Herpes simplex virus 1 DNA is in unstable nucleosomes throughout the lytic infection cycle, and the instability of the nucleosomes is independent of DNA replication.

Herpes simplex virus 1 (HSV-1) DNA is chromatinized during latency and consequently regularly digested by micrococcal nuclease (MCN) to nucleosome-size fragments. In contrast, MCN digests HSV-1 DNA in lytically infected cells to mostly heterogeneous sizes. Yet HSV-1 DNA coimmunoprecipitates with histones during lytic infections.

During lytic infections, herpes simplex virus type 1 DNA is in complexes with the properties of unstable nucleosomes.

The genomes of herpes simplex virus type 1 (HSV-1) are regularly chromatinized during latency such that their digestion with micrococcal nuclease (MCN) releases nucleosome-sized DNA fragments. In lytically infected cells, in contrast, MCN releases HSV-1 DNA in primarily heterogeneously sized fragments. Consistently, only a small percentage of this HSV-1 DNA coimmunoprecipitates with histones.

Five years of progress on cyclin-dependent kinases and other cellular proteins as potential targets for antiviral drugs.

In 1997-1998, the pharmacological cyclin-dependent kinase (CDK) inhibitors (PCIs) were independently discovered to inhibit replication of human cytomegalovirus, herpes simplex virus type 1 and HIV-1. The results from small clinical trials against cancer were then suggesting that PCIs could be safe enough to be used clinically. It was thus hypothesized that PCIs could have the potential to be developed as novel antivirals targeting cellular proteins.

Antiviral drugs that target cellular proteins may play major roles in combating HIV resistance.

Despite the significant progresses made in antiretroviral therapy, current drugs still cannot cure or prevent HIV infection. And all drugs continue to select for drug-resistant HIV strains. Consequently, new antiretroviral drugs are constantly being developed.

Roscovitine inhibits activation of promoters in herpes simplex virus type 1 genomes independently of promoter-specific factors.

Flavopiridol, roscovitine, and other inhibitors of Cyclin-Dependent Kinases (CDK) inhibit the replication of a variety of viruses in vitro while proving nontoxic in human clinical trials of their effects against cancer. Consequently, these and other Pharmacological CDK inhibitors (PCIs) have been proposed as potential antivirals. Flavopiridol potently inhibits all tested CDKs and inhibits the transcription of most cellular and viral genes.