In 1911 Rous showed that a cell-free filtrate from a chicken sarcoma could still induce tumours, later named Rous Sarcoma Virus (RSV). At the time, most scientists believed cancer arose only from internal mutations and was not contagious, so his results were shocking. His work suggested that viruses can rewrite cellular genetic information and initiate tumour formation, opening a new branch of cancer research. This concept eventually led to preventive tools such as the human papillomavirus (HPV) vaccine. Rous thus connected virology with oncology and profoundly influenced medicine and public health.

RSV is a positive-strand RNA retrovirus whose genome is reverse-transcribed and integrated into the host genome as a provirus. Rous’ filtration experiment, a classical proof of sub-bacterial pathogen size, showed that tumorigenic capacity resided in an infectious particle. Decades later, the RSV oncoprotein v-Src was identified as a mutated version of the host tyrosine kinase c-Src, helping to establish the oncogene concept. Research on RNA tumour viruses led to the discovery of reverse transcriptase, elucidation of cell signalling pathways, and the hunt for tumour-suppressor genes. Rous’ discovery is therefore regarded as the cornerstone of molecular oncology and viral carcinogenesis.

Labelled-particle studies defined RSV as a 100–120 nm enveloped RNA virus, later shown to carry Gag, Pol, Env and the oncogene Src. Constitutive v-Src kinase activity persistently activates FAK, PI3K and Ras pathways, disrupting adhesion and cell-cycle checkpoints. Rous’ work established CEF culture as a retrovirology model and temperature-sensitive tsRSV mutants for gene-function assays. Mapping of RSV proviral insertion sites pioneered insertional mutagenesis screens to identify host oncogenic drivers. These techniques foreshadow today’s RNA-seq-based and transposon-tag insertion screening approaches.