Review Part 3: Human herpesvirus‐6 in multiple non‐neurological diseases

Ablashi, Dharam V.; Devin, Courtney L.; Yoshikawa, Tetsushi; Lautenschlager, Irmeli; Luppi, Mario; Kühl, Uwe; Komaroff, Anthony L.

doi:10.1002/jmv.21860

Cited by 48 publications

(39 citation statements)

References 114 publications

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“…The importance of the finding was amplified by the fact that this virus, finally designated human herpesvirus 6 (HHV-6), was initially isolated from patients with lymphoproliferative disorders and AIDS, raising the key question of its pathogenicity. Since that time, the knowledge about this virus and associated diseases has considerably improved, as extensively reported in previously published overviews and books which remain relevant references (2)(3)(4)(5)(6)(7)(8)(9)(10). However, many questions on those domains are still pending and constitute true challenges for present and future research.…”

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confidence: 99%

Laboratory and Clinical Aspects of Human Herpesvirus 6 Infections

2015

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SUMMARY Human herpesvirus 6 (HHV-6) is a widespread betaherpesvirus which is genetically related to human cytomegalovirus (HCMV) and now encompasses two different species: HHV-6A and HHV-6B. HHV-6 exhibits a wide cell tropism in vivo and, like other herpesviruses, induces a lifelong latent infection in humans. As a noticeable difference with respect to other human herpesviruses, genomic HHV-6 DNA is covalently integrated into the subtelomeric region of cell chromosomes (ciHHV-6) in about 1% of the general population. Although it is infrequent, this may be a confounding factor for the diagnosis of active viral infection. The diagnosis of HHV-6 infection is performed by both serologic and direct methods. The most prominent technique is the quantification of viral DNA in blood, other body fluids, and organs by means of real-time PCR. Many active HHV-6 infections, corresponding to primary infections, reactivations, or exogenous reinfections, are asymptomatic. However, the virus may be the cause of serious diseases, particularly in immunocompromised individuals. As emblematic examples of HHV-6 pathogenicity, exanthema subitum, a benign disease of infancy, is associated with primary infection, whereas further virus reactivations can induce severe encephalitis cases, particularly in hematopoietic stem cell transplant recipients. Generally speaking, the formal demonstration of the causative role of HHV-6 in many acute and chronic human diseases is difficult due to the ubiquitous nature of the virus, chronicity of infection, existence of two distinct species, and limitations of current investigational tools. The antiviral compounds ganciclovir, foscarnet, and cidofovir are effective against active HHV-6 infections, but the indications for treatment, as well as the conditions of drug administration, are not formally approved to date. There are still numerous pending questions about HHV-6 which should stimulate future research works on the pathophysiology, diagnosis, and therapy of this remarkable human virus.

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confidence: 99%

Laboratory and Clinical Aspects of Human Herpesvirus 6 Infections

2015

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“…Other herpesvirus infection In addition to CMV, infections with other b-herpesviruses, such as human herpesvirus 6 (HHV-6) and human herpesvirus 7 (HHV-7), may have an impact on allograft function (81,82). Infection by HHV-6 and HHV-7 is almost universal in adults, and HHV-6 replication is commonly detected in SOT recipients (83,84). Infection by HHV-6 is usually asymptomatic, although severe disease (gastrointestinal, central nervous system disease) has occasionally been reported (85,86).…”

Section: Type Of Organ Transplantmentioning

confidence: 99%

The Impact of Infection on Chronic Allograft Dysfunction and Allograft Survival After Solid Organ Transplantation

Martín-Gandul

Mueller

Pascual

et al. 2015

American Journal of Transplantation

131

103

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Infectious diseases after solid organ transplantation (SOT) are a significant cause of morbidity and reduced allograft and patient survival; however, the influence of infection on the development of chronic allograft dysfunction has not been completely delineated. Some viral infections appear to affect allograft function by both inducing direct tissue damage and immunologically related injury, including acute rejection. In particular, this has been observed for cytomegalovirus (CMV) infection in all SOT recipients and for BK virus infection in kidney transplant recipients, for community-acquired respiratory viruses in lung transplant recipients, and for hepatitis C virus in liver transplant recipients. The impact of bacterial and fungal infections is less clear, but bacterial urinary tract infections and respiratory tract colonization by Pseudomonas aeruginosa and Aspergillus spp appear to be correlated with higher rates of chronic allograft dysfunction in kidney and lung transplant recipients, respectively. Evidence supports the beneficial effects of the use of antiviral prophylaxis for CMV in improving allograft function and survival in SOT recipients. Nevertheless, there is still a need for prospective interventional trials assessing the potential effects of preventive and therapeutic strategies against bacterial and fungal infection for reducing or delaying the development of chronic allograft dysfunction.

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“…HHV-6B is the major causative agent of exanthem subitum (roseola infantum), which is characterized by high fever, diarrhoea, and a mild skin rash along the trunk, neck, and face (Yamanishi et al, 1988). HHV-6A has been associated with several adult diseases, including cofactor in AIDS progression, and various neurological disorders including encephalitis, ataxia, seizure, liver disfunction, and chronic fatigue syndrome; however, the causal link between human diseases and virus infection remains to be fully elucidated (De Bolle et al, 2005;Ablashi et al, 2010).…”

Section: Human Herpesvirus 6 (Hhv-6)mentioning

confidence: 99%