miRNAs Have Such Rock Star Status That Real Rock Stars Write About Them

Tonight I went to a concert in which the two bands I went to see were fronted by biologists: Bad Religion (Greg Graffin Ph.D) and Offspring ("Dexter" Holland soon to be Ph.D). 

I go curious as to what they've been publishing in the biomedical literature and found a cool paper published during 2013 in PLoS ONE whose first author is Bryan Holland of Offspring.

I read the paper and it is fascinating. 

The subject of the paper is the phenomenon of miRNA's. These are non-coding (i.e. non-protein making) short pieces of RNA that function to regulate genes. What Holland's paper focuses is on  is miRNA's within the genome of HIV.  The paper argues that 8 miRNA like sequences found in HIV may bind to cellular targets and be responsible for dysregulation of cellular genes. This dysregulation may play a role in HIV's ability to evade host defense, something it does quite readily.

I find the whole topic of RNA fascinating because as the myriad functions of RNA (tRNA, ribozymes, RNAi, miRNA, siRNAs, snRNPs, etc) are detailed it is clear how versatile this molecule is giving a lot of validity that our modern DNA world evolved from an RNA one.

Getting to the Brain by Hijacking miRNA: The EEE story

The mechanism by which Eastern Equine Encephalitis (EEE), a deadly mosquito-borne viral disease with a 50% mortality rate, causes its characteristic illness is the subject of a pathbreaking article in Nature by authors from Pitt's Center for Vaccine Research

The paper is focused on the role of miRNAs and their interaction with viral RNA. miRNAs are small pieces of RNA that cells use to regulate the expression of genes. miRNAs have not been thought to have a role in controlling viral genes. In the case of EEE, however, William Klimstra and colleagues found an miRNA that binds to the virus, blunting its ability to infect specific cells of the immune system and, consequently, stops the triggering of an immune response.

This suppression of host immune defenses by exploiting--or hijacking, as the authors put it--host miRNAs allows the virus to reek havoc in the central nervous system causing the signs and symptoms of encephalitis.

Furthermore, the viral sequences that bind the miRNA serve a dual purpose, enhancing replication in the mosquito vector.

The elegance and ingenuity of this viral mechanism is truly fascinating and it will be important to determine if other viruses use similar mechanisms.