Viral Integration

Dear Colleagues:

Retrovirus DNA integration of reverse transcribed viral RNA into cellular DNA has affected the evolution of numerous biological systems. Retroviruses also cause major human diseases, including HIV-1/AIDS and human T-cell leukemia virus type-1/adult T-cell leukemia-lymphoma. The viral integrase mediates the insertion of the two viral DNA ends into the host genome that produces persistent expression of the retrovirus genome for virus replication, as well as affecting cellular gene expression. These integration effects have significantly enhanced interest to understand the structural diversity of integrase–viral DNA complexes termed intasomes. Understanding of retrovirus integration mechanisms has been propelled by X-ray crystallography and single-particle cryo-electron microscopy of intasomes. Continued development of HIV-1 integrase strand transfer inhibitors and potential allosteric inhibitors requires high-resolution structures to combat drug-resistance mutations. The clinical use of retrovirus vectors for human gene therapies and anti-cancer thearpies will surely be enhanced in the future. The entire spectrum of retrovirus integration aspects from its harmful to beneficial effects on human health will necessitate further investigation of retrovirus integration mechanisms.

Viral genome integration is also a common feature of Hepadnaviruses. They are hepatotropic DNA viruses that replicate their DNA genome via a reverse transcriptase. The human representative, hepatitis B virus, causes major human diseases, including liver cirrhosis and hepatocellular carcinoma. By contrast to retroviruses, the viral genomic archive, which is the template for transcription and genome replication, is an episomal covalently closed circular DNA. Viral genome integration is not required for viral replication but is involved in the development of hepatocellular carcinoma. Understanding the consequences of HBV integration on the pathobiology of HBV-induced liver disease and liver oncogenesis should open new avenues to identify early predictors of liver cancer and to study novel strategies to prevent liver cancer development in chronically infected patients.

Prof. Dr. Duane P. Grandgenett
Prof. Dr. Fabien Zoulim
Guest Editors

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