Serological Diagnosis of Human Polyomavirus Infection

Lundstig, Annika; Dillner, Joakim

doi:10.1007/0-387-32957-9_7

Cited by 35 publications

(27 citation statements)

References 21 publications

(3 reference statements)

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“…Anti-agnoprotein IgG was detected in only 15% and 7.5% of HD and KT patients, respectively, which was significantly lower than the 63% and 80% seropositivity for VP1 and the 42% and 62% seropositivity for LTD1, respectively. In adult populations similar to our study groups, BKV seroprevalence rates of between 60 and 90% have been reported using assays which detect antibody responses directed against the major capsid protein VP1 by EIA or by inhibiting its interaction with receptor-like glycosylated surface structures of type O erythrocytes, i.e., by hemagglutination inhibition (18,23,25,32). The higher VP1-type response may partly be due to the fact that the host immune system is more readily and even systemically (re)exposed to viral surface proteins which typically contain neutralizing epitopes (11).…”

Section: Discussionsupporting

confidence: 80%

Human Polyomavirus Type 1 (BK Virus) Agnoprotein Is Abundantly Expressed but Immunologically Ignored

Leuenberger

Andresen

Gosert

et al. 2007

Clin Vaccine Immunol

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Impaired BK virus (BKV)-specific immunity is a key risk factor of polyomavirus-associated nephropathy. We hypothesized that BKV agnoprotein might constitute an important immune target, as it is highly expressed after infection in vitro. We demonstrate abundant expression of BKV agnoprotein in vivo by immunostaining of kidney transplant (KT) biopsy specimens. Antibody responses to the recombinant affinity-purified BKV agnoprotein, large tumor (LT), and VP1 antigens in 146 sera from 38 KT patients and in 19 sera from 16 healthy donors (HD) were compared by enzyme immunoassay. In HD, low titers of anti-agnoprotein immunoglobulin G (IgG) were found in 15% of sera, compared to 41% for anti-LT antigen and 63% for anti-VP1. No anti-BKV IgM was detectable. In KT patients, anti-agnoprotein IgG and IgM were found in 8% and 3.6% of sera, compared to 63% and 18% for anti-LT IgG and IgM and 80% and 41% for anti-VP1 IgG and IgM, respectively. Anti-LT antigen and anti-VP1, but not anti-agnoprotein, activities increased during and after BKV viremia in KT patients. To investigate specific cellular immune responses, we compared levels of gamma interferon production in peripheral blood mononuclear cells (PBMC) of 10 HD and 30 KT patients by enzyme-linked immunospot assay. In HD, the median numbers of gamma interferon spot-forming units per million PBMC for the agnoprotein, LT antigen, and VP1 peptides were 1, 23, and 25, respectively, whereas the responses in KT patients were 2, 24, and 99, respectively. We conclude that BKV agnoprotein, though abundantly expressed in vivo, is poorly recognized immunologically.The human polyomavirus BK virus (BKV) is the primary etiological agent of polyomavirus-associated nephropathy (PVAN), which causes irreversible graft loss in 1 to 10% of kidney transplant (KT) patients (15, 31). BKV was first discovered in 1970 in the urine of a KT patient with the initials B.K. who had ureteric stenosis and abundant decoy cell shedding (9). However, BKV asymptomatically infects 60 to 90% of the human population (23) and establishes a state of nonreplicative infection in the renourinary tract (13, 15). Intermittent low-level urinary replication with BKV loads of Յ10e6 per ml is detected in 5% of immunocompetent individuals, whereas high-level replication with BKV loads of Ն10e7 per ml is found in 20 to 60% of immunosuppressed patients (15). In KT patients, high-level urine BKV replication is found in 30%, which may be followed by BKV viremia in 13% and by histologically confirmed PVAN in 8% of patients (18). The risk factors for PVAN are not conclusively defined and likely involve complementing determinants of the triad of recipient, graft, and virus (17). Disruption of the balance between the BKV replication and host immune control is generally viewed as a key element of PVAN pathogenesis (5). In the absence of validated antivirals, reducing maintenance immunosuppression represents the primary treatment option for presumptive or definitive PVAN (3,39).BKV belongs to the genus Polyomavirus of the Polyomavir...

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Section: Discussionsupporting

confidence: 80%

Human Polyomavirus Type 1 (BK Virus) Agnoprotein Is Abundantly Expressed but Immunologically Ignored

Leuenberger

Andresen

Gosert

et al. 2007

Clin Vaccine Immunol

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“…Seropositivity for JCV was first determined using hemagglutination inhibition assays, but this has since been replaced by enzyme-linked immunosorbent assays (ELISAs), using recombinant VLPs (182,290). More recently, a two-step anti-JCV antibody assay has been developed in an attempt to stratify disease risk by antibody presence.…”

Section: Analysis Of the Viral Genomementioning

confidence: 99%

Molecular Biology, Epidemiology, and Pathogenesis of Progressive Multifocal Leukoencephalopathy, the JC Virus-Induced Demyelinating Disease of the Human Brain

et al. 2012

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SUMMARY Progressive multifocal leukoencephalopathy (PML) is a debilitating and frequently fatal central nervous system (CNS) demyelinating disease caused by JC virus (JCV), for which there is currently no effective treatment. Lytic infection of oligodendrocytes in the brain leads to their eventual destruction and progressive demyelination, resulting in multiple foci of lesions in the white matter of the brain. Before the mid-1980s, PML was a relatively rare disease, reported to occur primarily in those with underlying neoplastic conditions affecting immune function and, more rarely, in allograft recipients receiving immunosuppressive drugs. However, with the onset of the AIDS pandemic, the incidence of PML has increased dramatically. Approximately 3 to 5% of HIV-infected individuals will develop PML, which is classified as an AIDS-defining illness. In addition, the recent advent of humanized monoclonal antibody therapy for the treatment of autoimmune inflammatory diseases such as multiple sclerosis (MS) and Crohn's disease has also led to an increased risk of PML as a side effect of immunotherapy. Thus, the study of JCV and the elucidation of the underlying causes of PML are important and active areas of research that may lead to new insights into immune function and host antiviral defense, as well as to potential new therapies.

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“…The most common method for studying seroprevalence of polyomaviruses is enzyme-linked immunosorbent assay (ELISA) using VP1 capsomers or VP1-based virus-like particles (VLPs) as the capture antigen [e.g. (15)(16)(17)(18)(19)(20)(21)(22)(23)]. Of these two possibilities, VLP-based ELISA is likely more sensitive as VP1 VLPs morphologically resemble mature infectious particles and thus present conformational epitopes (24).…”

Section: Seroepidemiology Of the Novel Hpyvsmentioning

confidence: 99%

The novel human polyomaviruses HPyV6, 7, 9 and beyond

Ehlers

Wieland

2013

APMIS

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Ehlers B, Wieland U. The novel human polyomaviruses HPyV 6, 7, 9 and beyond. APMIS 2013; 121: 783-95. Since the discovery of Merkel cell polyomavirus and its causative association with Merkel cell carcinoma (MCC), six human polyomaviruses (HPyVs) have been identified that, so far, lack any disease association, which include the human polyomaviruses (HPyV) 6, 7, 9, 10 and 12 as well as the Saint Louis polyomavirus (STLPyV). PCR studies revealed that HPyV6 and HPyV7 are shed from the skin of healthy subjects and of patients suffering from various skin tumours. HPyV6, 7 and 9 were sporadically detected in body fluids and excretions of immunocompromised patients and healthy subjects. HPyV10 was identified in papillomavirusinduced anal condylomas, and variants of HPyV10, named MWPyV and MX polyomavirus (human) (MXPyV), as well as STLPyV were detected in faeces of diarrheal and healthy children. HPyV12 was discovered in organs of the digestive tract of patients suffering from various malignant diseases. Serological studies using capsomer-based or virus-like particle (VLP)-based enzyme-linked immunosorbent assay (ELISA) revealed that HPyV6, 7, 9 and 12 are circulating in the human population. As all other HPyVs, the novel polyomaviruses encode small and large T antigens and thus are potentially oncogenic. However, several studies have revealed a lack of association of HPyV6, 7 and 9 with numerous human tumours. In the future, it will be important to unravel the cell types and body compartments of the novel HPyVs′ reservoir and to search for possible associations with cancer and non-malignant diseases.

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Serological Diagnosis of Human Polyomavirus Infection

Cited by 35 publications

References 21 publications

Human Polyomavirus Type 1 (BK Virus) Agnoprotein Is Abundantly Expressed but Immunologically Ignored

Human Polyomavirus Type 1 (BK Virus) Agnoprotein Is Abundantly Expressed but Immunologically Ignored

Molecular Biology, Epidemiology, and Pathogenesis of Progressive Multifocal Leukoencephalopathy, the JC Virus-Induced Demyelinating Disease of the Human Brain

The novel human polyomaviruses HPyV6, 7, 9 and beyond

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