Re: Extrahepatic replication of hepatitis C virus

[Guest guest]

Hey Liz, can you please tell me where this excerpt came from? I'd be interested to know who wrote this, and be able to find some more of the details as to how they came to these conclusions. Thanks, Chriselizabethnv1 <elizabethnv1@...> wrote: Extrahepatic replication of hepatitis C virus HCV is not strictly hepatotropic, as it can also replicate in peripheral blood mononuclear cells (PBMC). Several groups of researchers have detected HCV-RNA negative strand, which is a viral replicative intermediate, within PBMC, and it was also demonstrated that viral genomic sequences present in PBMC are often different from those found in serum and the liver [15-18]. HCV RNA has also been detected in PBMC and hematopoietic progenitor cells by in situ hybridization [19].

Furthermore, the same minor quasispecies variants of strain H77, which were selected in lymphoblastoid cells in vitro, were found to be replicating in vivo in PBMC of chimpanzees inoculated with the same parent strain [20]. Within the population of PBMC, the cells harboring replicating virus have been identified primary as monocytes/macrophages and B cells, although T cells can also be infected, particularly in long-lasting infection [21-23]. The above cells may manifest functional changes in chronic hepatitis C patients, although it is unclear whether this is directly caused by HCV infection. B-cell dysfunction is thus characterized by low-titer and delayed onset antibody response and an increased frequency of naive B cells [24,25], whereas monocyte-derived dendritic cells demonstrate impaired allostimulatory function [21,26]. It was recently shown that primary human macrophages can be infected by HCV in vitro, as evidenced by

the detection of viral replicative forms, an occasional evolution of viral sequences during cell culture, and positive staining of infected cells for viral non-structural protein 3 (NS3) [27,28]. Moreover, HCV infection of macrophages in vitro may induce TNF-?and IL-8 [29].It's a pleasure having you join in our conversations. We hope you have found the support you need with us. If you are using email for your posts, for easy access to our group, just click the link-- Hepatitis C/Happy Posting

[Guest guest]

http://vir.sgmjournals.org/cgi/content/full/81/7/1631

Re: Extrahepatic replication of hepatitis C virus

Hey Liz, can you please tell me where this excerpt came from? I'd be interested to know who wrote this, and be able to find some more of the details as to how they came to these conclusions.

Thanks,

Chriselizabethnv1 <elizabethnv1@...> wrote:

Extrahepatic replication of hepatitis C virus HCV is not strictly hepatotropic, as it can also replicate in peripheral blood mononuclear cells (PBMC). Several groups of researchers have detected HCV-RNA negative strand, which is a viral replicative intermediate, within PBMC, and it was also demonstrated that viral genomic sequences present in PBMC are often different from those found in serum and the liver [15-18]. HCV RNA has also been detected in PBMC and hematopoietic progenitor cells by in situ hybridization [19]. Furthermore, the same minor quasispecies variants of strain H77, which were selected in lymphoblastoid cells in vitro, were found to be replicating in vivo in PBMC of chimpanzees inoculated with the same parent strain [20]. Within the population of PBMC, the cells harboring replicating virus have been identified primary as monocytes/macrophages and B cells, although T cells can also be infected, particularly in long-lasting infection [21-23]. The above cells may manifest functional changes in chronic hepatitis C patients, although it is unclear whether this is directly caused by HCV infection. B-cell dysfunction is thus characterized by low-titer and delayed onset antibody response and an increased frequency of naive B cells [24,25], whereas monocyte-derived dendritic cells demonstrate impaired allostimulatory function [21,26]. It was recently shown that primary human macrophages can be infected by HCV in vitro, as evidenced by the detection of viral replicative forms, an occasional evolution of viral sequences during cell culture, and positive staining of infected cells for viral non-structural protein 3 (NS3) [27,28]. Moreover, HCV infection of macrophages in vitro may induce TNF-?and IL-8 [29].It's a pleasure having you join in our conversations. We hope you have found the support you need with us. If you are using email for your posts, for easy access to our group, just click the link-- Hepatitis C/Happy Posting

[Guest guest]

I also found studies backing this information at the pubmed site , and

the National Institute for Health .

[Guest guest]

Thank you doll! Now could you tell me what it says? LOL I'll keep this handy for the next time I can't get to sleep. Seriously, thank you!elizabethnv1 <elizabethnv1@...> wrote: http://vir.sgmjournals.org/cgi/content/full/81/7/1631 Re: Extrahepatic replication of hepatitis C virus Hey Liz, can you please tell me where this excerpt came from? I'd be interested to know who wrote this, and be able to find some more of the details as to how they came to these conclusions. Thanks, Chriselizabethnv1 <elizabethnv1@...> wrote: Extrahepatic replication of hepatitis C virus HCV is not strictly hepatotropic, as it can also replicate in peripheral blood mononuclear

cells (PBMC). Several groups of researchers have detected HCV-RNA negative strand, which is a viral replicative intermediate, within PBMC, and it was also demonstrated that viral genomic sequences present in PBMC are often different from those found in serum and the liver [15-18]. HCV RNA has also been detected in PBMC and hematopoietic progenitor cells by in situ hybridization [19]. Furthermore, the same minor quasispecies variants of strain H77, which were selected in lymphoblastoid cells in vitro, were found to be replicating in vivo in PBMC of chimpanzees inoculated with the same parent strain [20]. Within the population of PBMC, the cells harboring replicating virus have been identified primary as monocytes/macrophages and B cells, although T cells can also be infected, particularly in long-lasting infection [21-23]. The above cells may manifest functional changes in chronic hepatitis C patients, although it is unclear

whether this is directly caused by HCV infection. B-cell dysfunction is thus characterized by low-titer and delayed onset antibody response and an increased frequency of naive B cells [24,25], whereas monocyte-derived dendritic cells demonstrate impaired allostimulatory function [21,26]. It was recently shown that primary human macrophages can be infected by HCV in vitro, as evidenced by the detection of viral replicative forms, an occasional evolution of viral sequences during cell culture, and positive staining of infected cells for viral non-structural protein 3 (NS3) [27,28]. Moreover, HCV infection of macrophages in vitro may induce TNF-?and IL-8 [29].It's a pleasure having you join in our conversations. We hope you have found the support you need with us. If you are using email for your posts, for easy access to our group, just click the link--

Hepatitis C/Happy Posting

[Guest guest]

Thank you doll! Now could you tell me what it says? LOL I'll keep this handy for the next time I can't get to sleep. Seriously, thank you!elizabethnv1 <elizabethnv1@...> wrote: http://vir.sgmjournals.org/cgi/content/full/81/7/1631 Re: Extrahepatic replication of hepatitis C virus Hey Liz, can you please tell me where this excerpt came from? I'd be interested to know who wrote this, and be able to find some more of the details as to how they came to these conclusions. Thanks, Chriselizabethnv1 <elizabethnv1@...> wrote: Extrahepatic replication of hepatitis C virus HCV is not strictly hepatotropic, as it can also replicate in peripheral blood mononuclear

cells (PBMC). Several groups of researchers have detected HCV-RNA negative strand, which is a viral replicative intermediate, within PBMC, and it was also demonstrated that viral genomic sequences present in PBMC are often different from those found in serum and the liver [15-18]. HCV RNA has also been detected in PBMC and hematopoietic progenitor cells by in situ hybridization [19]. Furthermore, the same minor quasispecies variants of strain H77, which were selected in lymphoblastoid cells in vitro, were found to be replicating in vivo in PBMC of chimpanzees inoculated with the same parent strain [20]. Within the population of PBMC, the cells harboring replicating virus have been identified primary as monocytes/macrophages and B cells, although T cells can also be infected, particularly in long-lasting infection [21-23]. The above cells may manifest functional changes in chronic hepatitis C patients, although it is unclear

whether this is directly caused by HCV infection. B-cell dysfunction is thus characterized by low-titer and delayed onset antibody response and an increased frequency of naive B cells [24,25], whereas monocyte-derived dendritic cells demonstrate impaired allostimulatory function [21,26]. It was recently shown that primary human macrophages can be infected by HCV in vitro, as evidenced by the detection of viral replicative forms, an occasional evolution of viral sequences during cell culture, and positive staining of infected cells for viral non-structural protein 3 (NS3) [27,28]. Moreover, HCV infection of macrophages in vitro may induce TNF-?and IL-8 [29].It's a pleasure having you join in our conversations. We hope you have found the support you need with us. If you are using email for your posts, for easy access to our group, just click the link--

Hepatitis C/Happy Posting