Somewhat related is the many variants of each geno that aren't sufficiently unique, that is, far enough from the nearest genotype or subtype residence on the genome and in the necessary quantities to be classified as a new geno/subtype. Another way of saying this is that not all G1a for example, are identical to one another.
However, the variants of a wild-type virus are thought to be so similar in most cases that the immune system identifies them as one and the same and responds accordingly.
The host-mediated immune responses will determine through natural selection processes which 'version' of G1a each person will have. This is the same method that can give rise to a new G/S.
ML
It is an interesting read, answers a few questions for me, and adds a few more? Thanks for the question and the answer/
Deb
That's the way I read it. And the antibodies may not protect against reinfection either. I found the entire article quite interesting. As I recall - it's been a week - it focuses on therapeutic and prophylactic vaccine research and Th1 response and CD4 and Cd8 cells that play such a significant role in clearing HCV.
Mike
“Therefore, not surprisingly, many quasispecies of HCV can exist within a single infected individual. It is believed that the ability of the virus to rapidly and constantly change in response to immune pressure may out pace the host's own ability to produce effective neutralizing antibodies. While neutralizing antibodies may be detected in an infected individual, given the rapid mutational rate of the virus, they may be more reflective of a former HCV viral variant rather than the current”
Am I interpreting this correct? To me it is saying that the antibodies that are produced to fight off HCV in one person my not be the same antibodies that would fight HCV in another person, even if they have the same Gen. Type due to the rapid and constant change of the virus. Even though people my have the same Gen. Type the virus has mutated or adapted to each persons Immune System.
I don't know whether this addresses your question but it seems related.
See: Immunotherapy for HCV Infection: Next Steps
Posted 11/04/2008
http://www.medscape.com/viewarticle/581892_1
"....While it is known that neutralizing antibodies are generated during HCV infection and that they can be detected within 7-8 weeks postinfection.[27] they are not able to protect against reinfection.[28,29] In fact, HCV-specific antibody responses can be completely absent following the resolution of infection.[30,31] Several factors may be responsible for the apparent lack of antibody-mediated protection in HCV infection. First, HCV is highly variable, therefore, effective neutralizing antibodies produced in response to one variant of HCV may not necessarily protect against another, which may explain the propensity of convalescent humans to become reinfected. Further adding to the genetic diversity of the virus is the high mutational rate of HCV. Calculations based on chronically infected individuals estimate that the average mutational rate of HCV is 0.001 substitutions per genomic site per year, averaging 8-18 mutations per year.[32] In addition, it has been shown that certain proteins of the virus may change at a more rapid rate than others, including proteins of the viral envelope, which are critical targets for neutralizing antibodies.[33] Therefore, not surprisingly, many quasispecies of HCV can exist within a single infected individual. It is believed that the ability of the virus to rapidly and constantly change in response to immune pressure may out pace the host's own ability to produce effective neutralizing antibodies. While neutralizing antibodies may be detected in an infected individual, given the rapid mutational rate of the virus, they may be more reflective of a former HCV viral variant rather than the current infecting virus...."