HIV‐1 infection of primary effusion lymphoma cell line triggers Kaposi's sarcoma‐associated herpesvirus (KSHV) reactivation

Merat, Rastine; Amara, Ali; Lebbe, Célèste; Morel, Patrice; Saı̈b, Ali

doi:10.1002/ijc.10086

Cited by 51 publications

(38 citation statements)

References 21 publications

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“…It was reported recently that BC-3 cells, derived from a human primary effusion lymphoma and chronically infected with HHV-8, are permissive to HIV infection (Merat et al, 2002). Our results confirm that BC-3 cells support HIV replication, as shown by p24 production and release of infectious virus in culture supernatant.…”

Section: Discussionsupporting

confidence: 88%

“…Jurkat T cells were used as representative of cells naturally permissive to HIV infection. The B cell line BC-3, derived from PEL and chronically infected with HHV-8, was used as representative of HHV-8 target of infection and because of its permissiveness to HIV (Merat et al, 2002). For non-permissive cells, a neuronal cell line derived from a human glioblastoma (A172) was used.…”

Section: Methodsmentioning

confidence: 99%

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Human herpesvirus-8 (Kaposi's sarcoma-associated virus) ORF50 increases in vitro cell susceptibility to human immunodeficiency virus type 1 infection

Caselli

Galvan

Santoni

et al. 2003

Journal of General Virology

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ORF50, an immediate-early gene of human herpesvirus-8 (HHV-8), encodes a transactivating protein necessary for virus reactivation and lytic replication. ORF50 was reported recently to synergize with human immunodeficiency virus type 1 (HIV-1) tat at a post-transcriptional level. To study the effects of these molecular interactions on HIV replication and biology, cellular clones stably transformed with ORF50 were obtained by transfection of cell lines of different origin. These clones were infected subsequently with HIV. Experiments showed that ORF50 enhances HIV replication in T and B cells (Jurkat and BC-3 cells) and induces susceptibility and transient permissiveness in non-susceptible glial (A172) cells. Upregulation of viral receptors and co-receptors did not account for increased sensitivity to HIV infection and therefore the action of ORF50 might be modulated by the intracellular environment. Interestingly, non-susceptible cells transformed with ORF50 showed transient production of HIV particles that could spread to adjacent cells by direct contact. These findings show that HHV-8 ORF50 has an enhancing effect on HIV replication in vitro and suggest that the two viruses might interact in co-infected patients.

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Section: Discussionsupporting

confidence: 88%

Section: Methodsmentioning

confidence: 99%

Human herpesvirus-8 (Kaposi's sarcoma-associated virus) ORF50 increases in vitro cell susceptibility to human immunodeficiency virus type 1 infection

Caselli

Galvan

Santoni

et al. 2003

Journal of General Virology

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“…The current facts are that (i) Tat did activate KSHV replication and Tat did not directly activate ORF50 (Fig. 2 and 3) (24,28,42,62); (ii) the induction of KSHV lytic RNA (ORF50, ORF26, and ORF29 mRNA) was delayed (from 3 to 24 h) (Fig. 2); (iii) inflammatory cytokines and receptors induced by HIV-1 play important roles in AIDS-KS pathogenesis by promoting KSHV replication and inducing KS cell malignancy (22,43,46).…”

Section: Overexpression Of Tat In Pel Cell Lines Induces Kshv Lytic Cmentioning

confidence: 82%

“…Since Ensoli and colleagues previously demonstrated extracellular Tat could promote the growth and proliferation of KS tumor cells (6,19), the role of Tat as a cofactor in enhancing KSHV replication in PEL cell lines is always a highly controversial and arguable subject (24,28,42,62). For instance, studies from three groups consistently demonstrated that both intracellular and extracellular Tat could strongly activate KSHV well (24,28,42). On the contrary, one group showed an absolutely contradictory observation that either intracellular or extracellular Tat alone failed to induce KSHV replication (62).…”

Section: Discussionmentioning

confidence: 99%

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Intracellular Tat of Human Immunodeficiency Virus Type 1 Activates Lytic Cycle Replication of Kaposi's Sarcoma-Associated Herpesvirus: Role of JAK/STAT Signaling

Zeng

Zhang

Huang

et al. 2007

J Virol

111

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Human immunodeficiency virus type 1 (HIV-1) infection significantly increases the risk of Kaposi's sarcoma (KS) occurrence in individuals infected with Kaposi's sarcoma-associated herpesvirus (KSHV). KSHV infection appears to be necessary but not sufficient for KS development without other cofactors. However, factors that facilitate KSHV to cause KS have not been well defined. Previously, we determined that human herpesvirus 6 was one of the cofactors that activated lytic cycle replication of KSHV. Here, we demonstrate that the Tat protein of HIV-1 is a potentially important factor in the pathogenesis of KS, as determined by production of lytic phase mRNA transcripts and viral proteins in BCBL-1 cells. Mechanistic studies showed ectopic expression of Tat induced the production of human interleukin-6 (huIL-6) and its receptor (huIL-6Ra) and activated STAT3 signaling. Neutralization of huIL-6 or huIL-6R or inhibition of STAT3 signaling enhanced the replication. In addition, IL-4/STAT6 signaling also partially contributed to Tat-induced KSHV replication. These findings suggest that Tat may participate in KS pathogenesis by inducing KSHV replication and increasing KSHV viral load. These data also suggest that JAK/STAT signaling may be of therapeutic value in AIDS-related KS patients.

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Effect of multiple herpesvirus infections on the progression of HIV disease in a cohort of HIV seroconverters

Suligoi

Dorrucci

Uccella

et al. 2002

Journal of Medical Virology

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The effects of herpesviruses infection on the progression of HIV disease remain controversial, with some studies showing accelerated progression and others showing no effect. Furthermore, the effect of concurrent infection with more than one herpesvirus on the progression of HIV disease has never been investigated. To this end, the rates of progression of HIV disease were determined after stratifying for the presence of up to five different herpesvirus infections. The study population consisted of 359 HIV-infected persons for whom the date of seroconversion was estimated (part of the Italian Seroconversion Study). One serum sample from each participant was tested for antibodies to five herpesviruses: HSV-2, CMV, HHV-6, HHV-7, and HHV-8. Univariate analysis showed that HSV-2 and HHV-8 were significantly associated with progression to AIDS, yet when adjusting for age at HIV seroconversion and for the presence of the other herpesvirus infections, only HHV-8 infection showed a significant association. The age-adjusted risk of progression to AIDS with Kaposi's sarcoma increased with the number of herpesvirus infections and was significant in individuals with four infections. The risk of progression to AIDS without Kaposi's sarcoma also increased with the number of infections, although not significantly. Similar results were found when considering CD4+ cell count <200 x 10(6) cells/L as the endpoint. Concurrent infection with more than one herpesvirus does not appear to have a significant effect on the course of HIV disease, except for the known association between HHV-8 and Kaposi's sarcoma. However, even after excluding Kaposi's sarcoma from the AIDS-defining endpoints, a slightly increased risk for participants with four herpesvirus infections remained.

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HIV‐1 infection of primary effusion lymphoma cell line triggers Kaposi's sarcoma‐associated herpesvirus (KSHV) reactivation

Cited by 51 publications

References 21 publications

Human herpesvirus-8 (Kaposi's sarcoma-associated virus) ORF50 increases in vitro cell susceptibility to human immunodeficiency virus type 1 infection

Human herpesvirus-8 (Kaposi's sarcoma-associated virus) ORF50 increases in vitro cell susceptibility to human immunodeficiency virus type 1 infection

Intracellular Tat of Human Immunodeficiency Virus Type 1 Activates Lytic Cycle Replication of Kaposi's Sarcoma-Associated Herpesvirus: Role of JAK/STAT Signaling

Effect of multiple herpesvirus infections on the progression of HIV disease in a cohort of HIV seroconverters

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