Abelson murine leukemia virus

Abelson murine leukemia virus (A-MuLV or Ab-MLV) is a retrovirus that has been extensively studied for its ability to induce leukemia in mice. This virus is a member of the Murine leukemia virus family, which are part of the larger group of Retroviridae. The Abelson virus was first identified in the 1960s by Herbert T. Abelson and Louise P. Salzman. The discovery of A-MuLV has significantly contributed to the understanding of cancer, particularly the mechanisms behind leukemogenesis, the process by which normal cells transform into cancerous leukocytes.

Overview[edit | edit source]

A-MuLV is characterized by its ability to transform lymphocytes, a type of white blood cell, leading to the development of leukemia in mice. The virus carries a specific oncogene, known as v-abl, derived from the cellular gene c-abl. The c-abl gene encodes a tyrosine kinase, which is a critical enzyme involved in cell signaling pathways that regulate cell growth and division. When the v-abl oncogene is introduced into cells by the virus, it leads to the uncontrolled proliferation of these cells, a hallmark of cancer.

Genetic Structure and Function[edit | edit source]

The genome of A-MuLV consists of RNA that, upon infection of a host cell, is reverse-transcribed into DNA by the enzyme reverse transcriptase. This DNA is then integrated into the host's genome, where the v-abl oncogene is expressed. The v-abl protein is a mutated form of the normal c-abl tyrosine kinase and is constitutively active, meaning it continuously signals cells to divide, leading to the development of leukemia.

Research and Implications[edit | edit source]

Research on A-MuLV has provided invaluable insights into the molecular biology of cancer. Studies of the virus have helped to elucidate the role of oncogenes in cancer development and the importance of tyrosine kinases in cell signaling pathways. Furthermore, understanding the mechanism of action of the v-abl oncogene has led to the development of targeted cancer therapies, such as imatinib (Gleevec), which specifically inhibits the BCR-ABL tyrosine kinase, a human homolog of v-abl involved in chronic myeloid leukemia.