Human Herpesvirus 6 Latency Characterized by High Viral Load: Chromosomal Integration in Many, but Not All, Cells

Luppi, Mario; Barozzi, Patrizia; Bosco, Raffaella; Vallerini, Daniela; Potenza, Leonardo; Forghieri, Fabio; Torelli, Giuseppe

doi:10.1086/506952

Cited by 25 publications

(12 citation statements)

References 10 publications

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“…The incidence of CIHHV-6 is not exactly known, although a recent study of blood donors from the United Kingdom estimated an incidence between 0.2%-1% [24] . It is suggested that CIHHV-6 may also be vertically transmitted (mother to child transmission) [25] , since it was found in germ cell lines, however, this has not been confirmed by other investigators [26] . Individuals with CIHHV-6 have a characteristic persistently high levels of HHV-6 DNA in the blood, sera, and hair follicles, without causing clinical illness [27] .…”

Section: Latency and Chromosomally-integrated Hhv-6mentioning

confidence: 86%

Human herpesvirus 6 infections after liver transplantation

Massih¹,

Razonable²

2009

WJG

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Section: Latency and Chromosomally-integrated Hhv-6mentioning

confidence: 86%

Human herpesvirus 6 infections after liver transplantation

Massih¹,

Razonable²

2009

WJG

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“…Once again, this important observation has been criticized, since all experiments were made using only peripheral blood cells (41). This argument was frequently used, as peripheral blood cells could be infected and/or integrated during the course of an individual's lifetime or during embryogenesis, yielding cells that harbor, at least for some subjects, less than one copy of HHV-6 DNA per cell, which is not compatible with the inherited transmission of CIHHV-6 on May 12, 2018 by guest http://jvi.asm.org/ (65,67). However, considering the current body of evidence, the demonstration of positive fluorescent in situ hybridization of HHV-6 probes in the chromosomes of fibroblasts (22), the detection of viral DNA in the hair follicles of CIHHV-6 patients (Ն1 copy/hair follicle) (101), and the fact that high loads of viral DNA can be found in several tissues throughout the bodies of subjects with CIHHV-6 (44), little doubt persists that CIHHV-6 can be inherited.…”

Section: Chromosomal Integration Of Hhv-6mentioning

confidence: 99%

Herpesviruses and Chromosomal Integration

Morissette

Flamand

2010

J Virol

204

164

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Herpesviruses are members of a diverse family of viruses that colonize all vertebrates from fish to mammals. Although more than one hundred herpesviruses exist, all are nearly identical architecturally, with a genome consisting of a linear double-stranded DNA molecule (100 to 225 kbp) protected by an icosahedral capsid made up of 162 hollow-centered capsomeres, a tegument surrounding the nucleocapsid, and a viral envelope derived from host membranes. Upon infection, the linear viral DNA is delivered to the nucleus, where it circularizes to form the viral episome. Depending on several factors, the viral cycle can proceed either to a productive infection or to a state of latency. In either case, the viral genetic information is maintained as extrachromosomal circular DNA. Interestingly, however, certain oncogenic herpesviruses such as Marek's disease virus and Epstein-Barr virus can be found integrated at low frequencies in the host's chromosomes. These findings have mostly been viewed as anecdotal and considered exceptions rather than properties of herpesviruses. In recent years, the consistent and rather frequent detection (in approximately 1% of the human population) of human herpesvirus 6 (HHV-6) viral DNA integrated into human chromosomes has spurred renewed interest in our understanding of how these viruses infect, replicate, and propagate themselves. In this review, we provide a historical perspective on chromosomal integration by herpesviruses and present the current state of knowledge on integration by HHV-6 with the possible clinical implications associated with viral integration.

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“…About 2 % of the HHV6 subtype "A" carrier persons harbour the viral genome in the germline, too [207][208][209]. In some individuals, however, chromosomal integration can be detected in many, but not in all cells of the body [113]. It has to be mentioned, that conventional perinatal or transplacental HHV6 transmission is also present in the population [228].…”

Section: Vertical Transmission Of Viruses (Perinatal or Transplacental?)mentioning

confidence: 99%

“…A series of publications reported the presence of viral nucleic acids in fetal hydrops (HHV6) [5] or in the amniotic fluid, cord blood and neonatal blood samples (Papillomaviruses [3,4,166,222], herpesviruses [6,63,66,113,114,152,206,222] Later, however, the majority of viral DNA was detected in the meconium and cell debris of the amniotic fluid samples [222] taken at birth at the end of normal pregnancies.…”

Section: The Perinatal Transmission and Transplacental Transfer Of VImentioning

confidence: 99%

Heterogeneous Pathways of Maternal-fetal Transmission of Human Viruses (Review)

Younes

Csire

Kapusinszky

et al. 2009

Pathol. Oncol. Res.

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Several viruses can pass the maternal-fetal barrier, and cause diseases of the fetus or the newborn. Recently, however, it became obvious, that viruses may invade fetal cells and organs through different routes without acute consequences. Spermatozoa, seminal fluid and lymphocytes in the sperm may transfer viruses into the human zygotes. Viruses were shown to be integrated into human chromosomes and transferred into fetal tissues. The regular maternal-fetal transport of maternal cells has also been discovered. This transport might implicate that lymphotropic viruses can be released into the fetal organs following cellular invasion. It has been shown that many viruses may replicate in human trophoblasts and syncytiotrophoblast cells thus passing the barrier of the maternal-fetal interface. The transport of viral immunocomplexes had also been suggested, and the possibility has been put forward that even anti-idiotypes mimicking viral epitopes might be transferred by natural mechanisms into the fetal plasma, in spite of the selective mechanisms of apical to basolateral transcytosis in syncytiotrophoblast and basolateral to apical transcytosis in fetal capillary endothelium. The mechanisms of maternal-fetal transcytosis seem to be different of those observed in differentiated cells and tissue cultures. Membrane fusion and lipid rafts of high cholesterol content are probably the main requirements of fetal transcytosis. The long term presence of viruses in fetal tissues and their interactions with the fetal immune system might result in post partum consequences as far as increased risk of the development of malignancies and chronic pathologic conditions are discussed.

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Human Herpesvirus 6 Latency Characterized by High Viral Load: Chromosomal Integration in Many, but Not All, Cells

Cited by 25 publications

References 10 publications

Human herpesvirus 6 infections after liver transplantation

Human herpesvirus 6 infections after liver transplantation

Herpesviruses and Chromosomal Integration

Heterogeneous Pathways of Maternal-fetal Transmission of Human Viruses (Review)

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