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HCV Infection May Predict Coronary Artery Disease
NATIONAL HARBOR, MD. – Coronary artery disease was significantly more prevalent in patients with hepatitis C virus infection, compared with control subjects, based on a retrospective review. The findings were presented at the annual meeting of the American College of Gastroenterology.
"An association of coronary artery disease [CAD] with hepatitis C has been suggested, but definitive data are still lacking," said Dr. Sanjaya Satapathy, who conducted the study while at Long Island Jewish Medical Center in New Hyde Park, N.Y.
To estimate the prevalence of CAD in hepatitis C patients, Dr. Satapathy and his colleagues reviewed data from 934 individuals with hepatitis C infection who were seen at a single center between May 2002 and December 2008. Of these patients, 63 had undergone coronary angiography. The investigators compared their data with data from 63 matched controls without hepatitis C.
Overall severity of CAD according to the combined Reardon severity score was significantly greater in the hepatitis C virus (HCV) group than in the controls (6.3 vs. 2.6, respectively), suggesting that being HCV-positive increases the severity of, or risk for, CAD, Dr. Satapathy said.
The researchers defined CAD in two different ways for their analysis. CAD defined as stenosis greater than 50% was found in 44 of the HCV cases (70%) compared with 30 controls (48%). CAD defined as stenosis greater than 75% was found in 42 patients with hepatitis C (67%) compared with 29 controls (46%).
In addition, the prevalence of multivessel coronary artery disease was significantly higher in the HCV patients compared with the controls (57% vs. 16%, respectively). The prevalence of single-vessel involvement was greater in the control group.
"HCV seropositive status is a strong predictor for CAD," Dr. Satapathy said. However, "HCV patients are more likely to remain undertreated with antiplatelet and lipid-lowering agents," he noted.
The study was limited by the retrospective design and small sample size, said Dr. Satapathy. However, the findings suggest that CAD is significantly more common and severe in HCV-positive patients, and this should be considered by clinicians treating these patients, he said.
http://tinyurl.com/cg4ca3n
"An association of coronary artery disease [CAD] with hepatitis C has been suggested, but definitive data are still lacking," said Dr. Sanjaya Satapathy, who conducted the study while at Long Island Jewish Medical Center in New Hyde Park, N.Y.
To estimate the prevalence of CAD in hepatitis C patients, Dr. Satapathy and his colleagues reviewed data from 934 individuals with hepatitis C infection who were seen at a single center between May 2002 and December 2008. Of these patients, 63 had undergone coronary angiography. The investigators compared their data with data from 63 matched controls without hepatitis C.
Overall severity of CAD according to the combined Reardon severity score was significantly greater in the hepatitis C virus (HCV) group than in the controls (6.3 vs. 2.6, respectively), suggesting that being HCV-positive increases the severity of, or risk for, CAD, Dr. Satapathy said.
The researchers defined CAD in two different ways for their analysis. CAD defined as stenosis greater than 50% was found in 44 of the HCV cases (70%) compared with 30 controls (48%). CAD defined as stenosis greater than 75% was found in 42 patients with hepatitis C (67%) compared with 29 controls (46%).
In addition, the prevalence of multivessel coronary artery disease was significantly higher in the HCV patients compared with the controls (57% vs. 16%, respectively). The prevalence of single-vessel involvement was greater in the control group.
"HCV seropositive status is a strong predictor for CAD," Dr. Satapathy said. However, "HCV patients are more likely to remain undertreated with antiplatelet and lipid-lowering agents," he noted.
The study was limited by the retrospective design and small sample size, said Dr. Satapathy. However, the findings suggest that CAD is significantly more common and severe in HCV-positive patients, and this should be considered by clinicians treating these patients, he said.
http://tinyurl.com/cg4ca3n
So I guess the question then becomes: What happens after we become SVR? Do we resolve the brain endothelial cell and CNS infection, as we do in the liver, or does the brain remain infected? Additionally, even if the brain infection is resolved, what effect might there be on future function and health? In other words, does the brain recover after SVR? Thanks for the study Mike.
DoubleDose
DoubleDose
Gastroenterology. 2011 Nov 30.
Hepatitis C Virus Infects the Endothelial Cells of the Blood-Brain Barrier.
Hepatitis C Research Group, Institute for Biomedical Research, University of Birmingham, Birmingham, UK.
Hepatitis C Virus (HCV) infection leads to progressive liver disease and is associated with a variety of extrahepatic syndromes, including central nervous system (CNS) abnormalities. However, it is unclear whether such cognitive abnormalities are a function of systemic disease, impaired hepatic function, or virus infection of the CNS.
METHODS:
We measured levels of HCV RNA and expression of the viral entry receptor in brain tissue samples from 10 infected individuals (and 3 uninfected individuals, as controls) and human brain microvascular endothelial cells using quantitative PCR and immunochemical and confocal imaging analyses. HCV pseudoparticles and cell culture-derived HCV were used to study the ability of endothelial cells to support viral entry and replication.
RESULTS:
Using quantitative PCR we detected HCV RNA in brain tissue of infected individuals at significantly lower levels than in liver samples. Brain microvascular endothelia and brain endothelial cells expressed all of the recognized HCV entry receptors. Two independently derived brain endothelial cell lines, hCMEC/D3 and HBMEC, supported HCV entry and replication. These processes were inhibited by antibodies against the entry factors CD81, scavenger receptor-BI, and Claudin-1; by interferon; and by reagents that inhibit NS3 protease and NS5B polymerase. HCV infection promotes endothelial permeability and cellular apoptosis.
CONCLUSIONS:
Human brain endothelial cells express functional receptors that support HCV entry and replication. Virus infection of the CNS might lead to HCV-associated neuropathologies.
Hepatitis C Virus Infects the Endothelial Cells of the Blood-Brain Barrier.
Hepatitis C Research Group, Institute for Biomedical Research, University of Birmingham, Birmingham, UK.
Hepatitis C Virus (HCV) infection leads to progressive liver disease and is associated with a variety of extrahepatic syndromes, including central nervous system (CNS) abnormalities. However, it is unclear whether such cognitive abnormalities are a function of systemic disease, impaired hepatic function, or virus infection of the CNS.
METHODS:
We measured levels of HCV RNA and expression of the viral entry receptor in brain tissue samples from 10 infected individuals (and 3 uninfected individuals, as controls) and human brain microvascular endothelial cells using quantitative PCR and immunochemical and confocal imaging analyses. HCV pseudoparticles and cell culture-derived HCV were used to study the ability of endothelial cells to support viral entry and replication.
RESULTS:
Using quantitative PCR we detected HCV RNA in brain tissue of infected individuals at significantly lower levels than in liver samples. Brain microvascular endothelia and brain endothelial cells expressed all of the recognized HCV entry receptors. Two independently derived brain endothelial cell lines, hCMEC/D3 and HBMEC, supported HCV entry and replication. These processes were inhibited by antibodies against the entry factors CD81, scavenger receptor-BI, and Claudin-1; by interferon; and by reagents that inhibit NS3 protease and NS5B polymerase. HCV infection promotes endothelial permeability and cellular apoptosis.
CONCLUSIONS:
Human brain endothelial cells express functional receptors that support HCV entry and replication. Virus infection of the CNS might lead to HCV-associated neuropathologies.
Thanks for the abstract Mike, and reminding us that there are more ramifications to having the virus than just liver failure. I think it is simplistic for people to categorize HCV as a "liver virus" because that more or less connotes liver-only. Yes the virus infects and attacks the liver, but as we have been finding, also attacks joints and connective tissue, the brain, blood vessels, salivary glands and cells, and possibly the central nervous system, etc. I think of HCV as a system-wide virus that has a particularly nasty effect on the liver in many cases. I think they have shown a relationship with HCV and strokes, and cerebral hemmorhages, often fatal. The woman that was CEO of the Body Shop had HCV, and died of cerebral hemmorhage. Its a nasty virus, and its why we do the treatment.
Now if we can only figure out how to FEEL better after we have beaten the virus, then we are home free!
DoubleDose
Now if we can only figure out how to FEEL better after we have beaten the virus, then we are home free!
DoubleDose
Hepatology. 2011 Nov 26.
Hepatitis C and non-Hodgkin lymphoma:
Department of Medicine, Memorial Sloan-Kettering Cancer Center (MSKCC), 1275 York Avenue, New York, NY 10065, USA.
Abstract
Hepatitis C virus (HCV) is a commonly transmitted infection that has both hepatic and extrahepatic repercussions. These range from the inflammatory to the oncologic with an undisputed link to hepatitis, liver cirrhosis and hepatocellular carcinoma. Its role in the development of B-cell non-Hodgkin lymphoma (B-NHL) is becoming better understood, and with it, there are opportunities for research, therapy, and even prevention. CONCLUSION: Research in the field has progressed significantly over the last decade with the number of patients diagnosed with HCV and B-NHL rising incrementally. It is therefore becoming crucial to fully understand the pathobiologic link of HCV in B-cell lymphomagenesis and its optimal management in the oncologic setting. (HEPATOLOGY 2011.).
Copyright © 2011 American Association for the Study of Liver Diseases.
http://www.ncbi.nlm.nih.gov/pubmed/22120959
Mike
Hepatitis C and non-Hodgkin lymphoma:
Department of Medicine, Memorial Sloan-Kettering Cancer Center (MSKCC), 1275 York Avenue, New York, NY 10065, USA.
Abstract
Hepatitis C virus (HCV) is a commonly transmitted infection that has both hepatic and extrahepatic repercussions. These range from the inflammatory to the oncologic with an undisputed link to hepatitis, liver cirrhosis and hepatocellular carcinoma. Its role in the development of B-cell non-Hodgkin lymphoma (B-NHL) is becoming better understood, and with it, there are opportunities for research, therapy, and even prevention. CONCLUSION: Research in the field has progressed significantly over the last decade with the number of patients diagnosed with HCV and B-NHL rising incrementally. It is therefore becoming crucial to fully understand the pathobiologic link of HCV in B-cell lymphomagenesis and its optimal management in the oncologic setting. (HEPATOLOGY 2011.).
Copyright © 2011 American Association for the Study of Liver Diseases.
http://www.ncbi.nlm.nih.gov/pubmed/22120959
Mike
"When I see all of the threads and posts about the side effects of treatment I immediately think of the side effects of having HCV. It's not just about the liver...... as so many people seem to believe."
Absolutely true. Many people who go thru tx have no idea how or what else has been affected due to their HepC dx. Not that it's a good example but Natalie Cole comes to mind. Just think she started tx and was 4 or 5 months into it and blamo, her kidneys failed her to the point that she needed a kidney transplant, and was on dialysis. Of course everytime I read her story it's different. Maybe the story is right in her book version, but I won't buy it b/c she has done nothing for the HepC struggle except give out bad information.
http://www.webmd.com/hepatitis/news/20090521/natalie-cole-recovering-after-kidney-transplant
Absolutely true. Many people who go thru tx have no idea how or what else has been affected due to their HepC dx. Not that it's a good example but Natalie Cole comes to mind. Just think she started tx and was 4 or 5 months into it and blamo, her kidneys failed her to the point that she needed a kidney transplant, and was on dialysis. Of course everytime I read her story it's different. Maybe the story is right in her book version, but I won't buy it b/c she has done nothing for the HepC struggle except give out bad information.
http://www.webmd.com/hepatitis/news/20090521/natalie-cole-recovering-after-kidney-transplant
Hi; I don't know about hep c and cad but I am sure the infection effects many parts of the body. I began Incivek in August within a week joint problems that had developed over the years melted away. That is when I first felt this treatment was different. I have been undetectable since week 4. The side effects have been unbelievable but if I achieve SVR it will be well worth all of it.
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TITLE: "Hepatitis C virus enters human peripheral neuroblastoma cells - evidence for extra-hepatic cells sustaining hepatitis C virus penetration. "
Author: Burgel, B.;Friesland, M.;Koch, A. ;Manns, M. P.;Wedemeyer, H.;Weissenborn, K.;Schulz-Schaeffer, W. J.;Pietschmann, T.;Steinmann,l;
Ciesek, S., et al.
Citation: Journal of Viral Hepatitis Aug2011, Vol. 18 Issue 8, p562-570
Year: 2011
Abstract: Summary. Patients with chronic hepatitis C virus (HCV) infection show an increased incidence of nervous system disorders such as chronic fatigue syndrome, depression and cognitive dysfunction. It is unclear whether this is because of HCV replication in the brain and in peripheral neuronal cells or to more indirect effects of HCV infection on the central or peripheral nervous system. The aim of this study was to investigate whether cells originating from these tissues are permissive for HCV cell entry, RNA replication and virus assembly. Among eight cell lines analysed, the human peripheral neuroblastoma cell line SKNMC expressed all HCV entry factors and was efficiently infected with HCV pseudoparticles (HCVpp) independent of the HCV genotype. All remaining cell types including human neuroblastoma and glioblastoma cell lines and microglial cells lacked expression of at least one host factor essential for HCV entry. When transfected with HCV luciferase reporter virus RNA, inoculated with HCV reporter viruses or challenged with high-titre cell culture-derived HCV, none of these cells supported detectable HCV RNA replication. Thus, in conclusion, this comprehensive screening did not reveal evidence directly strengthening the notion that HCV enters and replicates in the central nervous system. However, productive viral entry into the peripheral neuroblastoma cell line SKNMC indicates that HCV may penetrate into certain nonhepatic cell types which may serve as viral reservoirs and could modulate viral pathogenesis. Analysed, the human peripheral neuroblastoma cell line SKNMC expressed all HCV entry factors and was efficiently infected with HCV pseudoparticles (HCVpp) independent of the HCV genotype. All remaining cell types including human neuroblastoma and glioblastoma cell lines and microglial cells lacked expression of at least one host factor essential for HCV entry.
ISSN: 13520504
TITLE: "Molecular and Bioinformatic Evidence of Hepatitis C Virus Evolution in Brain."
Author: Fishman, Sarah L.;Murray, Jacinta M.;Eng, Francis J.;Walewski,Jose L.; Morgello, Susan;Branch, Andrea D. et al.
Citation: Journal of Infectious Diseases 2/15/2008, Vol. 197 Issue 4, p597-607
Year: 2008
Abstract: Background. Neurocognitive deficits in patients with hepatitis C virus (HCV) infection prompted a search tor HCV in brain. Results. HCV was present in the brains of 7 (54%) of 13 patients with viremia, as determined by 5' UTR and E1 (envelope 1) gene analysis. Brain HCV RNA consensus sequences differed from those in plasma and liver in 4 (57%) of 7 patients. The quality of HCV RNA from postmortem brain and liver was assessed and demonstrated to be suitable for sequence analysis. Quasispecies analysis revealed that several mutations present in clones from >1 brain region were absent in clones from liver and plasma. Brain-specific mutations defined several families of related sequences. The patterns of brain-specific mutations in these families were consistent with the evolution of HCV RNA from a common ancestor. Single-nucleotide-polymorphism analysis confirmed that a prominent brain-specific mutation constituted ̃10% of HCV RNA in cerebellum and medulla but that this mutation was undetectable in the liver and plasma of the same patient. Conclusions. This study introduces novel methods for assessing RNA from postmortem samples. It increases the reported cases of HCV in the brain, provides the first E1 sequences from the brain, and contributes to the growing evidence that HCV replicates and evolves within the brain.