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Geno Types
I did a little research on geno types and the way I understand it is there is only one hep-c and the different geno type you have is really how you as an individual and your genes react to the virus. Now I may be reading this all wrong. It wouldn't be the first time.
The genotype is the specific genetic makeup (the specific genome) of an individual, in the form of DNA. Together with the environmental variation that influences the individual, it codes for the phenotype of that individual. Non-hereditary mutations are not classically understood as representing the individuals' genotype. Hence, scientists and doctors sometimes talk for example about the (geno)type of a particular cancer, thus separating the disease from the diseased. While codons for different amino acids may change in a random mutation (changing the sequence coding a gene), this doesn't necessarily alter the phenotype.
Typically, one refers to an individual's genotype with regard to a particular gene of interest and, in polyploid individuals, it refers to what combination of alleles the individual carries (see homozygous, heterozygous). Any given gene will usually cause an observable change in an organism, known as the phenotype. The terms genotype and phenotype are distinct for at least two reasons:
To distinguish the source of an observer's knowledge (one can know about genotype by observing DNA; one can know about phenotype by observing outward appearance of an organism).
Genotype and phenotype are not always directly correlated. Some genes only express a given phenotype in certain environmental conditions. Conversely, some phenotypes could be the result of multiple genotypes. The genotype is commonly mixed up with the Phenotype which refers to the physical appearance
The distinction between genotype and phenotype is commonly experienced when studying family patterns for certain hereditary diseases or conditions, for example, hemophilia. Sometimes people who do not have hemophilia can have children with the disease, because the parents each "carried" hemophilia genes in their body, even though these genes have no effect on the parents health. The parents in this case are called carriers. Healthy people who are not carriers and healthy people who are carriers of the hemophilia gene have the same outer appearance (ie they do not have the disease), therefore they are said to have the same phenotype. However, the carriers have the gene and the other healthy people do not (they have different genotypes).
With careful experimental design, one can use statistical methods to correlate differences in the genotypes of populations with differences in their observed phenotype. These association studies can be used to determine the genetic risk factors associated with a disease. They may even be able to differentiate between populations who may or may not respond favorably to a particular drug treatment. Such an approach is known as personalized medicine.
Inspired by the biological concept and usefulness of genotypes, computer science employs simulated genotypes in genetic programming and evolutionary algorithms. Such techniques can help evolve mathematical solutions to certain types of otherwise difficult problems.
[edit
The genotype is the specific genetic makeup (the specific genome) of an individual, in the form of DNA. Together with the environmental variation that influences the individual, it codes for the phenotype of that individual. Non-hereditary mutations are not classically understood as representing the individuals' genotype. Hence, scientists and doctors sometimes talk for example about the (geno)type of a particular cancer, thus separating the disease from the diseased. While codons for different amino acids may change in a random mutation (changing the sequence coding a gene), this doesn't necessarily alter the phenotype.
Typically, one refers to an individual's genotype with regard to a particular gene of interest and, in polyploid individuals, it refers to what combination of alleles the individual carries (see homozygous, heterozygous). Any given gene will usually cause an observable change in an organism, known as the phenotype. The terms genotype and phenotype are distinct for at least two reasons:
To distinguish the source of an observer's knowledge (one can know about genotype by observing DNA; one can know about phenotype by observing outward appearance of an organism).
Genotype and phenotype are not always directly correlated. Some genes only express a given phenotype in certain environmental conditions. Conversely, some phenotypes could be the result of multiple genotypes. The genotype is commonly mixed up with the Phenotype which refers to the physical appearance
The distinction between genotype and phenotype is commonly experienced when studying family patterns for certain hereditary diseases or conditions, for example, hemophilia. Sometimes people who do not have hemophilia can have children with the disease, because the parents each "carried" hemophilia genes in their body, even though these genes have no effect on the parents health. The parents in this case are called carriers. Healthy people who are not carriers and healthy people who are carriers of the hemophilia gene have the same outer appearance (ie they do not have the disease), therefore they are said to have the same phenotype. However, the carriers have the gene and the other healthy people do not (they have different genotypes).
With careful experimental design, one can use statistical methods to correlate differences in the genotypes of populations with differences in their observed phenotype. These association studies can be used to determine the genetic risk factors associated with a disease. They may even be able to differentiate between populations who may or may not respond favorably to a particular drug treatment. Such an approach is known as personalized medicine.
Inspired by the biological concept and usefulness of genotypes, computer science employs simulated genotypes in genetic programming and evolutionary algorithms. Such techniques can help evolve mathematical solutions to certain types of otherwise difficult problems.
[edit
Hey! How are you? Hope you're not TOO down about the Mavs kickin' some Kings bu**!
I hope you enjoy the game!
Janice
I hope you enjoy the game!
Janice
Well, perhaps one wants to consider the quasi-species as well then, of which there are thought to be millions of different varieties of HCV.
A paper I recently read is that the Genotype is the classification which displays consistent markers that allow for sub-classification of the HCV, whereas with the quasi-species there are so many varieties that further sub-classification would be virtually impossible.
That same paper also explained that some nonresponders and relapsers may have viruses which have mutated into quasi-species which can replicate better/faster than others and thus do not respond to tx as well as those who have quasi-species that have not undergone this mutation.
Before one gets to cagey though, I should point out that I believe it also indicated that there has not been any evidence of HCV becoming drug resistant at this point, simply that the replication rate varies. But in lieu of nonresponders, I do question how such a claim can be made unless there is means to validate that virus destruction is still occurring even when viral breakthroughs are evidenced in a person's tx making them a nonresponder.
A paper I recently read is that the Genotype is the classification which displays consistent markers that allow for sub-classification of the HCV, whereas with the quasi-species there are so many varieties that further sub-classification would be virtually impossible.
That same paper also explained that some nonresponders and relapsers may have viruses which have mutated into quasi-species which can replicate better/faster than others and thus do not respond to tx as well as those who have quasi-species that have not undergone this mutation.
Before one gets to cagey though, I should point out that I believe it also indicated that there has not been any evidence of HCV becoming drug resistant at this point, simply that the replication rate varies. But in lieu of nonresponders, I do question how such a claim can be made unless there is means to validate that virus destruction is still occurring even when viral breakthroughs are evidenced in a person's tx making them a nonresponder.
I have genotype 1A and also 1B. It just depends on who you get it from I think really...what tree branch you are down on and how many times the person you get it from is affected, and the person before them that they got it from was affected etc.
Techinically if you got it over and over (infection) from ten different people you could have ten different genotypes (or however many there are out there).
But under that are different STRAINS (not sure if I am wording it exactly right but you get the concept).
I mean if I am geno 1B and I share a needle with someone else who is 1B for example - but our bloods have never been exposed ever anywhere...then I'd probably technically have more than ONE hep genotype 1B....
Like swine flu and bird flu or whatever all the names are. It might be something that makes it harder for us to achieve SVR or something............just a thought. I often wonder WHY some geno 1As and not the OTHERs for example and I really do believe some infective strains are just more virulent than others.
It's the only thing that makes sense to me.
And it's only because I am a combo genotype person that I've thought about it. I know for a fact that a lot of addicts say "oh you have hcv I do too - it's ok for us to use the same needle we both have it" without ANY understanding...that it's like saying I have an orange and you have an apple - yeah you both have fruit but.................
;)
Techinically if you got it over and over (infection) from ten different people you could have ten different genotypes (or however many there are out there).
But under that are different STRAINS (not sure if I am wording it exactly right but you get the concept).
I mean if I am geno 1B and I share a needle with someone else who is 1B for example - but our bloods have never been exposed ever anywhere...then I'd probably technically have more than ONE hep genotype 1B....
Like swine flu and bird flu or whatever all the names are. It might be something that makes it harder for us to achieve SVR or something............just a thought. I often wonder WHY some geno 1As and not the OTHERs for example and I really do believe some infective strains are just more virulent than others.
It's the only thing that makes sense to me.
And it's only because I am a combo genotype person that I've thought about it. I know for a fact that a lot of addicts say "oh you have hcv I do too - it's ok for us to use the same needle we both have it" without ANY understanding...that it's like saying I have an orange and you have an apple - yeah you both have fruit but.................
;)
Upbeat: Truthfully I don't understand your point. The only thing I understand is that I have a virus, and just like the influenza virus it mutates and changes, thats why we have different genotypes. I maybe (am probably) wrong but I don't think the virus mutated into geno 2 once it got in my system. I think I was exposed to genotype 2. (Luckily I guess, we'll see)
Child24Angel-Of course you didn't expose or carry Hepc to Nick.
BUG
Child24Angel-Of course you didn't expose or carry Hepc to Nick.
BUG
The Hawk is right.
If you take the quote above and apply it to the virus itself you are closer to the mark. Its the virus that comes in several strains, or genotypes. The history of HCV emergence suggests that each genotype arose in a specific geographical zone. Genotype 1 and subtypes [a, b, etc] arose in sub-Saharan Africa. Genotype 3 arose in South East Asia, etc.
Each genotype requires different treatment, and has different statistical clearance rates. Genotype 1 is the toughest [and probably the most prolific].
This is a huge subject, and I'm no expert, but hopefully this will give you a better idea of what you are reading/hearing.
If you take the quote above and apply it to the virus itself you are closer to the mark. Its the virus that comes in several strains, or genotypes. The history of HCV emergence suggests that each genotype arose in a specific geographical zone. Genotype 1 and subtypes [a, b, etc] arose in sub-Saharan Africa. Genotype 3 arose in South East Asia, etc.
Each genotype requires different treatment, and has different statistical clearance rates. Genotype 1 is the toughest [and probably the most prolific].
This is a huge subject, and I'm no expert, but hopefully this will give you a better idea of what you are reading/hearing.
I'm not sure if you got it right. My understanging is the different genotypes are like different strains, which is why you can get more than one. Although my reading makes it sound like one of the big problems in fighting Hep C is the fact it alters from one person to the next by how it responds with your particular body. I could be totally off, but thats what got through into my fuzzy brain.
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