Human herpesvirus 7 is a T-lymphotropic virus and is related to, but significantly different from, human herpesvirus 6 and human cytomegalovirus.

Berneman, Zwi; Ablashi, Dharam V.; Li, Ge; Eger-Fletcher, Maureen; Reitz, Marvin S.; Hung, Chia Chun; Brus, I; Komaroff, Anthony L.; Gallo, Robert C.

doi:10.1073/pnas.89.21.10552

Cited by 229 publications

(171 citation statements)

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“…The virus then persists in the body and is shed in the saliva (22)(23)(24)(25)(26). Mainly because HHV-7 has been isolated from peripheral blood lymphocytes and grows in CD4 ϩ T lymphocytes (3,27,28), and by analogy with HHV-6B, it has been postulated that HHV-7 is harbored in latent form in T lymphocytes. In vitro the susceptibility to HHV-7 is restricted to CD4 ϩ T lymphocytes (refs.…”

mentioning

confidence: 99%

CD68⁺cells of monocyte/macrophage lineage in the environment of AIDS-associated and classic-sporadic Kaposi sarcoma are singly or doubly infected with human herpesviruses 7 and 6B

Kempf

Adams

Wey

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

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Earlier studies have shown that Kaposi sarcomas contain cells infected with human herpesvirus (HHV) 6B, and in current studies we report that both AIDSassociated and classic-sporadic Kaposi sarcoma contain HHV-7 genome sequences detectable by PCR. To determine the distribution of HHV-7-infected cells relative to those infected with HHV-6, sections from paraffin-embedded tissues were allowed to react with antibodies to HHV-7 virion tegument phosphoprotein pp85 and to HHV-6B protein p101. The antibodies are specific for HHV-7 and HHV-6B, respectively, and they retained reactivity for antigens contained in formalin-fixed, paraffin-embedded tissue samples. We report that (i) HHV-7 pp85 was present in 9 of 32 AIDS-associated Kaposi sarcomas, and in 1 of 7 classical-sporadic HIV-negative Kaposi sarcomas; (ii) HHV-7 pp85 was detected primarily in cells bearing the CD68 marker characteristic of the monocyte͞ macrophage lineage present in or surrounding the Kaposi sarcoma lesions; and (iii) in a number of Kaposi sarcoma specimens, tumor-associated CD68 ؉ monocytes͞macro-phages expressed simultaneously antigens from both HHV-7 and HHV-6B, and therefore appeared to be doubly infected with the two viruses. CD68 ؉ monocytes͞macrophages infected with HHV-7 were readily detectable in Kaposi sarcoma, but virtually absent from other normal or pathological tissues that harbor macrophages. Because all of the available data indicate that HHV-7 infects CD4 ؉ T lymphocytes, these results suggest that the environment of the Kaposi sarcoma (i) attracts circulating peripheral lymphocytes and monocytes, triggers the replication of latent viruses, and thereby increases the local concentration of viruses, (ii) renders CD68 ؉ monocytes͞macrophages susceptible to infection with HHV-7, and (iii) the combination of both events enables double infections of cells with both HHV-6B and HHV-7.

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confidence: 99%

CD68⁺cells of monocyte/macrophage lineage in the environment of AIDS-associated and classic-sporadic Kaposi sarcoma are singly or doubly infected with human herpesviruses 7 and 6B

Kempf

Adams

Wey

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

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“…Human herpesvirus 7 (HHV-7) was first isolated from CD4 þ T cells obtained from a healthy adult in 1990 [Frenkel et al, 1990]. HHV-7 is distinct molecularly from these two variants of HHV-6 [Berneman et al, 1992]. Although both HHV-6 B and HHV-7 cause exanthem subitum [Yamanishi et al, 1988;Tanaka et al, 1994], a common childhood febrile disease, the clinical features of primary HHV-6 A infection remain unclear.…”

Section: Introductionmentioning

confidence: 99%

Latent infection of human herpesvirus 7 in CD4⁺ T lymphocytes

Miyake

Yoshikawa

Sun

et al. 2005

Journal of Medical Virology

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To determine the cell populations in peripheral blood that are infected latently with human herpesvirus 7 (HHV-7), the real-time polymerase chain reaction (PCR) was used to determine the quantities of viral DNA in adherent and nonadherent cells from 71 healthy volunteers. Realtime PCR, which detected the U31 gene of HHV-7, was developed to measure viral load. The majority of non-adherent cells (14/16; 87.5%) contained HHV-7 DNA, while most of the adherent cells did not (1/16; 6.3%). HHV-7 viral load in non-adherent cells was significantly higher than that in adherent cells (P < 0.0001). Then, HHV-7 DNA load was compared between the CD4-positive and -negative cell fractions derived from the non-adherent cells of 26 healthy adults. As in the previous experiment, only 2 (7.7%) of the 26 adherent cell specimens contained small amounts of HHV-7 DNA (27.7 copies/1 Â 10 6 cells and 208.7 copies/1 Â 10 6 cells). In contrast, 88.5% of CD4 þ T cell samples (23/26 specimens) were positive for HHV-7 DNA, ranging from 0.4 to 3,542.8 copies/1 Â 10 6 cells. Viral DNA was detected in only 3 (11.5%) of the 26 CD4 À T cell specimens, with 8.4, 63.5, and 74.1 copies/1 Â 10 6 cells. HHV-7-positive DNA loads were significantly higher in the CD4 þ T cells than those observed in the CD4 À T cells (P ¼ 0.0005). The relationship between HHV-7 viral loads in nonadherent cells and those in saliva was investigated. Comparison of HHV-7 DNA load between blood CD4 þ T cells and saliva revealed that the HHV-7 DNA load in saliva correlated with that present in CD4 þ T cells (r ¼ 0.415; P ¼ 0.0174).

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“…HHV-6 and HHV-7 belong to the family Herpesviride, subfamily Betaherpesvirinae, genus Roseolovirus (Berneman et al, 1992). The viruses are ubiquitous (seroprevalence rate in adults is 60-90%) lymphotropic and immunomodulating and can be reactivated in immunocompromised and immunosuppressed hosts (Dockrell and Paya, 2001;Yamanishi et al, 2001;Lusso et al, 2006).…”

Section: Effect Of Hhv-6 and Hhv-7 Infection On The Post-transplant Pmentioning

confidence: 99%

“…PCR amplification for the viruses was carried out using 1 µg DNA and 10 µl plasma DNA (corresponding to 100 µl of plasma). The detection of HHV-6 and HHV-7 DNA was performed according to Secchiero et al (1995) and Berneman et al (1992), respectively. Positive (virus genomic DNA, Advanced Biotechnologies Inc, Columbia, MD, USA) and negative (DNA without virus-specific sequences) as well as water controls were included in each experiment.…”

Section: Patientsmentioning

confidence: 99%

Effect of HHV-6 and HHV-7 Infection on the Posttransplant Process and the Development of Complications in Patients after Autologous Stem Cell Transplantation / HHV-6 Un HHV-7 Infekcijas Ietekme Uz Pēctransplantācijas Klīnisko Gaitu Un Komplikāciju Attīstību Pacientiem Pēc Autologas Cilmes Šūnu Transplantācijas

Trociukas

Èapenko

Zazerska

et al. 2016

Proceedings of the Latvian Academy of Sciences. Section B. Natural, Exact, and Applied Sciences.

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Communicated by Ludmila VîksnaThe relationship between HHV-6 and HHV-7 reactivation and development of post-autologous peripheral stem cell transplantation complications was examined. The presence of viral genomic sequences in whole peripheral blood and cell free plasma was determined by nested PCR, load by real-time PCR, virus specific antibodies and cytokines in serum by ELISA, and HHV-6 variants by restriction endonuclease analysis. Clinical features, reactivation of viruses and serum TNF-a, and IL-6 concentrations were determined in seventy-six patients with Roseolovirus infection before and after transplantation. Anti-HHV-6 antibodies were found in 62 of 76 (81.6%) patients before transplantation. A significantly higher rate of single HHV-7 infection was found in patients with viral infection in comparison with single HHV-6 infection (p = 0.0003) and concurrent (HHV-6 and HHV-7) infection (p = 0.0017). Complications after transplantation developed in 30.3% of patients and reactivation of viruses was detected in all of these patients. Significant increase of HHV-6 and HHV-7 reactivation with simultaneous increase of pro-inflammatory cytokines serum levels suggests that both viruses may be involved in the development of complications after autologous peripheral blood stem cell transplantation via their immunomodulatory ability. The kinetics of the Roseolovirus reactivation may reflect the potential role of HHV-7 as a co-factor for

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Human herpesvirus 7 is a T-lymphotropic virus and is related to, but significantly different from, human herpesvirus 6 and human cytomegalovirus.

Cited by 229 publications

References 27 publications

CD68⁺cells of monocyte/macrophage lineage in the environment of AIDS-associated and classic-sporadic Kaposi sarcoma are singly or doubly infected with human herpesviruses 7 and 6B

CD68⁺cells of monocyte/macrophage lineage in the environment of AIDS-associated and classic-sporadic Kaposi sarcoma are singly or doubly infected with human herpesviruses 7 and 6B

Latent infection of human herpesvirus 7 in CD4⁺ T lymphocytes

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Human herpesvirus 7 is a T-lymphotropic virus and is related to, but significantly different from, human herpesvirus 6 and human cytomegalovirus.

Cited by 229 publications

References 27 publications

CD68+cells of monocyte/macrophage lineage in the environment of AIDS-associated and classic-sporadic Kaposi sarcoma are singly or doubly infected with human herpesviruses 7 and 6B

CD68+cells of monocyte/macrophage lineage in the environment of AIDS-associated and classic-sporadic Kaposi sarcoma are singly or doubly infected with human herpesviruses 7 and 6B

Latent infection of human herpesvirus 7 in CD4+ T lymphocytes

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CD68⁺cells of monocyte/macrophage lineage in the environment of AIDS-associated and classic-sporadic Kaposi sarcoma are singly or doubly infected with human herpesviruses 7 and 6B

CD68⁺cells of monocyte/macrophage lineage in the environment of AIDS-associated and classic-sporadic Kaposi sarcoma are singly or doubly infected with human herpesviruses 7 and 6B

Latent infection of human herpesvirus 7 in CD4⁺ T lymphocytes