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Ganciclovir Plus Arginine Butyrate in Treating Patients With Cancer or Lymphoproliferative Disorders Associated With the Epstein Barr Virus

ABSTRACT: RATIONALE: The Epstein Barr virus can cause cancer and lymphoproliferative disorders. Ganciclovir is an antiviral drug that acts against the Epstein Barr virus. Arginine butyrate may make virus cells more sensitive to ganciclovir. Combining ganciclovir and arginine butyrate may kill more Epstein Barr virus cells and tumor cells. PURPOSE: Phase I trial to study the effectiveness of arginine butyrate plus ganciclovir in treating patients who have cancer or lymphoproliferative disorders that are associated with the Epstein Barr virus.

DISEASE(S): Leukemia,Precancerous Condition,Small Intestine Cancer,Angioimmunoblastic T-cell Lymphoma,Precancerous Conditions,Lymphoma,Intestinal Neoplasms

PROVIDER: 2005372 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Project description:Arboviruses are defined by their ability to replicate in both mosquito vectors and mammalian hosts. There is good evidence that arboviruses “prime” their progeny for infection of the next host, such as differential glycosylation of their outer glycoproteins or packaging of host ribosomal subunits. We and others have previously shown that mosquito derived viruses more efficiently infect mammalian cells than mammalian derived viruses. These observations are coherent with arboviruses acquiring host-specific adaptations, and we hypothesized that virus derived from either the mammalian host or mosquito vector will elicit different responses when infecting the mammalian host. Here we perform an RNA-sequencing analysis of the transcriptional response of Human Embryonic Kidney 293 (HEK-293) cells to infection with either mosquito (Aedes albopictus, C7/10) or mammalian (Baby Hamster Kidney, BHK) derived Sindbis virus (SINV). We show that C7/10 derived virus infection leads to a more robust transcriptional response in HEK-293s as compared to infection with the BHK derived virus. Surprisingly, despite more efficient infection, we found an increase in interferon-β (IFN-β) and interferon stimulated gene (ISG) transcripts in response to C7/10 derived virus infection versus BHK derived virus infection. However, translation of interferon stimulated genes was lower in HEK-293s infected with C7/10 derived virus, starkly contrasting with the transcriptional response. This inhibition of ISG translation is reflective of a more rapid overall shut-off of host cell translation following infection with C7/10 derived virus. Finally, we show that C7/10 derived virus infection of HEK-293 cells leads to elevated levels of phosphorylated eukaryotic translation elongation factor-2 (eEF2), identifying a potential mechanism leading to the more rapid shut-off of host translation. We postulate that the rapid shut-off of host translation in mammalian cells infected with mosquito derived virus acts to counter the IFN-β stimulated transcriptional response.

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Ganciclovir Plus Arginine Butyrate in Treating Patients With Cancer or Lymphoproliferative Disorders Associated With the Epstein Barr Virus

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