The Story behind the Science: On the discovery of respiratory syncytial virus.

Respiratory syncytial virus (RSV) was discovered in 1956 by the laboratory of Robert Chanock after its isolation from children with upper respiratory infections. Here, we review the events leading to its discovery including its prior isolation as chimpanzee coryza virus and its subsequent association with human disease.

CDK2 regulates HIV-1 transcription by phosphorylation of CDK9 on serine 90.

Background: HIV-1 transcription is activated by the viral Tat protein that recruits host positive transcription elongation factor-b (P-TEFb) containing CDK9/cyclin T1 to the HIV-1 promoter. P-TEFb in the cells exists as a lower molecular weight CDK9/cyclin T1 dimer and a high molecular weight complex of 7SK RNA, CDK9/cyclin T1, HEXIM1 dimer and several additional proteins. Our previous studies implicated CDK2 in HIV-1 transcription regulation.

Acceleration of adenovirus replication and increased virion production by treatment with the steroid hormone 17 beta-estradiol.

We report here that concentration of an estrogen known to promote enhanced transformation and to increase oncogenicity of rat embryo cells, accelerate the production and increase the yield of progeny virions in adenovirus type 12 (Ad 12)-infected HEp-2 cells. Further, measurement of the incorporation of radioactive RNA and DNA precursors indicated that macromolecular synthesis in the estrogen-treated, infected cells was accelerated. Possible explanations for this observation are discussed.

Cyclic AMP mediates the direct antiproliferative action of mismatched double-stranded RNA.

Previous experiments have demonstrated that double-stranded RNAs (dsRNAs) can exert an antiproliferative effect on human tumor cells, independent of interferon (IFN) induction. However, the mechanism by which dsRNAs inhibit tumor growth has not been elucidated. As a first step in determining the molecular events responsible for growth arrest, we have explored the role of signal transduction through the cAMP system in the antiproliferative effect of the mismatched dsRNA, r(I)n.