF 1 mice receiving B19 NS1 as compared to those mice receiving PBS. Additionally, significant increases of Tumor Necrosis Factor –α (TNF-α), TNF-α receptor, IκB kinase –α (IKK-α), nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor (IκB) and nuclear factor-kappa B (NF-κB) were detected in livers from NZB/W F1 mice receiving B19 NS1 as compared to those mice receiving PBS. Accordingly, significant increases of matrix metalloproteinase-9 (MMP9) and U-plasminogen activator (uPA) were also detected in livers from NZB/W F1 mice receiving B19 NS1 as compared to those mice receiving PBS. Contrarily, no significant variation on livers from NZB/W F1 mice receiving B19 VP1u or VP2 was observed as compared to those mice receiving PBS. These findings firstly demonstrated the aggravated effects of B19 NS1 but not VP1u or VP2 protein on hepatic injury and provide a clue in understanding the role of B19 NS1 on hepatic injury in SLE.

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Acute Hepatitis as a Manifestation of Parvovirus B19 Infection

Cited by 42 publications

References 13 publications

New Parvovirus Associated with Serum Hepatitis in Horses after Inoculation of Common Biological Product

New Parvovirus Associated with Serum Hepatitis in Horses after Inoculation of Common Biological Product

The Perils of Pathogen Discovery: Origin of a Novel Parvovirus-Like Hybrid Genome Traced to Nucleic Acid Extraction Spin Columns

Human Parvovirus B19 NS1 Protein Aggravates Liver Injury in NZB/W F1 Mice

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