Navigation Links
Flu's evolution strategy strikes perfect balance

Scientists have uncovered the flu's secret formula for effectively evolving within and between host species: balance. The key lies with the flu's unique replication process, which has evolved to produce enough mutations for the virus to spread and adapt to its host environment, but not so many that unwanted genomic mutations lead to the flu's demise (catastrophic mutagenesis). These findings overturn long-held assumptions about how the virus evolves.

Better understanding how the flu virus replicates and evolves to infect new hosts will help scientists find new ways to fight the flu. One option is the development of therapies that take advantage of the new findings by promoting mutagenesis treatments designed to generate increased mutations that will ultimately kill the virus.

"These new findings give us insights into how we may be able to control viral evolution," said Baek Kim, Ph.D., professor in the department of Microbiology and Immunology at the University of Rochester Medical Center and lead study author. "This research presents an attractive strategy for tackling the flu making the influenza virus kill itself by amplifying the number of mutations made beyond the desired level, which is lethal for the virus."

In the new study, published in the online journal PLoS One, scientists disprove the widely accepted idea that the flu virus evolves so efficiently due to its error-prone replication process. The virus requires a high number of genomic mutations to jump from one species to another, such as from a pig to a human, and up until this point scientists believed the error-prone replication process facilitated the mutations needed for the flu to spread. In reality, its replication process is not prone to errors; rather, the virus goes through multiple rounds of RNA genome replication in each viral infection cycle, allowing it to produce more than enough genomic mutations necessary for viral evolution and host adaptation.

The flu's accurate replication process also keeps the virus in check. Given the flu's multiple rounds of RNA replication per infection, too many mutations would result if the process was highly prone to error, leading to catastrophic mutagenesis.

"The perception has always been that the flu virus mutates a lot, and in order to do that it has to have an enzyme that makes a lot of mistakes, but Kim's work shows that is not the case at all," said David Topham, Ph.D., associate professor of Microbiology and Immunology at Rochester and an expert on how the body fights the flu. "There is a selection pressure, perhaps related to the flu's multiple replication strategy, which helps certain mutations develop and avoid immunity so that the virus can spread."

Topham, Kim and John Treanor, M.D., chief of the Infectious Diseases Division of the Department of Medicine at Rochester, lead the New York Influenza Center of Excellence (NYICE), which funded the current research. NYICE is one of five centers nationwide designated by the National Institutes of Health to further our understanding of the flu virus through basic research and surveillance studies, and to facilitate the nation's preparations for a potential pandemic.

To pin down the mechanisms behind flu virus evolution, researchers conducted unique biochemical analyses comparing flu virus replication to HIV replication, which has been well characterized in past research. While both viruses require efficient mutation production to adapt and thrive in their host environments, they replicate their genetic information very differently. HIV has evolved so that the virus only has a few chances to replicate its genome per infection and generate sufficient mutations, while the flu virus has ample chances to make and accumulate genomic mutations in each viral infection cycle.

At the center of the new finding are the polymerases, or enzymes, responsible for viral replication. Because the AIDS virus only has a few opportunities to replicate its genome in each infection cycle, its polymerases are highly error prone in order to generate sufficient mutations within its limited replication window. In contrast, the flu virus polymerases are high-fidelity enzymes they are accurate and not prone to error. Even without copious changes in genetic material, the flu's multiple replication strategy allows the virus to produce genomic mutations sufficient for viral evolution and host adaptation.

"Kim's team has developed some very important new methodology for studying the function of the flu polymerase that could easily result in the development of new antivirals or other methods to control influenza," said Treanor. "I think this research will stimulate a lot of additional research about the flu polymerase."


Contact: Emily Butler
University of Rochester Medical Center

Related biology news :

1. Natural S-Equol suggested as critical component in SE5-OH for reducing menopausal hot flushes
2. Evolution is driven by gene regulation
3. Clones on task serve greater good, evolutionary study shows
4. Adaptation to parasites drive African fishes along different evolutionary paths
5. Uncertainty drives the evolution of cooperative breeding in birds
6. Structure of 450 million year old protein reveals evolutions steps
7. Scientists retrace evolution with first atomic structure of an ancient protein
8. Hidden interactions between predators and prey: evolution causes cryptic dynamics in ecology
9. Migrating squid drove evolution of sonar in whales and dolphins, researchers argue
10. Old developmental pathways spawn revolutionary evolutionary changes
11. Systems Biology poised to revolutionize the understanding of cell function and disease
Post Your Comments:
(Date:5/12/2016)... 2016 , a brand of ... results from the Q1 wave of its quarterly wearables ... consumers, receptivity to a program where they would receive ... insurance company. "We were surprised to see ... Michael LaColla , CEO of Troubadour Research, "primarily because ...
(Date:4/26/2016)... and LONDON , April ... part of EdgeVerve Systems, a product subsidiary of ... today announced a partnership to integrate the Onegini ...      (Logo: ) ... their customers enhanced security to access and transact ...
(Date:4/14/2016)... 14, 2016 BioCatch ™, ... today announced the appointment of Eyal Goldwerger ... Goldwerger,s leadership appointment comes at a time ... the deployment of its platform at several of the ... which discerns unique cognitive and physiological factors, is a ...
Breaking Biology News(10 mins):
(Date:6/23/2016)... ... June 23, 2016 , ... Mosio, a ... eBook, “Clinical Trials Patient Recruitment and Retention Tips.” Partnering with experienced clinical research ... by providing practical tips, tools, and strategies for clinical researchers. , “The landscape ...
(Date:6/23/2016)... 2016 /PRNewswire/ - FACIT has announced the creation ... biotechnology company, Propellon Therapeutics Inc. ("Propellon" or "the ... a portfolio of first-in-class WDR5 inhibitors for the ... WDR5 represent an exciting class of therapies, possessing ... for cancer patients. Substantial advances have been achieved ...
(Date:6/23/2016)... ... 23, 2016 , ... Charm Sciences, Inc. is pleased to ... AOAC Research Institute approval 061601. , “This is another AOAC-RI approval of the ... Vice President of Regulatory and Industrial Affairs. “The Peel Plate methods perform comparably ...
(Date:6/23/2016)... 23, 2016   EpiBiome , a precision microbiome ... in debt financing from Silicon Valley Bank (SVB). The ... to advance its drug development efforts, as well as ... "SVB has been an incredible strategic partner to ... traditional bank would provide," said Dr. Aeron Tynes ...
Breaking Biology Technology: