Objective: To test the hypothesis that different preceding infections influence the neurophysiologic classification and clinical features of Guillain–Barre syndrome (GBS) Methods: We tested pretreatment sera, 7 ± 3 (mean ± SD) days from onset, from 229 patients with GBS in a multicenter trial of plasma exchange and immunoglobulin, for serological markers of infection, adhesion molecules, and cytokine receptors, and compared these with neurophysiologic and clinical features Results: Recent infection by Campylobacter jejuni was found in 53 patients (23%), cytomegalovirus in 19 (8%), and Epstein–Barr virus in four (2%) Patients with C jejuni infection were more likely than others to have neurophysiologic criteria of axonal neuropathy or inexcitable nerves, antiganglioside GM 1 antibodies, pure motor GBS, lower CSF protein, and worse outcome Patients with cytomegalovirus infection were younger and more likely than others to have raised serum concentrations of molecules important in T lymphocyte activation and migration, soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble leukocyte selectin, and soluble interleukin-2 receptor (sIL-2R) Concentrations of sICAM-1 and soluble tumor necrosis factor receptor were higher in patients with inexcitable nerves than those with demyelinating neurophysiology Logistic regression analysis showed death or inability to walk unaided at 48 weeks were associated with diarrhea, inexcitable nerves, severe arm weakness, age over 50, raised sIL-2R concentration and absence of immunoglobulin (Ig) M antiganglioside GM 1 antibodies Conclusions: Subtypes of GBS defined by preceding infections were only approximately associated with different patterns of clinical, neurophysiologic, and immunologic features A single infectious agent caused more than one type of pathology in GBS, implying interaction with additional host factors Most patients had no identified infection

Preceding infections, immune factors, and outcome in Guillain-Barré syndrome

Serological tests for antibodies specific for Epstein-Barr virus (EBV) antigens are frequently used to define infection status and for the differential diagnosis of other pathogens responsible for mononucleosis syndrome. Using only three parameters [viral capsid antigen (VCA) IgG, VCA IgM and EBV nuclear antigen (EBNA)-1 IgG],it is normally possible to distinguish acute from past infection: the presence of VCA IgM and VCA IgG without EBNA-1 IgG indicates acute infection, whereas the presence of VCA IgG and EBNA-1 IgG without VCA IgM is typical of past infection. However, serological findings may sometimes be difficult to interpret as VCA IgG can be present without VCA IgM or EBNA-1 IgG in cases of acute or past infection, or all the three parameters may be detected simultaneously in the case of recent infection or during the course of reactivation. A profile of isolated EBNA-1 IgG may also create some doubts. In order to interpret these patterns correctly, it is necessary to determine IgG avidity, identify anti-EBV IgG and IgM antibodies by immunoblotting, and look for heterophile antibodies, anti-EA (D) antibodies or viral genome using molecular biology methods. These tests make it possible to define the status of the infection and solve any problems that may arise in routine laboratory practice.

Serological diagnosis of Epstein-Barr virus infection: Problems and solutions

SUMMARY

Four species of human bocavirus (HBoV) have been recently discovered and classified in the Bocavirus genus (family Parvoviridae, subfamily Parvovirinae). Although detected both in respiratory and stool samples worldwide, HBoV1 is predominantly a respiratory pathogen, whereas HBoV2, HBoV3, and HBoV4 have been found mainly in stool. A variety of signs and symptoms have been described in patients with HBoV infection including rhinitis, pharyngitis, cough, dyspnea, wheezing, pneumonia, acute otitis media, fever, nausea, vomiting, and diarrhea. Many of these potential manifestations have not been systematically explored, and they have been questioned because of high HBoV co-infection rates in symptomatic subjects and high HBoV detection rates in asymptomatic subjects. However, evidence is mounting to show that HBoV1 is an important cause of lower respiratory tract illness. The best currently available diagnostic approaches are quantitative PCR and serology. This concise review summarizes the current clinical knowledge on HBoV species. Copyright © 2011 John Wiley & Sons, Ltd.

Human bocavirus—the first 5 years

Post-transplant lymphoproliferative disorder (PTLD) is a rare but frequently fatal complication of iatrogenic immunosuppression. PTLD encompasses a spectrum of B cell lymphoproliferations ranging from reactive plasmacytic hyperplasia to monomorphic B cell lymphoma.1 The tumours are almost always associated with Epstein-Barr Virus (EBV), and similar lymphoproliferative disorders also occur in other congenital and acquired immunodeficiency states.2 These malignancies reflect an imbalance in the normal control of EBV infection, although the virus is also linked to a subset of Hodgkin's disease and T cell lymphomas in apparently immunocompetent individuals.3–5 Other EBV associated tumours occurring in particular areas of the world include Burkitt's lymphoma in equatorial Africa and nasopharyngeal carcinoma in South East Asia.2 This review discusses the biology of EBV infection in the normal and immunocompromised host and the risk factors and pathogenesis of EBV associated PTLD.

EBV is an enveloped herpesvirus with a 172 kb double stranded DNA genome.2 A defining feature of herpesviruses is their ability to maintain a latent infection with the virus genome retained in host cells without production of infectious virions. EBV targets B lymphocytes through the CD21 receptor and establishes a latent infection both in vivo and in vitro.

### EBV INFECTION IN VITRO

In vitro infection of B lymphocytes with EBV results in the establishment of an immortalised B lymphoblastoid cell line in which the majority of cells contain a non-replicating episomal form of the EBV genome and only a small proportion of cells contain replicating virus. Lymphoblastoid cell lines express a panel of EBV encoded latent antigens which comprise six nuclear proteins (Epstein-Barr nuclear antigens (EBNA)1, -2, -3A, -3B, -3C, and leader protein (LP)) and three latent membrane antigens (LMP1, -2A, and -2B). Abundantly expressed small non-polyadenylated RNAs termed Epstein-Barr virus early RNA (EBER) 1 and 2 are transcribed but not translated, and …

https://jcp.bmj.com/content/jclinpath/53/4/248.full.pdf

The role of EBV in post-transplant malignancies: a review

We identified a new polyomavirus in skin lesions from a patient with trichodysplasia spinulosa (TS). Apart from TS being an extremely rare disease, little is known of its epidemiology. On the basis of knowledge regarding other polyomaviruses, we anticipated that infections with trichodysplasia spinulosa–associated polyomavirus (TSV) occur frequently and become symptomatic only in immunocompromised patients. To investigate this hypothesis, we developed and used a Luminex-based TSV viral protein 1 immunoassay, excluded cross-reactivity with phylogenetically related Merkel cell polyomavirus, and measured TSV seroreactivity. Highest reactivity was found in a TS patient. In 528 healthy persons in the Netherlands, a wide range of seroreactivities was measured and resulted in an overall TSV seroprevalence of 70% (range 10% in small children to 80% in adults). In 80 renal transplant patients, seroprevalence was 89%. Infection with the new TSV polyomavirus is common and occurs primarily at a young age.

/pdf/seroprevalence-of-trichodysplasia-spinulosa-associated-3v6qo2uj6p.pdf

Seroprevalence of trichodysplasia spinulosa-associated polyomavirus.

DNA of the polyomaviruses WU (WUPyV) and KI (KIPyV) and of human bocavirus (HBoV) has been detected with varying frequency in respiratory tract samples of children. However, only little is known about the humoral immune response against these viruses. Our aim was to establish virus-specific serological assays and to determine the prevalence of immunoglobulin G (IgG) against these three viruses in the general population. The capsid proteins VP1 of WUPyV and KIPyV and VP2 of HBoV were cloned into baculovirus vectors and expressed in Sf9 insect cells. IgG antibodies against WUPyV VP1, KIPyV VP1, and HBoV VP2 were determined by immunofluorescence assays in 100 plasma samples of blood donors. The median age of the blood donors was 31 years (range 20 - 66 yrs), 52% were male. 89% of the samples were positive for WUPyV IgG (median age 31 yrs, 49.4% male), 67% were positive for KIPyV IgG (median age 32 yrs, 46.3% male), and 76% were positive for HBoV IgG (median age 32 yrs, 51.3% male). For WUPyV and HBoV, there were no significant differences of the seropositivity rates with respect to age groups or gender. For KIPyV, the seropositivity rate increased significantly from 59% in the age group 20 - 29 years to 100% in the age group > 50 years. High prevalences of antibodies against WUPyV, KIPyV, and HBoV were found in plasma samples of healthy adults. The results indicate that primary infection with these viruses occurs during childhood or youth. For KIPyV, the seropositivity appears to increase further during adulthood.

/pdf/high-prevalence-of-antibodies-against-polyomavirus-wu-59238ri1f4.pdf

High prevalence of antibodies against polyomavirus WU, polyomavirus KI, and human bocavirus in German blood donors

To shed light on primate foamy virus (FV) evolution, we determined the complete nucleotide sequence of the gorilla simian foamy virus (SFVgor). Starting from a conserved region in the integrase (IN) domain of the pol gene we cloned the viral genome to the 5′ and 3′ LTR into plasmid vectors and elucidated its nucleotide sequence. The sequences of both LTRs were determined by nucleotide sequencing of separate PCR products from the primer-binding site or the bel region and LTRs. All protein motifs conserved among the primate FV were identified in SFVgor. Using phylogenetic analysis of the Gag, Pol and Env amino acid sequences, we demonstrate that SFVgor consistently clusters in accordance with a scenario of virus–host co-divergence.

Complete nucleotide sequence and evolutionary analysis of a gorilla foamy virus.

Serological diagnosis of herpes virus infections is hampered by concurrent expression of IgM for heterologous members of this virus family. To assess the frequency of such multiple diagnostic findings and to understand their etiology, we sought by using IgG, IgM, and IgG avidity test serodiagnoses for Epstein-Barr virus (EBV) among immunocompetent or immune-suppressed patients with well-documented cytomegalovirus (CMV) primary infection. Controls had primary infection by EBV or had acute septic or severe respiratory infection. Among EBV-seropositive patients with CMV primary infection, a large proportion (13/56, 23%) showed antibody profiles of EBV reactivation: seroconversion of VCA IgM and/or > or = fourfold rise of VCA IgG, together with high or intermediate avidity of VCA IgG. Most of the CMV patients with EBV serodiagnosis showed also diagnostic HHV-6 antibody rises. In contrast to the frequently occurring CMV-induced EBV immunoreactivation, EBV primary infections did not appear to induce immunoreactivations of CMV (0/22). Only one (2%) CMV patient had a significant varicella zoster virus (VZV) antibody rise. The studies show that CMV is a particularly active inducer of some, but not all, members of the herpes virus family and suggest that the in vivo interplay between CMV and EBV occurs unidirectionally. The high frequency of heterologous herpes virus immunoreactivations poses demands on laboratory diagnosis.

Immunoreactivation of Epstein-Barr virus due to cytomegalovirus primary infection

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High prevalence of antibodies against polyomavirus WU, polyomavirus KI, and human bocavirus in German blood donors

Complete nucleotide sequence and evolutionary analysis of a gorilla foamy virus.

Immunoreactivation of Epstein-Barr virus due to cytomegalovirus primary infection