Villarete L, Somasundaram T, Ahmed R
Department of Microbiology and Immunology, University of California, Los Angeles.
J Virol. 1994 Nov;68(11):7490-6. doi: 10.1128/JVI.68.11.7490-7496.1994.
Viral variants with different biological properties predominate in the central nervous system (CNS) and lymphoid tissues of carrier mice infected at birth with the Armstrong strain of lymphocytic choriomeningitis virus. The CNS isolates have the same phenotype as the parental strain and cause acute infections in adult mice, while the spleen-derived isolates cause chronic infections associated with suppressed T-cell responses and susceptibility to opportunistic infections. Our previous studies have identified a single amino acid change in the viral glycoprotein, a phenylalanine-to-leucine (F-->L) mutation at residue 260, that correlates with the tissue-specific selection and the persistent and immunosuppressive phenotype of the spleen isolates (R. Ahmed, C.S. Hahn, T. Somasundaram, L. Villarete, M. Matloubian, and J. H. Strauss, J. Virol. 65:4242-4247, 1991). In this study, we screened viral isolates obtained from the spleen, liver, kidney, and brain of carrier mice for the presence of this mutation and determined the temporal selection of variants as they appear in these organs. We found that this F-->L amino acid change is common to > 90% of the spleen and liver isolates and is selected for rapidly by day 32 postinfection (p.i.). Although the kinetics observed in the kidney are relatively slower than in the spleen and liver, this F-->L mutation predominates in the kidney-derived isolates by 250 days p.i. In contrast, the majority of the CNS isolates retain the parental sequence up to 250 days p.i. In addition, most of the brain isolates replicated efficiently in a neuronal cell line, and this enhanced growth phenotype in neurons correlated with the parental F genotype. This linkage with neurotropism, along with our earlier finding that the F-->L mutation is necessary for enhanced infection of macrophages (M. Matloubian, S. R. Kolhekar, T. Somasundaram, and R. Ahmed, J. Virol. 67:7340-7349, 1993), provides a cellular basis for the molecular changes associated with tissue-specific selection. Taken together, these results suggest that tropism for macrophages is a critical determinant in selection of variants with the F-->L mutation in tissues such as spleen and liver, and tropism for neurons is important in retention of the F genotype in the CNS.
出生时感染淋巴细胞性脉络丛脑膜炎病毒阿姆斯特朗株的携带小鼠,其不同生物学特性的病毒变体在中枢神经系统(CNS)和淋巴组织中占主导地位。CNS分离株具有与亲代毒株相同的表型,并在成年小鼠中引起急性感染,而脾脏来源的分离株则引起与T细胞反应受抑制和易患机会性感染相关的慢性感染。我们之前的研究已经确定病毒糖蛋白中有一个单一氨基酸变化,即第260位残基处的苯丙氨酸到亮氨酸(F→L)突变,这与组织特异性选择以及脾脏分离株的持续和免疫抑制表型相关(R. Ahmed、C.S. Hahn、T. Somasundaram、L. Villarete、M. Matloubian和J.H. Strauss,《病毒学杂志》65:4242 - 4247,1991年)。在本研究中,我们筛选了从携带小鼠的脾脏、肝脏、肾脏和大脑中获得的病毒分离株,以检测该突变的存在,并确定这些变体在这些器官中出现时的时间选择。我们发现,这种F→L氨基酸变化在超过90%的脾脏和肝脏分离株中很常见,并且在感染后第32天(p.i.)就迅速被选择。尽管在肾脏中观察到的动力学相对比在脾脏和肝脏中慢,但到感染后250天,这种F→L突变在肾脏来源的分离株中占主导地位。相比之下,大多数CNS分离株在感染后250天内都保留亲代序列。此外,大多数大脑分离株在神经元细胞系中能高效复制,并且这种在神经元中增强的生长表型与亲代F基因型相关。这种与嗜神经性的联系,以及我们早期发现F→L突变对于增强巨噬细胞感染是必需的(M. Matloubian、S.R. Kolhekar、T. Somasundaram和R. Ahmed,《病毒学杂志》67:7340 - 7349,1993年),为与组织特异性选择相关的分子变化提供了细胞基础。综上所述,这些结果表明,对巨噬细胞的嗜性是在脾脏和肝脏等组织中选择具有F→L突变变体的关键决定因素,而对神经元的嗜性对于CNS中F基因型的保留很重要。