Replicative Forms of TT Virus DNA in Bone Marrow Cells

Okamoto, Hiroaki; Takahashi, Masaharu; Nishizawa, Tsutomu; Tawara, Akio; Sugai, Yoshiki; Sai, Toshiaki; Tanaka, Takeshi; Tsuda, Fumio

doi:10.1006/bbrc.2000.2481

Cited by 80 publications

(62 citation statements)

References 26 publications

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“…A conserved motif, WX7HX3C X1CX5H, present in VP2 of CAV is also found in the TTV group (7,40,45). Later analysis of the TTV transcription pattern in COS-1 and bone marrow cells has revealed the existence of at least three species of spliced mRNA molecules of 2.9 to 3, 1.2, and 1.0 kb in length, with common 5Ј and 3Ј termini, suggesting that more ORFs emerged through mRNA splicing, even though their functions are not clear (24,42,46).…”

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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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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“…TTV was originally named after the initials of first patient TT, then transfusion-transmitted, and recently renamed "torque teno" virus [73]. Due to the high degree of genomic variability of the putative coding regions [74] and difficulties in expression of full-length TTV protein for antibody testing [75,76], the diagnosis of TTV infection has been dependent on PCR detection of viral DNA using primers specific for the noncoding regions [77]. TTV DNA was detected in 120/211 SLE patients and 66/199 healthy control donors (p < 0.0001).…”

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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“…Following the development of detection methods that can detect a wide range of different TTV genotypes, it has become apparent that TTV infection is ubiquitous in man, as well as in all other primate species [5]. Infection is characterised by persistent viraemia and the presence of replicating virus in a wide range of anotomical sites, including bone marrow, lymphoid tissue, lung and liver [6][7][8][9]. As an indication of its great replicative capacity in vivo, studies of the kinetics of clearance of viraemia during interferon-AE therapy have suggested that .10 10 TTV virions are produced every day, with 90% of the virus in plasma cleared and replenished over this period [10].…”

Section: Genetic Diversitymentioning

confidence: 99%

“…More recent studies have demonstrated virus replication in a wide range of tissues, with a growing consensus that the bone marrow, lung and lymphoid tissue contain the highest levels of replicating virus [6][7][8][9]. The importance of the bone marrow as the source of replicating virus is perhaps illustrated by the observation of a disappearance of TTV viraemia in the myelosuppressed period immediately after bone marrow transplantation [25].…”

Section: Disease Associations Of Ttvmentioning

confidence: 99%

TT virus infection: a novel virus-host relationship

Simmonds¹

2002

Journal of Medical Microbiology

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Replicative Forms of TT Virus DNA in Bone Marrow Cells

Cited by 80 publications

References 26 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

TT virus infection: a novel virus-host relationship

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