( derstand the functions of any microRNAs...)Virus uses tiny RNA to evade the immune system

SV40 is a relatively harmless monkey virus that can cause kidney infections in its natural simian host. In rodents, however, it can cause cancer. Although the SV40 genome has been found in some human tumors, its role in human cancer has been debated. The virus is better known as a model system that has greatly contributed to major scientific advances about how genes work.

To launch their study, Grundhoff wrote a computer program to screen the SV40 genome for possible microRNA precursors. MicroRNAs are made from messenger RNA molecules with distinctive hairpin folds. The hairpin structure is diced into a microRNA segment that works with another complex to disable other messenger RNAs with complementary sequences.

Among several dozen predicted microRNAs, the top candidate turned out to be abundantly expressed in human cells infected with SV40.

Sullivan soon found the target of the plentiful SV40 microRNA. It effectively targeted the messenger RNA for a protein known as T antigen, leading to its cleavage. "SV40 may be the world's most studied virus," Sullivan said, "and T antigen is its most studied part."

When SV40 enters a cell, it produces T antigen, which functions to trigger viral DNA replication. Unfortunately for the virus, T antigen also serves as a target for immune (T) cells, which can destroy infected cells and prevent the virus from spreading.

Conveniently, the microRNA that targets T antigen is made late in the infectious cycle, just when T antigen is no longer essential for virus replication. Further experiments showed that cytotoxic immune cells were more likely to kill cells infected with a mutant virus that cannot make the microRNA than the normal virus. Thus, microRNA-induced reductions in T antigen expression promote escape from antiviral T cells without affecting virus growth.

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Source:Howard Hughes Medical Institute