Parvovirus B19 and immune disorders

Pugliese, A.; Beltramo, Tiziana; Torre, Donato; Roccatello, Dario

doi:10.1002/cbf.1364

Cited by 20 publications

(13 citation statements)

References 16 publications

(17 reference statements)

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“…It should be noted that infection of the brain with B19 of humans is considered controversial and that B19 infections have been associated with certain human autoimmune diseases (24,30,31,41). In some cases with B19-associated meningoencephalitis B19 virus could not be detected in the brain (30,54), and an inappropriate host immune response is assumed as the cause of the brain lesion.…”

Section: Discussionmentioning

confidence: 99%

Leukoencephalopathy Associated with Parvovirus Infection in Cretan Hound Puppies

Schaudien¹,

Polizopoulou

Koutinas

et al. 2010

J Clin Microbiol

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Leukoencephalopathies in dogs encompass presumably inherited conditions such as leukodystrophies, hypomyelination or spongiform degeneration, but other causes, such as virus infections and toxic or nutritional factors, might also play a contributory role. In this report, we provide evidence of parvovirus infection and replication in the brains of five 6-week-old Cretan hound puppies suffering from a puppy shaker syndrome and leukoencephalopathy. Although these puppies belonged to two different litters, they were closely related, tracing back two generations to the same sire. Histologically, a mild to moderate lymphohistiocytic meningitis, with focal lymphohistiocytic leukoencephalitis in two animals, and a mild to moderate vacuolation with myelin loss, mainly in the white matter of the cerebellum was detected. Vacuolation was also found in the corpus callosum, fimbria hippocampi, mesencephalon, capsula interna, basal ganglia, and hypothalamus.

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Section: Discussionmentioning

confidence: 99%

Leukoencephalopathy Associated with Parvovirus Infection in Cretan Hound Puppies

Schaudien¹,

Polizopoulou

Koutinas

et al. 2010

J Clin Microbiol

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“…Whereas the causative role of infection with hepatitis B virus (HBV) and the development of polyarteritis nodosa (PAN) as well as hepatitis C virus (HCV) and mixed cryoglobulinemia are well established, 16–23 the role of other infectious agents is less clear. Infectious agents, such as human immunodeficiency virus, parvovirus B19, cytomegalovirus (CMV), varicella zoster virus, S. aureus , Rickettsiaceae, Treponema pallidum , and Borrelia burgdorferi , and numerous others have been variably associated with vasculitis 4,8,21,24–35 . One should always consider the increased susceptibility of a patient with autoimmune disease to infection with various pathogens, owing not only to immunosuppressive treatment but also to immune dysregulation in these patients 36 .…”

Section: Introductionmentioning

confidence: 99%

Infectious Serologies and Autoantibodies in Wegener's Granulomatosis and Other Vasculitides

Lidar

Lipschitz

Langevitz

et al. 2009

Annals of the New York Academy of Sciences

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In this study we assess the presence of antibodies against infectious agents as well as for a variety of autoantibodies in an attempt to establish associations between various vasculitides and infections in order to shed light on the etiopathogenesis of these diseases and perhaps implicate a potential cure. Sera from patients with Wegener's granulomatosis (WG), polyarteritis nodosa, microscopic polyangiitis, Churg Strauss, and giant cell arteritis were compared to healthy control sera. Serum samples were assessed, using the Bio-Rad BioPlex 2200, for the presence of Toxoplama gondii, cytomegalovirus (CMV), Epstein-Barr virus (EBV), Treponema pallidum, and Saccharomyces cerevisiae. Hepatitis B virus (HBV), hepatitis C virus (HCV), and anti-Helicobacter pylori antibodies were assessed by ELISA. In addition, sera were tested for a panel of antibodies associated with thrombophilia as well as various autoantibodies. The prevalence of antibodies toward HCV and H. pylori was significantly higher among patients with WG. IgG antibodies toward T. gondii and IgM antibodies toward CMV were significantly more common among WG patients than among controls. WG patients exhibited more antibodies toward EBV viral capsid antigen IgG and EBV early antigen IgG compared to sera from healthy controls. In WG, positive associations were disclosed between CMV IgG antibodies and the presence of gastrointestinal manifestations and renal involvement, and there was a higher Birmingham vasculitis activity score in association with elevated titers of EBV viral capsid antigen IgG antibodies. Otorhinolaryngeal manifestations were more common in those with positive IgG antibodies for EBV early antigen. Our results unveil novel associations between WG and various infectious agents, including HCV, H. pylori, T. gondii, CMV, and EBV. In addition to putative roles in initiation and exacerbation of the vasculitic process, it seems that these infectious agents also modulate the clinical phenotype of the disease.

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“…Since B19-infection is commonly detected in patients with SLE [41], these findings may provide a possible explanation on the effects of B19 NS1 in SLE patients with B19-infection.…”

Section: Discussionmentioning

confidence: 78%

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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Parvovirus B19 and immune disorders

Cited by 20 publications

References 16 publications

Leukoencephalopathy Associated with Parvovirus Infection in Cretan Hound Puppies

Leukoencephalopathy Associated with Parvovirus Infection in Cretan Hound Puppies

Infectious Serologies and Autoantibodies in Wegener's Granulomatosis and Other Vasculitides

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

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