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Hepatitis C - Are You smarter than a 5th grader?
Ask a question on this thread and let's see how smart/fast we really are.
Who discovered Hepatitis C?
Who discovered Hepatitis C?
Well, it's a moot point.
Harvey Alter was the first person who distinguished HCV as being different to HAV and HBV in the mid 70's. It became known as NonANonB.
In 1988/1989 Michael Houghton identified this 'new' virus as HCV, he cloned it and created the blood screening process that is used today.
Harvey Alter was the first person who distinguished HCV as being different to HAV and HBV in the mid 70's. It became known as NonANonB.
In 1988/1989 Michael Houghton identified this 'new' virus as HCV, he cloned it and created the blood screening process that is used today.
You are smarter than a 5th grader !!!!!!! : ). The winner creates the next
"smarter than a 5th grader" question. Tag your it :),
"smarter than a 5th grader" question. Tag your it :),
Is this the urban definition or the before 900 A.D. definition? Clarification please :).
Urban Dictionary Definition of Stir the Pot:
Stir the pot
Someone who loves to proliferate the tension and drama between 2 or more feuding people/groups in public to get a raise of people in hopes of starting a shitstorm of drama and uncomfortable conflict, sometimes for personal gain but oftentimes just for the thrill of confrontation.
http://www.urbandictionary.com/define.php?term=stir+the+pot
Stir the pot
Someone who loves to proliferate the tension and drama between 2 or more feuding people/groups in public to get a raise of people in hopes of starting a shitstorm of drama and uncomfortable conflict, sometimes for personal gain but oftentimes just for the thrill of confrontation.
http://www.urbandictionary.com/define.php?term=stir+the+pot
Back to who discovered Hep C.....
Advocate and Asle are both correct.
Dr. Alter co-discovered the Australia antigen, a key to detecting hepatitis B virus. Later, Dr. Alter spearheaded a project at the Clinical Center that created a storehouse of blood samples used to uncover the causes and reduce the risk of transfusion-associated hepatitis. He was principal investigator on studies that identified non-A, non-B hepatitis, now called hepatitis C. His work was instrumental in providing the scientific basis for instituting blood donor screening programs that have decreased the incidence of transfusion-transmitted hepatitis to near zero.
http://clinicalcenter.nih.gov/about/SeniorStaff/harvey_alter.html
Advocate and Asle are both correct.
Dr. Alter co-discovered the Australia antigen, a key to detecting hepatitis B virus. Later, Dr. Alter spearheaded a project at the Clinical Center that created a storehouse of blood samples used to uncover the causes and reduce the risk of transfusion-associated hepatitis. He was principal investigator on studies that identified non-A, non-B hepatitis, now called hepatitis C. His work was instrumental in providing the scientific basis for instituting blood donor screening programs that have decreased the incidence of transfusion-transmitted hepatitis to near zero.
http://clinicalcenter.nih.gov/about/SeniorStaff/harvey_alter.html
What does viral load mean in relationship to the the bodies blood volume?
I forgot to pos
Woops. bad Me. I forgot to post my sources.
Who discovered Hepatitis C?
The steps towards discovering the hepatitis C virus began in the mid-1970s, when Harvey J. Alter and his research team showed that many hepatitis cases were not due to the already known hepatitis A and B viruses. However, it wasn’t until 1987 that the identification of the virus and diagnostic tests were developed. These findings were confirmed in 1988 and the virus was named in 1989. The team credited with the discovery are Michael Houghton, Qui-Lim Choo and George Kuo from the Chiron Corporation, who worked in collaboration with Dr. D.W. Bradley from Centers for Disease Control. Research into the disease is ongoing in the hope of finding more effective treatments.
wanttoknowit.com/who-discovered-hepatitis-c/
Also,
discovery.yukozimo.com › Diseases
Woops. bad Me. I forgot to post my sources.
Who discovered Hepatitis C?
The steps towards discovering the hepatitis C virus began in the mid-1970s, when Harvey J. Alter and his research team showed that many hepatitis cases were not due to the already known hepatitis A and B viruses. However, it wasn’t until 1987 that the identification of the virus and diagnostic tests were developed. These findings were confirmed in 1988 and the virus was named in 1989. The team credited with the discovery are Michael Houghton, Qui-Lim Choo and George Kuo from the Chiron Corporation, who worked in collaboration with Dr. D.W. Bradley from Centers for Disease Control. Research into the disease is ongoing in the hope of finding more effective treatments.
wanttoknowit.com/who-discovered-hepatitis-c/
Also,
discovery.yukozimo.com › Diseases
@Mike...my personal theory?? My personal theory is that a person with a consistently low viral load, like I had(below 800,000) may actually have more liver damage,then a person with a huge viral load (think millions; 6~60 million)
Why? Because my immune system was always fighting the virus, everyday it was busy fighting the virus, which leads to scar tissue.
If our immune systems dont attack the virus, but instead, ignores it,then a person can actually have no damage. I know this guy, he is older,maybe 65 yr or older. He is an alcoholic, and thinks he caught Hep C over 40 yrs ago,when he used to use. I convinced him to get a biopsy, and he came back as a stage zero!
I tried so hard to cure myself, with all those "alternative treatments" that I read onthe internet, which were designed to boost the immune system. There I was, Ms Health, quit drinking 20 yrs ago, when I was diagnosed, always exercised regularly, ate great, took the vitamins, and myplatelets started to slid below normal when I went into menopause. Meanwhile, my Hubs was the opposite, and his labs were always fine. Of course, since he never had a biopsy, who knows what stage he was, but his viral load was much higher then mine~ moot point since we both treated, but I found that ironic
Why? Because my immune system was always fighting the virus, everyday it was busy fighting the virus, which leads to scar tissue.
If our immune systems dont attack the virus, but instead, ignores it,then a person can actually have no damage. I know this guy, he is older,maybe 65 yr or older. He is an alcoholic, and thinks he caught Hep C over 40 yrs ago,when he used to use. I convinced him to get a biopsy, and he came back as a stage zero!
I tried so hard to cure myself, with all those "alternative treatments" that I read onthe internet, which were designed to boost the immune system. There I was, Ms Health, quit drinking 20 yrs ago, when I was diagnosed, always exercised regularly, ate great, took the vitamins, and myplatelets started to slid below normal when I went into menopause. Meanwhile, my Hubs was the opposite, and his labs were always fine. Of course, since he never had a biopsy, who knows what stage he was, but his viral load was much higher then mine~ moot point since we both treated, but I found that ironic
I forgot to ad, I am responding to mikesimons Q:
What is your theory on why viral load doesn't correlate with liver damage?
What is your theory on why viral load doesn't correlate with liver damage?
It's not a theory. The hepatitis C virus is what causes liver damage. Viral load doesn't indicate there is liver damage.
http://www.medicinenet.com/hepatitis_c/page3.htm
How does liver damage occur in hepatitis C infection?
The presence of HCV in the liver triggers the human immune system, which leads to inflammation. Over time (usually decades), prolonged inflammation may cause scarring. Extensive scarring in the liver is called cirrhosis. When the liver becomes cirrhotic, it fails to perform its normal functions, (liver failure), and this leads to serious complications and even death. Cirrhotic livers also are more prone to become cancerous.
In conclusion, it's not the Hep C virus causing the damage to the liver, it's our own personal immune systems~~~
How does liver damage occur in hepatitis C infection?
The presence of HCV in the liver triggers the human immune system, which leads to inflammation. Over time (usually decades), prolonged inflammation may cause scarring. Extensive scarring in the liver is called cirrhosis. When the liver becomes cirrhotic, it fails to perform its normal functions, (liver failure), and this leads to serious complications and even death. Cirrhotic livers also are more prone to become cancerous.
In conclusion, it's not the Hep C virus causing the damage to the liver, it's our own personal immune systems~~~
Mechanism of pathogenesis and fibrogenesis in Hepatitis C Virus (HCV) infection. El Khobar, K. E. (2011).
Abstract
"Hepatitis C virus (HCV) is one of the most common causes of chronic liver disease worldwide. HCV infection causes liver fibrosis, cirrhosis and HCC, although the precise mechanism by which it does this has not been clearly defined. HCV proteins have been linked to dysregulation of several signal transduction pathways like the JAK/STAT cytokine pathway, the MAPKinase and AKT-mTOR survival factor pathway, and apoptotic pathway, also with high oxidative stress and ER stress in host cells. These findings link viral proteins as the causative agents in liver inflammation and fibrosis and showing possible association between HCV proteins and liver fibrosis. In the work described here, using the rAdHCV viruses to co-infect hepatocytes, the effect of HCV proteins on MAPK/ERK, PI3K/AKT, JAK/STAT signaling pathways, apoptosis, cell survival and oxidative stress were determined.
HCV proteins are able to upregulate both the ERK and AKT-mTOR pathways. These upregulation might result in increase viral persistence by facilitating viral replication and also survival of the cell. HCV proteins also caused upregulation of pSTAT3 (Tyr705), SOCS3, SOCS1, and PIAS1 in the absence of an increase in pSTAT1 (Tyr701). This deregulation of JAK/STAT signaling pathways may provide one mechanism where by HCV promotes its own persistence, evades the host anti-viral cytokine response and recruits other cellular pathways that ultimately result in liver fibrosis and subsequent oncogenic transformation. HCV infection also resulted in increased hepatocyte apoptosis, as shown by reduction of cell viability and increased levels of apoptotic marker, the cleaved caspase 3 and PARP which was accompanied by reduction in cIAP1 level. This HCV effect on cIAP1 reduction has not been reported previously and thus may provide a more comprehensive view on the association between HCV infection and apoptosis cell death. In contrast, expression of HCV proteins was not associated with increased oxidative stress. The effect of HCV on dysregulation of cell signaling pathways may, in part, underlie the mechanism of HCV associated pathogenesis and liver fibrosis."
dtl.unimelb.edu.au/dtl_publish/research/36/283950.html
Abstract
"Hepatitis C virus (HCV) is one of the most common causes of chronic liver disease worldwide. HCV infection causes liver fibrosis, cirrhosis and HCC, although the precise mechanism by which it does this has not been clearly defined. HCV proteins have been linked to dysregulation of several signal transduction pathways like the JAK/STAT cytokine pathway, the MAPKinase and AKT-mTOR survival factor pathway, and apoptotic pathway, also with high oxidative stress and ER stress in host cells. These findings link viral proteins as the causative agents in liver inflammation and fibrosis and showing possible association between HCV proteins and liver fibrosis. In the work described here, using the rAdHCV viruses to co-infect hepatocytes, the effect of HCV proteins on MAPK/ERK, PI3K/AKT, JAK/STAT signaling pathways, apoptosis, cell survival and oxidative stress were determined.
HCV proteins are able to upregulate both the ERK and AKT-mTOR pathways. These upregulation might result in increase viral persistence by facilitating viral replication and also survival of the cell. HCV proteins also caused upregulation of pSTAT3 (Tyr705), SOCS3, SOCS1, and PIAS1 in the absence of an increase in pSTAT1 (Tyr701). This deregulation of JAK/STAT signaling pathways may provide one mechanism where by HCV promotes its own persistence, evades the host anti-viral cytokine response and recruits other cellular pathways that ultimately result in liver fibrosis and subsequent oncogenic transformation. HCV infection also resulted in increased hepatocyte apoptosis, as shown by reduction of cell viability and increased levels of apoptotic marker, the cleaved caspase 3 and PARP which was accompanied by reduction in cIAP1 level. This HCV effect on cIAP1 reduction has not been reported previously and thus may provide a more comprehensive view on the association between HCV infection and apoptosis cell death. In contrast, expression of HCV proteins was not associated with increased oxidative stress. The effect of HCV on dysregulation of cell signaling pathways may, in part, underlie the mechanism of HCV associated pathogenesis and liver fibrosis."
dtl.unimelb.edu.au/dtl_publish/research/36/283950.html
I would love to know what you think, I think it is very interesting.
When I was first diagnosed my vl was 6M, went up to 12M at one point. Then I got the cyroglobunemia and that was fighting the HCV as well.
Thank God that is now gone.
If you have time and feel like it I would like to know what the theory is.
Thank you Dee
p.s. I know I am not smarter than a 5th grader
When I was first diagnosed my vl was 6M, went up to 12M at one point. Then I got the cyroglobunemia and that was fighting the HCV as well.
Thank God that is now gone.
If you have time and feel like it I would like to know what the theory is.
Thank you Dee
p.s. I know I am not smarter than a 5th grader
The time that I noticed my viral load increased, was when I was pregnant, it jumped up to 6 million. So I had it tested a few months after that last (and final) pregnancy,and it went down to 60,000~
I think it may be easier to catch a cold when we are pregnant, because our immune systems rev down, so as not to see the embryo as a foreign body(invader), and thus, attack it.
The "viral load" question posed was a good one, becuz I always hear people saying, "my viral load is low, so I'm not worried yet" or "my viral load is at 30 million, surely I will die soon!", both are false beliefs! A person with a viral load lower then 700,000 may go Und a tiny bit faster, like maybe 4% faster, then a person in the millions.
I think it may be easier to catch a cold when we are pregnant, because our immune systems rev down, so as not to see the embryo as a foreign body(invader), and thus, attack it.
The "viral load" question posed was a good one, becuz I always hear people saying, "my viral load is low, so I'm not worried yet" or "my viral load is at 30 million, surely I will die soon!", both are false beliefs! A person with a viral load lower then 700,000 may go Und a tiny bit faster, like maybe 4% faster, then a person in the millions.
"A person with a viral load lower then 700,000 may go Und a tiny bit faster, like maybe 4% faster, then a person in the millions. "
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Please post the links to the documented studies that corroborate that statement and those numbers. Thanks.
-----------------------------------------------
Please post the links to the documented studies that corroborate that statement and those numbers. Thanks.
http://www.webmd.com/hepatitis/c-hcv-viral-load
What Is a High Viral Load and Low Viral Load?
Dr. Pearlman: Anything over 800,000 IU/mL is high. Anything under that is low viral load … Those with low viral load have a better chance of responding to treatment.
What Is a High Viral Load and Low Viral Load?
Dr. Pearlman: Anything over 800,000 IU/mL is high. Anything under that is low viral load … Those with low viral load have a better chance of responding to treatment.
Yes, we know that the viral load can affect the response to treatment. I was wondering where you came up with the actual numbers, especially, where did you find the 4%.
http://www.healio.com/hepatology/chronic-hepatitis/news/online/%7BDC16145A-480E-48A6-BD9E-F2BCD654494F%7D/IL-28B-polymorphism-linked-with-boceprevir-interferon-response-in-HCV
Among previously untreated patients, sustained virologic response (SVR) following triple therapy was associated with the following baseline factors: Low viral load (OR=11.6, 1.5-87.8 for 400,000 IU/mL or less), IL-28B genotype (OR=2.6, 1.3-5.1 for CC compared with TT; OR=2.1, 1.2-3.7 for CC compared with CT), lack of cirrhosis (OR=4.3, 1.6-11.9), HCV genotype 1b (OR=2.0, 1.2-3.4) and non-black race (OR=2.0, 1.1-3.7) (95% CI for all). SVR was only associated with prior relapse compared with nonresponse among previous treatment failures at baseline (OR=2.6; 95% CI, 1.3-5.0).
When treatment response after 4 weeks was analyzed, IL-28B genotype was no longer predictive of response among untreated patients, while an HCV RNA decrease of 1 log10 or more was (OR=8.2, 4.5-15.0). Lower baseline RNA (OR=8.4, 1.0-68.6), no cirrhosis (OR=3.5, 1.1-11.3), BMI of 30 or less (OR=2.5, 1.4-4.2) and HCV genotype 1b (OR=2.1, 1.2-3.6) also were predictive factors. Among previous treatment failures, HCV-RNA decline (OR=2.7, 1.2-5.7) and prior relapse (OR=2.2, 1.1-4.4) were the only predictive factors (95% CI for all).
Among previously untreated patients, sustained virologic response (SVR) following triple therapy was associated with the following baseline factors: Low viral load (OR=11.6, 1.5-87.8 for 400,000 IU/mL or less), IL-28B genotype (OR=2.6, 1.3-5.1 for CC compared with TT; OR=2.1, 1.2-3.7 for CC compared with CT), lack of cirrhosis (OR=4.3, 1.6-11.9), HCV genotype 1b (OR=2.0, 1.2-3.4) and non-black race (OR=2.0, 1.1-3.7) (95% CI for all). SVR was only associated with prior relapse compared with nonresponse among previous treatment failures at baseline (OR=2.6; 95% CI, 1.3-5.0).
When treatment response after 4 weeks was analyzed, IL-28B genotype was no longer predictive of response among untreated patients, while an HCV RNA decrease of 1 log10 or more was (OR=8.2, 4.5-15.0). Lower baseline RNA (OR=8.4, 1.0-68.6), no cirrhosis (OR=3.5, 1.1-11.3), BMI of 30 or less (OR=2.5, 1.4-4.2) and HCV genotype 1b (OR=2.1, 1.2-3.6) also were predictive factors. Among previous treatment failures, HCV-RNA decline (OR=2.7, 1.2-5.7) and prior relapse (OR=2.2, 1.1-4.4) were the only predictive factors (95% CI for all).
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