Abstract:The mechanisms of viral persistence are complex and include infection of the lymphoid cells. In the case of hepatitis B virus, early observations have suggested that HBV may infect peripheral blood mononuclear cells (PBMC). In animal models studies in chronic hepatitis B patients have further confirmed that viral DNA replicative intermediates, as well as viral transcripts and proteins, can be detected in PBMC under certain conditions. The consequences of this lymphotropism are not fully understood, but it seem… Show more
“…Our data support the notion that HCV infects not only hepatic cells but also PBMCs, an extrahepatic target for HCV infection [38,39]. Both HCV positive-strand and negative-strand RNA were present in PBMCs [40].…”
We investigated the ability of CD8+ T cells to inhibit hepatitis C virus (HCV) replication in peripheral blood mononuclear cells (PBMCs). PBMCs isolated from 11 of 20 HCV-infected subjects had no detectable HCV RNA. Removal of CD8+ T cells from these PBMCs resulted in detection of HCV RNA, and depletion of CD8+ T cells from PBMCs that had detectable HCV RNA amplified HCV replication. Reconstitution of CD8- PBMCs with autologous CD8+ T cells led to inhibition of HCV replication. Interferon-gamma produced by CD8+ T cells was partially responsible for CD8+ T cell-mediated noncytotoxic anti-HCV activity in PBMCs. This noncytotoxic anti-HCV activity was confirmed in HCV replicon cells. Supernatants from CD8+ T cell cultures inhibited HCV RNA expression in the replicon cells. These findings may have important implications for the immunopathogenesis of HCV in both immune and hepatic cells and are relevant to the development of host innate immunity-based anti-HCV interventions.
“…Our data support the notion that HCV infects not only hepatic cells but also PBMCs, an extrahepatic target for HCV infection [38,39]. Both HCV positive-strand and negative-strand RNA were present in PBMCs [40].…”
We investigated the ability of CD8+ T cells to inhibit hepatitis C virus (HCV) replication in peripheral blood mononuclear cells (PBMCs). PBMCs isolated from 11 of 20 HCV-infected subjects had no detectable HCV RNA. Removal of CD8+ T cells from these PBMCs resulted in detection of HCV RNA, and depletion of CD8+ T cells from PBMCs that had detectable HCV RNA amplified HCV replication. Reconstitution of CD8- PBMCs with autologous CD8+ T cells led to inhibition of HCV replication. Interferon-gamma produced by CD8+ T cells was partially responsible for CD8+ T cell-mediated noncytotoxic anti-HCV activity in PBMCs. This noncytotoxic anti-HCV activity was confirmed in HCV replicon cells. Supernatants from CD8+ T cell cultures inhibited HCV RNA expression in the replicon cells. These findings may have important implications for the immunopathogenesis of HCV in both immune and hepatic cells and are relevant to the development of host innate immunity-based anti-HCV interventions.
“…23 Likewise, the lymphotropism for HBV infection cannot be overlooked. 28 As a result, a detectable lymph node should suggest not only chronic HCV infection but also chronic HBV infection. On further analysis, we found a high positive predictive rate and high specificity for both viral infections when the node was wider than 5 mm.…”
Lymph nodes in the hepatoduodenal ligament, especially those wider than 5 mm, suggest chronic HBV or HCV infection instead of only chronic hepatitis, especially in an endemic area such as Taiwan.
“…It has been reported that HCV is able to infect not only hepatocytes but also PBMCs (37,54). Immediately after discovery of the virus in 1989, different groups showed that HCV replicates in lymphoid cells by infecting macrophages and B and T lymphocytes (8,24,58).…”
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