Molecular mechanism of viral pathogenecity, cytotoxicity and establishment of persistent infection

建立了持续感染hPIV-2东芝株的HeLa细胞。传至50代时，始终可检测到多核巨细胞。HeLa/hPIV2/Toshiba细胞大部分处于稳定状态，但部分细胞出现CPE并最终死亡。因此，hPIV2持续感染细胞被认为是载体和稳定状态的混合体。副粘病毒持续感染的建立过程可分为5种类型，在持续感染过程中常出现稳定状态和携带状态的混合体。我们设计了一种定量方法来分析持续感染的建立效率。属于I型的hPIV2 CA和SV5 T1株的效率较高，为0.1~0.3，属于II型的SV5 WR的效率也很高，约为0.1，尽管该病毒不能立即建立持续感染(稳定状态)。IV型SV41的免疫效率约为0.0007，与hPIV2Toshiba株基本相同。在副粘病毒持续感染中，常发现稳定状态和载体状态的混合体。此外，还进一步详细分析了不同SeV pi株的建立效率。亲本重组仙台病毒(rSeV(PA)、rSeV(Ppi)和rSeV(HNpi)的效率低于检测下限，而rSeV(Lpi)的效率接近1。出乎意料的是，rSeV(Mpi)和rSeV(Fpi)能够形成持续感染的细胞，但效率在0.001左右，表明fpi和mpi蛋白都有助于建立持续感染SeVpi的效率。

HeLa cells persistently infected with hPIV-2 Toshiba strain were established. Until 50 passages, multinucleated giant cells were detected all the time. The greater part of HeLa/hPIV2/Toshiba cells are steady states, but some fractions show CPE and eventually die. Thus, hPIV2 persistently infected cells are considered to be a mixture of carrier and steady states. Establishing processes of persistent infection by paramyxoviruses were classified into 5types.A mixture of steady state and carrier state was often found in persistent infection by paramyxoviruses. We devised a quantitative method for analyzing establishing-efficiency of persistent infection. The efficiency of hPIV2 CA and SV5 T1 strains belonging to type I was high, that is, 0.1〜0.3 and the efficiency of SV5 WR belonging to type II was also high, approximately 0.1, though the virus had no ability to immediately establish persistent infection (steady state). The efficiency of SV41 belonging to type IV was about 0.0007 and was almost same as that of hPIV2 Toshiba strain. A mixture of steady state and carrier state is often found in persistent infection by paramyxoviruses. Furthermore, the establishing efficiency of various SeV pi strain was further analyzed in detail. The efficiency of parent recombinant Sendai virus (rSeV (PA) ), rSeV (Ppi) and rSeV (HNpi) was below the limit of detection, while that of rSeV (Lpi) was nearly 1. Unexpectedly, rSeV (Mpi) and rSeV (Fpi) were found to be capable of forming persistently-infected cells, although the efficiency was around 0.001, indicating that both Fpi and Mpi proteins contribute to the establishing efficiency of persistent infection of SeVpi.