PATHOGENESIS OF SV40 INFECTIONS IN MACAQUES W/ AIDS

灵长类多瘤病毒包括JCV和BKV，它们感染 人类和猕猴的密切相关的SV 40。 在免疫功能正常 宿主，原发性感染发生在生命早期， 临床症状 然后病毒作为潜伏感染持续存在，主要是 在肾脏。 病毒脱落的再激活可发生在怀孕期间， 慢性疾病或免疫功能低下，可能或可能不相关 临床症状。 JCV与进行性多灶性相关 白质脑病（PML），一种中枢神经系统脱髓鞘疾病， 神经系统（CNS）由于少突胶质细胞感染，高达5% 艾滋病患者。 BKV引起间质性肾炎和/或 出血性膀胱炎，特别是在移植受者中。 同样，SV 40与PML和肾炎相关， SIV感染的猕猴与猿艾滋病。 先前的研究表明 SV 40在原发性感染中引起间质性肾炎， 在SIV感染的猕猴中潜伏感染的重新激活。 我们 现在认识到SV 40脑膜脑炎的第二个CNS表现 影响大脑灰质，无脱髓鞘，不同于 PML。 这种病变可能是SV 40的主要表现， 与SV 40诱导的间质性肾炎结合。 原位 SV 40杂交结合胶质细胞免疫组化 在同一切片上发现了大量的酸性蛋白质，表明许多 脑膜脑炎病变中的感染细胞 星形胶质细胞，与PML相反，在PML中，大多数受感染的细胞 是少突胶质细胞 分离的SV 40的初步序列数据 同时患有脑膜脑炎和肾病的猕猴表明， 这两种病变是由同一种病毒引起的 这与PML相关的不同。

The primate polyomaviruses include JCV and BKV, which infect humans, and the closely related SV40 of macaques. In immunocompetent hosts, primary infection occurs early in life, with mild or absent clinical signs. The virus then persists as a latent infection mainly in kidney. Reactivation with viral shedding can occur with pregnancy, chronic diseases or immunocompromise, and may or may not be associated with clinical signs. JCV is associated with progressive multifocal leukoencephalopathy (PML), a demyelinating disease of the central nervous system (CNS) due to infection of oligodendrocytes, in up to 5% of AIDS patients. BKV causes interstitial nephritis and/or hemorrhagic cystitis, particularly in transplant recipients. Similarly, SV40 is associated with both PML and nephritis in SIV-infected macaques with simian AIDS. Previous studies indicated that SV40 causes interstitial nephritis in primary infections, and PML upon reactivation of a latent infection in SIV-infected macaques. We now recognize a second CNS manifestation of SV40 a meningoencephalitis affecting cerebral gray matter, without demyelination, distinct from PML. This lesion can be a primary manifestation of SV40 in conjunction with SV40-induced interstitial nephritis. In situ hybridization for SV40, coupled with immunohistochemistry for glial fibrillary acidic protein on the same section, demonstrates that many of the infected cells in the meningoencephalitic lesions are astrocytes, in contrast to PML, where the majority of infected cells are oligodendrocytes. Preliminary sequence data on SV40 isolated from macaques with concurrent meningoencephalitis and renal disease suggest that these two lesions are caused by an identical strain of virus, which differs from that associated with PML.