Tiemessen C T, Kidd A H
Department of Virology, University of the Witwatersrand, Johannesburg, South Africa.
Arch Virol. 1993;128(1-2):1-13. doi: 10.1007/BF01309784.
The subgroup F adenoviruses were tested for their ability to induce interferon in semi-permissive human cells (Chang conjunctiva) and non-permissive cells (HEF, human embryo lung fibroblasts). These cells did not produce interferon spontaneously or in response to infection by either of these adenoviruses. It was concluded that interferon induction in response to subgroup F adenovirus infection is not a likely explanation of limited virus growth in culture. Adenovirus 40 and Ad41, unlike Ad2, were found to be sensitive to human lymphoblastoid interferon in Chang conjunctival cells. The addition of Ad2 to cells before pretreatment with interferon resulted in the partial and complete abrogation of Ad40 and Ad41 interferon sensitivity, respectively. The suppressive effect of Ad2 on the inhibitory action of interferon and the modulatory function of Ad2 in mixed infection with either Ad40 or Ad41 suggests the inadequate functioning of a subgroup F adenovirus gene product or products involved in suppression of the interferon-induced antiviral state.
对F亚组腺病毒进行了检测，以评估它们在半允许性人类细胞（张氏结膜细胞）和非允许性细胞（人胚肺成纤维细胞，HEF）中诱导干扰素的能力。这些细胞不会自发产生干扰素，也不会因感染这两种腺病毒中的任何一种而产生干扰素。得出的结论是，F亚组腺病毒感染诱导干扰素不太可能是培养中病毒生长受限的原因。与腺病毒2型不同，腺病毒40和腺病毒41在张氏结膜细胞中对人淋巴母细胞干扰素敏感。在用干扰素预处理细胞之前加入腺病毒2型，分别导致腺病毒40和腺病毒41对干扰素的敏感性部分和完全丧失。腺病毒2型对干扰素抑制作用的抑制效应以及在与腺病毒40或腺病毒41混合感染中的调节功能表明，F亚组腺病毒中一种或多种参与抑制干扰素诱导的抗病毒状态的基因产物功能不足。
