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Researchers from the Icahn School of Medicine at Mount Sinai identify a mechanism by which influenza A, a family of pathogens that includes the most deadly strains of flu worldwide, attack human cells to increase.
It was by studying the cells of patients with an RNA exosome mutation, which were contributed by six collaborating medical centers, that the investigators were able to understand how influenza A attacks the RNA exosome inside a cell’s nucleus for its own increase.
The genes affected in these rare cases of neurodegeneration is caused by a congenital RNA exosome mutation may offer future insight into more common brain disorders, such as Alzheimer’s and Parkinson’s diseases.
In the case of Influenza A, the loss of RNA exosome activity severely compromises viral infectivity, but also manifests in human neurodegeneration suggesting that viruses target essential proteins implicated in rare disease in order to ensure continual adaptation.
Influenza A is an RNA virus, it reproduces itself inside the nucleus. Most viruses replicate in a cell’s cytoplasm, outside the nucleus.
The researchers found that once inside the nucleus, influenza A attacks the RNA exosome, an essential protein complex that degrades RNA as a way to regulate gene expression.
The flu pathogen needs extra RNA to start the replication process so it steals these molecules from the hijacked exosome, Dr. Marazzi says.
Viruses make use of our by-products, rather than allowing the exosome to chew up and degrade excess RNA, it tags the exosome and steals the RNA it needs before it is destroyed.
“Without an RNA exosome, a virus cannot grow, so the agreement between the virus and host is that it is ok for the virus to use some of the host RNA because the host has other ways to suppress the virus that is produced.