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Ovine Pulmonary Adenomatosis Essay

1687 words - 7 pages

Ovine Pulmonary Adenomatosis (OPA) is an infectious lung cancer specific to sheep and is caused by jaagsiekte sheep retrovirus (JSRV). This is a type B retrovirus with a genome composed of linear, positive, single stranded RNA. Transmission is through inhalation of infectious virus or direct contact with infected respiratory secretions. It is found in many countries including the UK, in particular Scotland. The incubation period is long therefore it can take years for clinical signs to develop. Sheep are often 2-4 years before symptoms such as weight loss and heavy breathing occur. In my essay I will explore the mechanisms of transformation, the theories of immune evasion and the role of ...view middle of the document...

The mechanisms of transformation use the env protein, although no sequence homologous to a cellular oncogene has been detected in JSRVs genome. There are 3 pathways involved in JSRV transformation. I will explore the Akt pathway in detail.
The Hyal2-RON pathway involves hyaluronidase 2 (Hyal2), a gene that encodes a glycosylphosphatidylinositol (GPI) anchored protein on the cell surface which can act as an entry receptor for JSRV. Hyal2 is a member of a family that degrade hyaluronic acids of the vertebrates’ extracellular matrix. In the absence of JSRV env the Hyal2 receptor protein is associated with the RON receptor tyrosine kinase. This complex has low Ron kinase activity and negatively regulates RON receptor signalling, rendering it functionally silent. Hence pathways resulting in cellular transformation are not activated. However when JSRV is present Env cleavage by cellular furin protease occurs, before JSRV env protein binds and sequesters the Hyal2 receptor. This liberates an ocogenic factor (RON). The liberated RON becomes functionally active and consequently activates the PI3K-Akt and MAPK pathways.

The PI3K-Akt signalling pathway is determinant in cellular proliferation and survival. The mechanisms involved are very complex. Scientists previously hypothesised that the YXXM motif (tyrosine), a region in the cytoplasmic tail of TM, had a direct role in the activation of the Akt pathway. This was because the cytoplasmic tail of JSRV env has a tyrosine phosphorylated peptide motif that provides the binding site for the SH2 domain of the p85 subunit of PI3K. A study supported this theory, its results showing that mutation of this motif to phenylalanine or aspartic acid stopped any transforming activity of JSRV Env in NIH 3T3 cells. However scientists have now shown otherwise; the mutated motif was actually still transforming the cells, but less effectively. In short mutations of this motif do not prevent PI3K dependent Akt phosphorylation. Current research shows the tyrosine residue of YXXM motif is important in modulating the Env protein expression but it is not directly involved in PI3K activation. JSRV Env may activate PI3K through an unknown cellular adaptor molecule or by other signalling pathways directly triggered by JSRV Env. A chimera containing the membrane-spanning region (MSR) of enJSRV, when inserted into JSRV Env, led to a drop in transformation. This indicates regions other than the tyrosine motif are involved.

Despite the uncertainty of how PI3K binds to the Env, scientists have shown at the start of the Akt pathway Phosphatidyl-Inositol-3 Kinase (PI3K) is recruited to the cell membrane in response to a membrane stimulus, for example a growth factor or cytokine. Phosphorylated PI3K phosphorylates the second messenger phosphatidylinositol-4,5-biphosphate (PIP2) into phosphatidylinositol-3,4,5- triphosphate (PIP3). PIP3 then recruits phosphatidylinositol-dependent kinase 1 (PDK1) which then phosphorylates Akt. The...

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