Human Herpesvirus 6 Harbouring in Kidney

Asano, Yoshizo; Yoshikawa, Tetsushi; Suga, S.; Yazaki, Takehiko; Hirabayashi, Satoshi; Ono, Yoshinari; Tsuzuki, Kazuo; Oshima, Satoshi

doi:10.1016/s0140-6736(89)91993-4

Cited by 49 publications

(11 citation statements)

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“…In most children, primary infection occurs between 6 months and 2 years of age [Yoshikawa et al, 1989;Yoshikawa et al, 1990;Ueda et al, 1989;Okuno et al, 1989;Asano et al, 1990]. It is suggested that HHV-6 persist latently in salivary glands [Fox et al, 1990], lymph nodes [Eizuru et al, 1989], peripheral blood mononuclear cells [Kondo et al, 1991], and kidney [Asano et al, 1989b]. The virus probably remains latent in the body after the primary infection and then reactivates during immunosuppressed states like other human herpesviruses.…”

Section: Introductionmentioning

confidence: 99%

Human herpesvirus 6 infection after living related liver transplantation

et al. 2000

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The aim of the study was to investigate human herpesvirus-6 (HHV-6) infection after liver transplantation from living related donors, and to evaluate the reliability of the presence of HHV-6 DNA in plasma by the polymerase chain reaction (PCR) for monitoring active HHV-6 infection. EDTA peripheral blood was collected from 47 donor and recipient (16 males and 31 females, age 1-320 months) pairs at the time of transplantation and biweekly from these recipients after transplantation until 2 months after operation. Isolation of HHV-6 and serological assays were carried out to evaluate active HHV-6 infection in this study. The presence of the viral DNA in plasma was tested by nested PCR. Four clinical events, such as unexplained fever, thrombocytopenia, rejection, and central nervous system (CNS) involvement, were evaluated for clinical features of the virus infection. Risk factors for the virus activity after liver transplantation were also examined. HHV-6 activity was detected in 23 (49%) of the 47 recipients approximately 2-4 weeks after transplantation. All 9 isolates were HHV-6 variant B. The presence of the viral DNA in plasma correlated well with virus isolation and serology (P < 0.01). Only unexplained fever was associated statistically with HHV-6 activity after liver transplantation (P < 0. 01). If the recipient was seronegative to HHV-6 before transplantation, the recipient was more likely to develop the active virus infection after liver transplantation (P = 0.11). HHV-6 activity occurred in one-half of the recipients approximately 2-4 weeks after liver transplantation, and there was a close association between HHV-6 activity and unexplained fever following transplantation. Detection of the viral DNA in plasma by PCR is useful for monitoring active HHV-6 infection in these patients. Seronegative recipients were more likely to have evidence of active HHV-6 infection after liver transplantation.

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Section: Introductionmentioning

confidence: 99%

Human herpesvirus 6 infection after living related liver transplantation

et al. 2000

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“…As HHV-6 has been found in the renal tubular endothelial cells and kidney, 7 these clinical data imply a role of HHV-6 in hematuria that develops after HSCT. This suggests that HHV-6 is associated with urinary tract damage, but it cannot be considered as conclusive evidence because sporadic PCR positivity for HHV-6 in the urine was found in 9% of patients after HSCT.…”

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confidence: 67%

Human herpesvirus-6 as a possible cause of encephalitis and hemorrhagic cystitis after allogeneic hematopoietic stem cell transplantation

Kim

Lee

et al. 2002

Leukemia

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“…Although the precise mode of acquisition of primary HHV‐6 infection in seronegative recipients is not known, donor allograft is believed to be the likely source of transmission. HHV‐6 has been shown to develop latency in the kidney in vivo [38]. Furthermore, two renal transplant recipients who received the allografts from the same cadaveric donor were documented to have identical genomic patterns of their HHV‐6 isolates [24].…”

Section: Human Herpesvirus‐6mentioning

confidence: 99%

Human herpesviruses-6, -7 and -8 in organ transplant recipients

Singh

2000

Clinical Microbiology and Infection

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The newer herpesviruses are being increasingly recognized as significant opportunistic pathogens in organ transplant recipients. Published data support the role of human herpesvirus-6 as a potential cause of encephalitis and bone marrow suppression in transplant setting. An association of human herpesvirus-6 with fungal infections and cytomegalovirus infection has also been documented. Human herpesvirus-7 also appears to be an immunomodulatory agent and may facilitate the pathogenicity of cytomegalovirus. Unlike human herpesviruses -6 and -7, human herpesvirus -8 is not ubiquitous; its seroprevalence exhibits wide geographic variation. Human herpesvirus-8 has been causally associated with post-transplant Kaposi's sarcoma. The complete spectrum of pathogenicity and ultimately the effective prophylaxis and management of these viruses has yet to be fully elucidated.

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Human Herpesvirus 6 Harbouring in Kidney

Cited by 49 publications

References 3 publications

Human herpesvirus 6 infection after living related liver transplantation

Human herpesvirus 6 infection after living related liver transplantation

Human herpesvirus-6 as a possible cause of encephalitis and hemorrhagic cystitis after allogeneic hematopoietic stem cell transplantation

Human herpesviruses-6, -7 and -8 in organ transplant recipients

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