Lucchiari M A, Pereira C A
Instituto Butantan, Laboratorio de Imunologia Viral, São Paulo, Brazil.
Immunobiology. 1989 Nov;180(1):12-22. doi: 10.1016/S0171-2985(89)80026-9.
Resistance of mice to mouse hepatitis virus type 3 (MHV3) infection is genetically determined. Normal adult A/J mice are resistant, and BALB/c mice are susceptible. Higher titers of virus and interferon (IFN) in vivo were found in MHV3-infected BALB/c mice compared with A/J mice. In vitro activation of macrophages (M phi) by lipopolysaccharide (LPS) delayed MHV3 replication only in cells that originated from A/J mice, although cell populations from both A/J and BALB/c mice were able to synthesize comparable amounts of IFN-alpha/beta. Using specific antibodies, we have shown that the delayed MHV3 replication in LPS-activated A/J M phi was due, in part, to IFN-alpha/beta. A/J M phi were found to be more sensitive to IFN-gamma than to IFN-alpha/beta, and BALB/c M phi did not develop an antiviral state to either IFN. Cultured spleen cells from A/J mice synthesized more IFN-gamma than BALB/c spleen cells after specific or non-specific stimulation. The results indicate that IFN-activated M phi may play a crucial role in the resistance to MHV3 infection. Since IFN-gamma is produced in large amounts by A/J spleen cells after specific stimulation with MHV3 and is efficient in activating the A/J M phi, a T cell-dependent mechanism is likely to be involved.
小鼠对3型小鼠肝炎病毒（MHV3）感染的抗性是由基因决定的。正常成年A/J小鼠具有抗性，而BALB/c小鼠易感。与A/J小鼠相比，在感染MHV3的BALB/c小鼠体内发现了更高滴度的病毒和干扰素（IFN）。脂多糖（LPS）在体外对巨噬细胞（M phi）的激活仅在源自A/J小鼠的细胞中延迟了MHV3的复制，尽管来自A/J和BALB/c小鼠的细胞群体能够合成相当数量的IFN-α/β。使用特异性抗体，我们已经表明，LPS激活的A/J M phi中MHV3复制的延迟部分归因于IFN-α/β。发现A/J M phi对IFN-γ比对IFN-α/β更敏感，并且BALB/c M phi对这两种IFN均未产生抗病毒状态。在特异性或非特异性刺激后，来自A/J小鼠的培养脾细胞比BALB/c脾细胞合成更多的IFN-γ。结果表明，IFN激活的M phi可能在对MHV3感染的抗性中起关键作用。由于在用MHV3特异性刺激后，A/J脾细胞大量产生IFN-γ并且在激活A/J M phi方面有效，因此可能涉及一种T细胞依赖性机制。
