Ewert D, Duhadaway J
Wistar Institute, Philadelphia, PA 19104, USA.
Acta Virol. 1999 Apr-Jun;43(2-3):133-5.
Strains of Marek's disease virus (MDV), a herpesvirus, have been shown to augment the development of lymphoid leukosis induced by retroviruses, the avian leukosis virus (ALV) or the reticuloendotheliosis virus. In this study we explored the possibility that the ability to augment lymphoid leukosis may be correlated with the ability of different strains of MDV to block apoptosis. Subclones of the ALV-transformed B cell line, DT40, which was free of MDV DNA were infected with either R2/23 strain of MDV-1, SB1 strain of MDV-2, or turkey herpes virus (HVT), a MDV-3. We found that most of the normal DT40 cells and DT40 cells infected with the R2/23 became apoptotic when cultured in serum-reduced medium. By contrast, the frequency of apoptotic cells was greatly reduced in the DT40-SB1 and DT40-HVT subclones. These findings suggest that because the SB-1 strain persists in the ALV-infected cells, it may augment lymphoid leukosis by inhibiting apoptosis and providing a survival advantage to the B cells which have a deregulated myc proto-oncogene.
马立克氏病病毒(MDV)属于疱疹病毒,已被证明能增强由逆转录病毒、禽白血病病毒(ALV)或网状内皮组织增生症病毒诱导的淋巴细胞白血病的发展。在本研究中,我们探讨了增强淋巴细胞白血病的能力可能与不同MDV毒株阻断细胞凋亡的能力相关的可能性。用MDV-1的R2/23毒株、MDV-2的SB1毒株或MDV-3的火鸡疱疹病毒(HVT)感染不含MDV DNA的ALV转化B细胞系DT40的亚克隆。我们发现,大多数正常DT40细胞以及感染R2/23的DT40细胞在血清减少的培养基中培养时会发生凋亡。相比之下,DT40-SB1和DT40-HVT亚克隆中凋亡细胞的频率大大降低。这些发现表明,由于SB-1毒株在感染ALV的细胞中持续存在,它可能通过抑制细胞凋亡并为具有失调的myc原癌基因的B细胞提供生存优势来增强淋巴细胞白血病。