Feduchi E, Esteban M, Carrasco L
Centro de Biología Molecular, Universidad Autónoma de Madrid, Spain.
Virology. 1988 Jun;164(2):420-6. doi: 10.1016/0042-6822(88)90555-7.
Treatment of HeLa cells with human lymphoblastoid interferon (IFN-alpha) does not inhibit reovirus type 3 protein synthesis during virus infection. In contrast, reovirus translation is blocked by treatment of L cells with mouse IFN-alpha. The (2'-5')A synthetase activity is induced in HeLa cells by IFN-alpha treatment and is activated after reovirus infection, since cell lysates from these cells synthesize in vitro (2'-5')A oligonucleotides. The IFN-induced protein kinase activity is also triggered in those lysates upon dsRNA addition. Thus, contrary to DNA-containing viruses, such as vaccinia virus or adenovirus, reovirus infection does not destroy or reverse the IFN-induced antiviral state. In support of this conclusion, superinfection with poliovirus or vesicular stomatitis virus of reovirus-infected HeLa cells treated with IFN leads only to a blockade of translation of the former viruses. These results provide a remarkable example where in the same cells doubly infected with two different viruses, the antiviral state induced by IFN-alpha is manifested by selectively inhibiting translation of one kind of virus (poliovirus or vesicular stomatitis virus) without affecting the translation of reovirus type 3. In addition, these results indicate that the resistance of reovirus translation to inhibition by IFN is different from the mechanism of resistance induced by DNA-containing viruses.
用人淋巴母细胞干扰素（IFN-α）处理HeLa细胞，在病毒感染期间不会抑制呼肠孤病毒3型的蛋白质合成。相比之下，用小鼠IFN-α处理L细胞会阻断呼肠孤病毒的翻译。IFN-α处理可在HeLa细胞中诱导（2'-5'）A合成酶活性，并且在呼肠孤病毒感染后被激活，因为这些细胞的细胞裂解物可在体外合成（2'-5'）A寡核苷酸。在这些裂解物中加入双链RNA后，IFN诱导的蛋白激酶活性也会被触发。因此，与含DNA的病毒（如痘苗病毒或腺病毒）不同，呼肠孤病毒感染不会破坏或逆转IFN诱导的抗病毒状态。支持这一结论的是，用IFN处理的呼肠孤病毒感染的HeLa细胞再感染脊髓灰质炎病毒或水疱性口炎病毒，只会导致前一种病毒的翻译受阻。这些结果提供了一个显著的例子，即在同一细胞中被两种不同病毒双重感染时，IFN-α诱导的抗病毒状态表现为选择性抑制一种病毒（脊髓灰质炎病毒或水疱性口炎病毒）的翻译，而不影响呼肠孤病毒3型的翻译。此外，这些结果表明，呼肠孤病毒翻译对IFN抑制的抗性不同于含DNA病毒诱导的抗性机制。
