I do have one question and it may have been answered before? What the *ell is genotype 1a and where can I find a link or links that explains the genotyping and stages of this virus? I've been in a coma the last 9 weeks and have been asked this numerous times along the way and have as yet figured this out. Sorry, sitting in the corner with dunce cap on.
There is a test the doctors run in the beginning to check your levels and determine your genotype.. there are several different ones, and some are more resistant to the medications/ tx. Genotype 1 and 4 are those resistant type and ususally treat longer than type 2 or 3.. and it goes up even higher than 4. I have seen some post they were 10a.. not sure if that was a typo or not.
But ususally they find the genotype before starting treatment so they know which length of treatment you should be on.
For example geno type 1 will treat for 48 weeks, where 2 or 3 would be for 24, and it all depends on when you show UND to determine if should tx longer than the 48.. etc.. I am sure others will give you more defininate answers on this.
hey cable guy,
All I can add is that I was very surprised when my Doc. said "the liver IS one of the few organs that can repair itself." unlike kidneys and such. Not sure what comp. from scarring are though.
You have not been in too much of coma . your comments on here these last couple weeks (when I found this site) have been funny and right on.
Maybe u can help me figure out something. with all this geno typeing talk on here that I have no clue about yet. If you have hep C 30yrs plus, how probable is it I will need treatment now or later even? I just need some layman answers . It is driveing me nutty just waiting for biop.
Alo'ha , Geterdone,and all thanks. R.
Even in a single infected individual, HCV does not exist as a homogeneous species. Heterogeneous genomes - "quasispecies" - resulting from mutations due to high error rates in RNA replication are found within the same host. Many important biological features of several viruses are attributable to their quasispecies nature, including vaccination failure, persistent infection, and resistance to antiviral drugs.38 The amount of diversity of the quasispecies population has also been found to be related to the progression to liver disease.
The most striking feature of HCV is its ability to persist in the host. The mechanism(s) of viral persistence are unclear but cannot include viral integration into the host genome as with certain other viruses due to the lack of a DNA intermediate in its life cycle. Instead, persistence appears to result from HCV's ability to mutate rapidly under immune pressure, giving rise to related but immunologically distinct variants.11 Any one of these variants can become the predominant strain, and coexistence of multiple quasispecies allows HCV to escape the host immune response.
Most mutations occur in a short, hypervariable region of the E2/NS1 domain. The region represents only 8% of the domain but accounts for approximately half of the nucleotide changes in the entire envelope region.39 Because of the occurrence of this hypervariable region within the envelope where it would be most likely to be exposed to antibody, mutations in this region may serve to evade an immune response.11,39 It has been reported that the nucleotide substitution rate within the hypervariable region rises during acute infection at a time when HCV RNA levels in the serum are decreasing, possibly due to a host immune response.40 There is also evidence that HCV can escape immune clearance by down-regulating its replication while persisting quiescently in the liver.11
Genotypic analysis and prevalence
Traditionally, viruses have been classified according to antigenic characteristics, but with recent advances in molecular biology, genotypic classification through the analysis of genomic variation is now possible. Variations in the HCV genome fall into a series of specific patterns that have been classified into genotypes.41 Among the different HCV genotypes, the sequence of the 5' NC region is relatively conserved and is most often applied for diagnosis of HCV infection by PCR. In contrast, the sequences of NS3, NS5, and core regions are more variable and are therefore often used to define and distinguish among the HCV genotypes.42
Studies indicate that there are nine major HCV types (according to the general classification) designated 1 through 9.18
Some of these types are further divided into subtypes. The potential significance of this becomes apparent when considering virus-host interactions, severity of infection, and sensitivity to treatment. The clinical importance of HCV lies in its persistence and ability to cause chronic liver disease. The dramatic disparities in HCV disease course among infected persons and differences in disease patterns between countries with divergent dominant genotypes raise the possibility that the existence of various strains of HCV may be a critical factor in this variability.
In one study, 98 patients in the United States with chronic Hepatitis C infection were examined (Fig 1).41 Type 1 was the dominant genotype, present in 74% of patients, almost evenly divided between subtypes 1a and 1b. Two additional patients had a dual infection with types 1 and 2 while another case had both subtypes 1a and 1b.
One patient was untypeable. There was no correlation between infecting genotype and presumed cause, serum indices of necroinflammatory activity, age or sex of the patients, or known duration of infection. Patients with HCV genotype 2 had more severe liver disease histologically than did patients with other genotypes but paradoxically had significantly lower circulating levels of Hepatitis C viral RNA. 41 A second, independent study, also performed in the United States, found that HCV genotype 1 represented 70% of viral isolates, confirming that it accounts for the majority of infections in American patients. 4
Before I found medhelp, I was using another forum. A guy there said he'd been told several years ago to forget treatment, his cirrhosis was too far gone, and he should get his things in order, i.e. prepare for the end. Instead, he convinced his doctor to let him treat, got rid of HCV and his liver did indeed repair itself. It took him 8 years in total to accomplish.
My heptologist said once the hep is gone the scar tissue will start to soften as the liver repairs itself.
It takes time and care but it can be done!
My hepatologist told me that milk thistle lowers liver enzyme scores (ALT and AST)and that it's fine to take before and after treatment but not during. She doesn't believe it's known whether milk thistle actually repairs or regenerates the liver. Like many non-prescription drugs and herbs, it hasn't been studied enough because there are no pharmaceutical manufacturers to pay for the studies.
My doc at Yale says OK to take on tx. You've got to follow your intuition and see if your stats go up or down. No one knows. I believe they'r working for me.
Dr Weil says DEFINATELY TAKE IT WHILE ON TX!
THE PHARMA COS SCARE MDS INTO THINKING ALL HERBS ARE DANGEROUS. THERE WILL BE A BIG CAMPAIGN AGAINST HERBS & SUPPLEMENTS BY THE PHARMAS SOON. THE WORD I GOT IS THE MEDIA IS GOING TO COMPLY. DON'T BELIEVE IT.
Some folks around here are paranoid to the extreme and believe you are me. They have a gang here and Med Help booted me for the 90th time about two months back. Just a heads up. Hang in there. I've treated once -- genotype 1a, stage 2.
There's a lot of cruel people here that don't give a rat's ass if someone is sick. People who know better allow it to go on. Big news right?
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