The influenza virus genome consists of eight negative sense RNA segments. The segmentation allows efficient genetic exchange among influenza viruses co-infecting the same cell. But this strategy has its costs, namely, that each virion has to ensure that all eight segments are specifically packaged for a productive infection. Furthermore, all eight segments have to be capable of producing a functional protein. Or do they?
This group found that at high multiplicities of infection (MOI), the 3 measured proteins (HA, NA, and NS1), were all expressed in essentially all infected cells. However, at low MOI (.03) where a single virion has infected a cell, a surprisingly high number of cells did not express these proteins at detectable levels. They used this same method on a non-segmented negative sense RNA virus, vesicular stomatitis virus (VSV). In contrast to influenza, the majority of VSV-infected cells contained detectable levels of viral proteins, indicating this is possibly a result of the segmented lifestyle of the influenza virus.
These results were strengthened with a relatively sensitive procedure, flow cytometry, where only 46.9% of the infected cells expressed the proteins measured. Once the MOI of the influenza virus was increased to 1, there was a drastic increase in the number of infected cells expressing virus protein indicating that complementation or cooperation exists among influenza viruses.
Although this could be a detection problem of the methods used, if further research supports it, this could have very interesting conclusions to influenza biology. Defective interfering particles have been known to be produced naturally in viral infections, but this research suggests that the majority of influenza viruses are somewhat defective.
The authors end stating that the influenza virus …"exists less as a population of intact virus than as a swarm of complementation-dependent, semi-infectious virions". Could a segmented lifestyle be an evolutionary adaptation such that a cooperative inter-dependent virus swarm is selected over a more solitary population? How does the host react to such a diverse population? Is this influenza's answer to antigenic variation like that of bacteria or protozoans? Could this inter-dependence be a mechanism that influences other stages of the virus life cycle (ie packaging)? How are these proteins interacting within the cell? Any ideas? Please comment!
This group found that at high multiplicities of infection (MOI), the 3 measured proteins (HA, NA, and NS1), were all expressed in essentially all infected cells. However, at low MOI (.03) where a single virion has infected a cell, a surprisingly high number of cells did not express these proteins at detectable levels. They used this same method on a non-segmented negative sense RNA virus, vesicular stomatitis virus (VSV). In contrast to influenza, the majority of VSV-infected cells contained detectable levels of viral proteins, indicating this is possibly a result of the segmented lifestyle of the influenza virus.
These results were strengthened with a relatively sensitive procedure, flow cytometry, where only 46.9% of the infected cells expressed the proteins measured. Once the MOI of the influenza virus was increased to 1, there was a drastic increase in the number of infected cells expressing virus protein indicating that complementation or cooperation exists among influenza viruses.
Although this could be a detection problem of the methods used, if further research supports it, this could have very interesting conclusions to influenza biology. Defective interfering particles have been known to be produced naturally in viral infections, but this research suggests that the majority of influenza viruses are somewhat defective.
The authors end stating that the influenza virus …"exists less as a population of intact virus than as a swarm of complementation-dependent, semi-infectious virions". Could a segmented lifestyle be an evolutionary adaptation such that a cooperative inter-dependent virus swarm is selected over a more solitary population? How does the host react to such a diverse population? Is this influenza's answer to antigenic variation like that of bacteria or protozoans? Could this inter-dependence be a mechanism that influences other stages of the virus life cycle (ie packaging)? How are these proteins interacting within the cell? Any ideas? Please comment!
