Epstein-barr virus: The hematologic and oncologic consequences of virus-host interaction

Giller, Roger; Grose, Charles; Jones, James F.

doi:10.1016/s1040-8428(89)80009-5

Cited by 15 publications

(6 citation statements)

References 170 publications

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“…We further showed evidence that replication of the HK2 genome occurred in viral particles as well as in the infected cell (53), resembling the viral replication mechanism of spumaviruses (52). The infectious material of HK2 viruses can circularize and create episomal forms (51), similar to transforming viruses such as Epstein-Barr virus (EBV) and cytomegalovirus (CMV) (58,59). It is possible, then, that despite no proof of HK2 integration, replication and episomal formation of HK2 viruses could lead to carcinogenesis or other disturbances in cellular replication in human cells.…”

Section: Discussionmentioning

confidence: 84%

Susceptibility of Human Endogenous Retrovirus Type K to Reverse Transcriptase Inhibitors

Contreras-Galindo

Dube

Fujinaga

et al. 2017

J Virol

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Human endogenous retroviruses (HERVs) make up 8% of the human genome. The HERV type K (HERV-K) HML-2 (HK2) family contains proviruses that are the most recent entrants into the human germ line and are transcriptionally active. In HIV-1 infection and cancer, HK2 genes produce retroviral particles that appear to be infectious, yet the replication capacity of these viruses and potential pathogenicity has been difficult to ascertain. In this report, we screened the efficacy of commercially available reverse transcriptase inhibitors (RTIs) at inhibiting the enzymatic activity of HK2 RT and HK2 genomic replication. Interestingly, only one provirus, K103, was found to encode a functional RT among those examined. Several nucleoside analogue RTIs (NRTIs) blocked K103 RT activity and consistently inhibited the replication of HK2 genomes. The NRTIs zidovudine (AZT), stavudine (d4T), didanosine (ddI), and lamivudine (3TC), and the nucleotide RTI inhibitor tenofovir (TDF), show efficacy in blocking K103 RT. HIV-1-specific nonnucleoside RTIs (NNRTIs), protease inhibitors (PIs), and integrase inhibitors (IIs) did not affect HK2, except for the NNRTI etravirine (ETV). The inhibition of HK2 infectivity by NRTIs appears to take place at either the reverse transcription step of the viral genome prior to HK2 viral particle formation and/or in the infected cells. Inhibition of HK2 by these drugs will be useful in suppressing HK2 infectivity if these viruses prove to be pathogenic in cancer, neurological disorders, or other diseases associated with HK2. The present studies also elucidate a key aspect of the life cycle of HK2, specifically addressing how they do, and/or did, replicate. Endogenous retroviruses are relics of ancestral virus infections in the human genome. The most recent of these infections was caused by HK2. While HK2 often remains silent in the genome, this group of viruses is activated in HIV-1-infected and cancer cells. Recent evidence suggests that these viruses are infectious, and the potential exists for HK2 to contribute to disease. We show that HK2, and specifically the enzyme that mediates virus replication, can be inhibited by a panel of drugs that are commercially available. We show that several drugs block HK2 with different efficacies. The inhibition of HK2 replication by antiretroviral drugs appears to occur in the virus itself as well as after infection of cells. Therefore, these drugs might prove to be an effective treatment by suppressing HK2 infectivity in diseases where these viruses have been implicated, such as cancer and neurological syndromes.

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Section: Discussionmentioning

confidence: 84%

Susceptibility of Human Endogenous Retrovirus Type K to Reverse Transcriptase Inhibitors

Contreras-Galindo

Dube

Fujinaga

et al. 2017

J Virol

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“…[6][7][8] However, in such cases, clonal T-cell expansions are frequently the result of infection of the neoplastic cells by the virus, and they have not been directly related to the immune response against the virus. 6,9,10 In contrast to other viruses, human CMV (hCMV) has not been proven to be involved in human cancer. 11,12 However, recent studies from our and other groups in hCMV-seropositive healthy persons show the presence of TCR-V␤ (oligo)clonal expansions of hCMVspecific CD4 ϩ /cytotoxic/memory T cells in the peripheral blood (PB) of immunocompetent healthy adults.…”

Section: Introductionmentioning

confidence: 99%

Expanded cells in monoclonal TCR-αβ+/CD4+/NKa+/CD8−/+dim T-LGL lymphocytosis recognize hCMV antigens

Rodríguez-Caballero

García‐Montero

Bárcena

et al. 2008

Blood

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“…Epstein-Barr virus (EBV) enters cells through the complement receptor CR2 [133]. Cell adhesion molecule ICAM-1 functions as the ligand for lymphocyte function associated molecule-1 (LFA-I).…”

Section: Transfection O F Cancer Cells With Genes Encoding Selected Vmentioning

confidence: 99%

New Developments in the Virus Therapy of Cancer: A Historical Review

Sinkovics

Horváth²

1993

Intervirology

109

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Since the 1920s, viruses had been used for oncolysis. Natural human viral infections can rarely induce remissions of leukemias or lymphomas. Inoculation of tumor-bearing patients with live viruses very seldom resulted in durable complete remissions. Genetically engineered or tumor-adapted virus strains may perform better. Virally modified tumor cell membrane vaccines can induce in the host rejection strength antitumor immunity. Modern technology and much more work is needed before the optimal procedures for viral oncolysis or active antitumor immunization with virally modified tumor cell vaccines are learned and can be implemented in the clinical practice. Laboratory monitoring of the host’s immunological reactions accompanying failure and success of tumor rejection is essential for the recognition and duplication of the successful and for the avoidance of the unsuccessful interventions.

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Epstein-barr virus: The hematologic and oncologic consequences of virus-host interaction

Cited by 15 publications

References 170 publications

Susceptibility of Human Endogenous Retrovirus Type K to Reverse Transcriptase Inhibitors

Susceptibility of Human Endogenous Retrovirus Type K to Reverse Transcriptase Inhibitors

Expanded cells in monoclonal TCR-αβ+/CD4+/NKa+/CD8−/+dim T-LGL lymphocytosis recognize hCMV antigens

New Developments in the Virus Therapy of Cancer: A Historical Review

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