HEV is the most causative agent of acute viral hepatitis globally. HEV causes acute, chronic, and extrahepatic manifestations. Chronic HEV infection develops in immunocompromised patients such as organ transplant patients, HIV-infected patients, and leukemic patients. The source of chronic HEV infection is not known. Also, the source of extrahepatic manifestations associated with HEV infection is still unclear. Hepatotropic viruses such as HCV and HBV replicate in peripheral blood mononuclear cells (PBMCs) and these cells become a source of chronic reactivation of the infections in allograft organ transplant patients. Herein, we reported that PBMCs and bone marrow-derived macrophages (BMDMs), isolated from healthy donors (n= 3), are susceptible to HEV in vitro. Human monocytes (HMOs), human macrophages (HMACs), and human BMDMs were challenged with HEV-1 and HEV-3 viruses. HEV RNA was measured by qPCR, the marker of the intermediate replicative form (ds-RNA) was assessed by immunofluorescence, and HEV capsid protein was assessed by flow cytometry and ELISA. HEV infection was successfully established in primary HMOs, HMACs, and human BMDMs, but not in the corresponding cells of murine origin. Intermediate replicative form (ds RNA) was detected in HMOs and HMACs challenged with HEV. The HEV load was increased over time, and the HEV capsid protein was detected intracellularly in the HEV-infected cells and accumulated extracellularly over time, confirming that HEV completes the life cycle inside these cells. The HEV particles produced from the infected BMDMs were infectious to naive HMOs …

HEV is the most causative agent of acute viral hepatitis globally. HEV causes acute, chronic, and extrahepatic manifestations. Chronic HEV infection develops in immunocompromised patients such as organ transplant patients, HIV-infected patients, and leukemic patients. The source of chronic HEV infection is not known. Also, the source of extrahepatic manifestations associated with HEV infection is still unclear. Hepatotropic viruses such as HCV and HBV replicate in peripheral blood mononuclear cells (PBMCs) and these cells become a source of chronic reactivation of the infections in allograft organ transplant patients. Herein, we reported that PBMCs and bone marrow-derived macrophages (BMDMs), isolated from healthy donors (n= 3), are susceptible to HEV in vitro. Human monocytes (HMOs), human macrophages (HMACs), and human BMDMs were challenged with HEV-1 and HEV-3 viruses. HEV RNA was measured by qPCR, the marker of the intermediate replicative form (ds-RNA) was assessed by immunofluorescence, and HEV capsid protein was assessed by flow cytometry and ELISA. HEV infection was successfully established in primary HMOs, HMACs, and human BMDMs, but not in the corresponding cells of murine origin. Intermediate replicative form (ds RNA) was detected in HMOs and HMACs challenged with HEV. The HEV load was increased over time, and the HEV capsid protein was detected intracellularly in the HEV-infected cells and accumulated extracellularly over time, confirming that HEV completes the life cycle inside these cells. The HEV particles produced from the infected BMDMs were infectious to naive HMOs …

HEV is the most causative agent of acute viral hepatitis globally. HEV causes acute, chronic, and extrahepatic manifestations. Chronic HEV infection develops in immunocompromised patients such as organ transplant patients, HIV-infected patients, and leukemic patients. The source of chronic HEV infection is not known. Also, the source of extrahepatic manifestations associated with HEV infection is still unclear. Hepatotropic viruses such as HCV and HBV replicate in peripheral blood mononuclear cells (PBMCs) and these cells become a source of chronic reactivation of the infections in allograft organ transplant patients. Herein, we reported that PBMCs and bone marrow-derived macrophages (BMDMs), isolated from healthy donors (n= 3), are susceptible to HEV in vitro. Human monocytes (HMOs), human macrophages (HMACs), and human BMDMs were challenged with HEV-1 and HEV-3 viruses. HEV RNA was measured by qPCR, the marker of the intermediate replicative form (ds-RNA) was assessed by immunofluorescence, and HEV capsid protein was assessed by flow cytometry and ELISA. HEV infection was successfully established in primary HMOs, HMACs, and human BMDMs, but not in the corresponding cells of murine origin. Intermediate replicative form (ds RNA) was detected in HMOs and HMACs challenged with HEV. The HEV load was increased over time, and the HEV capsid protein was detected intracellularly in the HEV-infected cells and accumulated extracellularly over time, confirming that HEV completes the life cycle inside these cells. The HEV particles produced from the infected BMDMs were infectious to naive HMOs …

HEV is the most causative agent of acute viral hepatitis globally. HEV causes acute, chronic, and extrahepatic manifestations. Chronic HEV infection develops in immunocompromised patients such as organ transplant patients, HIV-infected patients, and leukemic patients. The source of chronic HEV infection is not known. Also, the source of extrahepatic manifestations associated with HEV infection is still unclear. Hepatotropic viruses such as HCV and HBV replicate in peripheral blood mononuclear cells (PBMCs) and these cells become a source of chronic reactivation of the infections in allograft organ transplant patients. Herein, we reported that PBMCs and bone marrow-derived macrophages (BMDMs), isolated from healthy donors (n= 3), are susceptible to HEV in vitro. Human monocytes (HMOs), human macrophages (HMACs), and human BMDMs were challenged with HEV-1 and HEV-3 viruses. HEV RNA was measured by qPCR, the marker of the intermediate replicative form (ds-RNA) was assessed by immunofluorescence, and HEV capsid protein was assessed by flow cytometry and ELISA. HEV infection was successfully established in primary HMOs, HMACs, and human BMDMs, but not in the corresponding cells of murine origin. Intermediate replicative form (ds RNA) was detected in HMOs and HMACs challenged with HEV. The HEV load was increased over time, and the HEV capsid protein was detected intracellularly in the HEV-infected cells and accumulated extracellularly over time, confirming that HEV completes the life cycle inside these cells. The HEV particles produced from the infected BMDMs were infectious to naive HMOs …

Description Cyclooxygenase-2 (COX-2) plays an important role in carcinogenesis, which catalyzes the conversion of arachidonic acid into prostaglandins. P53 is a tumor suppressor gene that contributes to apoptosis and cell cycle control. There is functional interaction between p53 and COX-2, which lead to abrogation of apoptosis and progression of malignancy. To assess the relationship between COX-2, p53 expression and the clinicopathololgic features in SLL and DLBCL. We immunohistochemically examined the expression of COX-2 and p53 in non-neoplastic lymphoid cells, lymph nodal low-grade (50 cases of SLL), intermediate and high-grade lymphomas (100 cases of DLBCL) and their corresponding bone marrow specimens. The expression of COX-2 and p53 was absent in the in non-neoplastic lymphoid cells. In contrast, their expression values increased progressively with the advancing grade of lymphoma (p  …

Description Cyclooxygenase-2 (COX-2) plays an important role in carcinogenesis, which catalyzes the conversion of arachidonic acid into prostaglandins. P53 is a tumor suppressor gene that contributes to apoptosis and cell cycle control. There is functional interaction between p53 and COX-2, which lead to abrogation of apoptosis and progression of malignancy. To assess the relationship between COX-2, p53 expression and the clinicopathololgic features in SLL and DLBCL. We immunohistochemically examined the expression of COX-2 and p53 in non-neoplastic lymphoid cells, lymph nodal low-grade (50 cases of SLL), intermediate and high-grade lymphomas (100 cases of DLBCL) and their corresponding bone marrow specimens. The expression of COX-2 and p53 was absent in the in non-neoplastic lymphoid cells. In contrast, their expression values increased progressively with the advancing grade of lymphoma (p  …

Description Cyclooxygenase-2 (COX-2) plays an important role in carcinogenesis, which catalyzes the conversion of arachidonic acid into prostaglandins. P53 is a tumor suppressor gene that contributes to apoptosis and cell cycle control. There is functional interaction between p53 and COX-2, which lead to abrogation of apoptosis and progression of malignancy. To assess the relationship between COX-2, p53 expression and the clinicopathololgic features in SLL and DLBCL. We immunohistochemically examined the expression of COX-2 and p53 in non-neoplastic lymphoid cells, lymph nodal low-grade (50 cases of SLL), intermediate and high-grade lymphomas (100 cases of DLBCL) and their corresponding bone marrow specimens. The expression of COX-2 and p53 was absent in the in non-neoplastic lymphoid cells. In contrast, their expression values increased progressively with the advancing grade of lymphoma (p  …

Description Cyclooxygenase-2 (COX-2) plays an important role in carcinogenesis, which catalyzes the conversion of arachidonic acid into prostaglandins. P53 is a tumor suppressor gene that contributes to apoptosis and cell cycle control. There is functional interaction between p53 and COX-2, which lead to abrogation of apoptosis and progression of malignancy. To assess the relationship between COX-2, p53 expression and the clinicopathololgic features in SLL and DLBCL. We immunohistochemically examined the expression of COX-2 and p53 in non-neoplastic lymphoid cells, lymph nodal low-grade (50 cases of SLL), intermediate and high-grade lymphomas (100 cases of DLBCL) and their corresponding bone marrow specimens. The expression of COX-2 and p53 was absent in the in non-neoplastic lymphoid cells. In contrast, their expression values increased progressively with the advancing grade of lymphoma (p  …

Description Cyclooxygenase-2 (COX-2) plays an important role in carcinogenesis, which catalyzes the conversion of arachidonic acid into prostaglandins. P53 is a tumor suppressor gene that contributes to apoptosis and cell cycle control. There is functional interaction between p53 and COX-2, which lead to abrogation of apoptosis and progression of malignancy. To assess the relationship between COX-2, p53 expression and the clinicopathololgic features in SLL and DLBCL. We immunohistochemically examined the expression of COX-2 and p53 in non-neoplastic lymphoid cells, lymph nodal low-grade (50 cases of SLL), intermediate and high-grade lymphomas (100 cases of DLBCL) and their corresponding bone marrow specimens. The expression of COX-2 and p53 was absent in the in non-neoplastic lymphoid cells. In contrast, their expression values increased progressively with the advancing grade of lymphoma (p  …

Description Cyclooxygenase-2 (COX-2) plays an important role in carcinogenesis, which catalyzes the conversion of arachidonic acid into prostaglandins. P53 is a tumor suppressor gene that contributes to apoptosis and cell cycle control. There is functional interaction between p53 and COX-2, which lead to abrogation of apoptosis and progression of malignancy. To assess the relationship between COX-2, p53 expression and the clinicopathololgic features in SLL and DLBCL. We immunohistochemically examined the expression of COX-2 and p53 in non-neoplastic lymphoid cells, lymph nodal low-grade (50 cases of SLL), intermediate and high-grade lymphomas (100 cases of DLBCL) and their corresponding bone marrow specimens. The expression of COX-2 and p53 was absent in the in non-neoplastic lymphoid cells. In contrast, their expression values increased progressively with the advancing grade of lymphoma (p  …