Stohlman S A, Woodward J G, Frelinger J A
Infect Immun. 1982 May;36(2):672-7. doi: 10.1128/iai.36.2.672-677.1982.
Peritoneal exudate cells from strains of mice both resistant and susceptible to challenge with mouse hepatitis virus strain JHM were examined for extrinsic and intrinsic antiviral activity. Thioglycolate-elicited and resident peritoneal cells from uninfected mice were able to suppress viral growth in a permissive cell. The active cell in both populations is an adherent, radiation-resistant, Thy-1.2 antigen- and Ia antigen-negative cell. The suppression of virus replication was not related to nonspecific cellular cytotoxicity directed against the permissive host cell, and no interferon was detected. The expression of extrinsic antiviral activity was not related to the ability of the host to resist mouse hepatitis virus infection by virtue of either age or genetic background. The expression of intrinsic antiviral activity, on the other hand, correlated with the ability of the host to resist virus challenge, indicating a characteristic distinction between these two in vitro mechanisms of macrophage-mediated antiviral activity with regard to host resistance to viral infection. Further, the ability of a macrophage to support viral replication itself was independent of the ability of the macrophage to suppress virus growth in another cell.
对感染小鼠肝炎病毒JHM株后有抗性和易感性的小鼠品系的腹腔渗出细胞进行了外在和内在抗病毒活性检测。来自未感染小鼠的巯基乙酸盐诱导的和常驻腹腔细胞能够抑制允许性细胞中的病毒生长。这两个细胞群体中的活性细胞是一种贴壁、抗辐射、Thy-1.2抗原和Ia抗原阴性的细胞。病毒复制的抑制与针对允许性宿主细胞的非特异性细胞毒性无关，且未检测到干扰素。外在抗病毒活性的表达与宿主凭借年龄或遗传背景抵抗小鼠肝炎病毒感染的能力无关。另一方面，内在抗病毒活性的表达与宿主抵抗病毒攻击的能力相关，这表明在巨噬细胞介导的抗病毒活性的这两种体外机制之间，就宿主对病毒感染的抗性而言存在特征性差异。此外，巨噬细胞自身支持病毒复制的能力与巨噬细胞在另一个细胞中抑制病毒生长的能力无关。
