Detection of TT Virus in Lymph Node Biopsies of B-Cell Lymphoma and Hodgkin's Disease, and its Association with EBV Infection

Garbuglia, Anna Rosa; Iezzi, T; Capobianchi, Maria Rosaria; Pignoloni, Patrizia; Pulsoni, Alessandro; Sourdis, John; Pescarmona, Edoardo; Vitolo, Domenico; Mandelli, Franco

doi:10.1177/039463200301600204

Cited by 58 publications

(40 citation statements)

References 34 publications

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“…At the same time, epidemiological associations of TTV with B-cell lymphoma, Hodgkin's disease, aplastic anemia, idiopathic pulmonary fibrosis, acute respiratory disease, and autoimmune rheumatic disorders have also been described (6,16,29,30,32,52). Although TTV is potentially related to many diseases, its actual function is still questioned.…”

mentioning

confidence: 99%

Torque Teno Virus (SANBAN Isolate) ORF2 Protein Suppresses NF-κB Pathways via Interaction with IκB Kinases

Zheng

Fang

et al. 2007

J Virol

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confidence: 99%

Torque Teno Virus (SANBAN Isolate) ORF2 Protein Suppresses NF-κB Pathways via Interaction with IκB Kinases

Zheng

Fang

et al. 2007

J Virol

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“…Co-infection of malignant B cells by EBV and TTV has recently been documented in nonHodgkin lymphomas and diffuse large B-cell lymphoma [78]. Expression of HRES-1/p28 is enhanced in EBV-transformed B cells [9].…”

Section: Hres-1/p28 With Viral Peptides and The 70 Kda Protein Of U1 mentioning

confidence: 99%

Molecular mimicry and immunomodulation by the HRES-1 endogenous retrovirus in SLE

et al. 2008

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Genetic and environmental factors are believed to influence development of systemic lupus erythematosus (SLE). Endogenous retroviruses (ERV) correspond to the integrated proviral form of infectious retroviruses, which are trapped within the genome due to mutations. ERV represent a key molecular link between the host genome and infectious viral particles. ERV-encoded proteins are recognized by antiviral immune responses and become targets of autoreactivity. Alternatively, ERV protein may influence cellular processes and the life cycle of infectious viruses. As examples, the HRES-1 human ERV encodes a 28-kDa nuclear autoantigen and a 24-kDa small GTP-ase, termed HRES-1/Rab4. HRES-1/p28 is a nuclear autoantigen recognized by crossreactive antiviral antibodies, while HRES-1/Rab4 regulates surface expression of CD4 and the transferrin receptor (TFR) through endosome recycling. Expression of HRES-1/Rab4 is induced by the tat gene of HIV-1, which in turn down-regulates expression of CD4 and susceptibility to reinfection by HIV-1. CD4 and the TFR play essential roles in formation of the immunological synapse (IS) during normal T-cell activation by a cognate MHC class II peptide complex. The key intracellular transducer of T-cell activation, Lck, is brought to the IS via binding to CD4. T-cell receptorζ (TCRζ) chain binds to the TFR. Abnormal T-cell responses in SLE have been associated with reduced lck and TCRζ chain levels. HRES-1 is centrally located on chromosome 1 at q42 relative to lupus-linked microsatellite markers and polymorphic HRES-1 alleles have been linked to the development of SLE. 1q42 is one of the three most common fragile sites in the human genome, and is inducible by DNA demethylation, a known mechanism of retroviral gene activation. Molecular mimicry and immunomodulation by a ERV, such as HRES-1, may contribute to self-reactivity and abnormal Tand B-cell functions in SLE. (Table I). HERVs are commonly designated as HERV followed by a single letter amino acid code corresponding to a tRNA. The 3′ terminus of tRNA is predicted to initiate reverse transcription by annealing to an 18 nucleotide long primer-binding site (PBS) at the 5′ LTR. While expression of murine ERV can lead to production of infectious virus and cause viremia, no production of infectious virion has been documented by HERV. High copy number of most ERV families makes it difficult to distinguish which members of a group are expressed. Although, no single provirus with intact LTRs and uninterrupted gag, pol, and env ORFs has been identified, the HERV-K ERV, as a family, has been shown to encode gag HHS Public Access Author Manuscript Author ManuscriptAuthor ManuscriptAuthor Manuscript the LTR region, is functionally analogous to the HIV-1 rev and HTLV-I/II rex proteins. HERV-K rev binds to both the nuclear export factor Crm1 and to a cis-acting viral RNA to activate nuclear export of unspliced RNAs [39]. Alternatively, the HERV-K LTR is also recognized by HIV-1 rev, suggesting a potential interaction between these exogeneous a...

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“…With respect to Hodgkin's lymphomas (HL) arising from ReedSternberg cells, about 60,000 new cases are diagnosed each year (1). An increase in the incidence of lymphomas has recently been observed and implication ofviral infections has been reported in the development of lymphoproliferative disorders (2). Advances in chemotherapy have led to a 5-year survival rate of 60-70% for NHL, and of more than 70% for HL (I).…”

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confidence: 99%

The Differential Expression of Galectin-1 and Galectin-3 in Normal Lymphoid Tissue and Non-Hodgkin's and Hodgkin's Lymphomas

D’Haene

Maris

Sandras

et al. 2005

Int J Immunopathol Pharmacol

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The WHO classification of lymphomas was established on the basis of clinical, morphological, immunohistochemical and genetic criteria. However, each entity displays its own spectrum of clinical aggressiveness. Treatment success varies widely and is not predictable. Since galectins are involved in oncogenesis and the. physiology of immune cells, we investigated whether galectin-1 and galectin-3 immunohistochemical expression could differ in 25 normal lymphoid tissues, 42 non-Hodgkin's and 14 Hodgkin's lymphomas. Immunohistochemical galectin expression was submitted to semi-quantitative and quantitative (computer-assisted microscopy) evaluations. This study is completed by an analysis (by means of quantitative RT-PCR) of galectin-3 mRNA expression in 3 normal lymph nodes, 3 follicular lymphomas (FLs) and 3 diffuse large B-celllymphomas (DLBCLs). The data show that in normal lymphoid tissue, lymphocytes do not express galectin-1 and rarely express galectin-3. In contrast, galectin-3 was expressed in 8 of the 16 DLBCL cases and in 1 of the 8 FL cases. Furthermore, galectin-3 mRNA was expressed 3-times more in the DLBCLs than in the FLs. While the blood vessel walls of the lymphomas expressed galectin-1, the vessel walls of normal lymphoid tissues did not. This expression of galectin-1 in blood vessel walls was correlated with vascular density. The present study thus shows that DLBCL can be distinguished from normal lymphoid tissue and other lymphomas on the basis of galectin-3 expression.

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Detection of TT Virus in Lymph Node Biopsies of B-Cell Lymphoma and Hodgkin's Disease, and its Association with EBV Infection

Cited by 58 publications

References 34 publications

Torque Teno Virus (SANBAN Isolate) ORF2 Protein Suppresses NF-κB Pathways via Interaction with IκB Kinases

Torque Teno Virus (SANBAN Isolate) ORF2 Protein Suppresses NF-κB Pathways via Interaction with IκB Kinases

Molecular mimicry and immunomodulation by the HRES-1 endogenous retrovirus in SLE

The Differential Expression of Galectin-1 and Galectin-3 in Normal Lymphoid Tissue and Non-Hodgkin's and Hodgkin's Lymphomas

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