PATHOGENESIS OF SV40 INFECTIONS IN MACAQUES W/ AIDS

灵长类多瘤病毒包括JCV和BKV，它们可以感染 人类，以及与猕猴密切相关的SV40。在免疫能力方面 宿主，原发感染发生在生命早期，轻度或无感染 临床症状。然后病毒主要以潜伏感染的形式持续存在 在肾脏里。病毒脱落的重新激活可能会在怀孕期间发生， 慢性病或免疫功能受损，可能与此相关，也可能不相关 有临床症状。JCV与进行性多灶性疾病有关 白质脑病(PML)是一种中枢神经系统脱髓鞘疾病 少突胶质细胞感染导致的神经系统(CNS)，高达5% 爱滋病患者。BKV引起间质性肾炎和/或 出血性膀胱炎，尤其是移植受者。 类似地，SV40与PML和肾炎有关 感染SIV的猕猴感染了猿猴艾滋病。先前的研究表明 SV40在原发感染中引起间质性肾炎，而PML 在SIV感染的猕猴中潜伏感染重新激活时。我们 现在认识到SV40 a脑膜脑炎的第二个中枢神经系统表现 影响大脑灰质，无脱髓鞘，与 PML。这种损害可以是SV40的主要表现。 合并SV40诱导的间质性肾炎。就地 SV40的杂交结合神经胶质细胞的免疫组织化学 纤维酸性蛋白在同一切片上，显示出许多 脑膜脑炎病变中感染细胞的比例为 星形胶质细胞，而不是PML，在PML中，大多数感染细胞 是少突胶质细胞。分离自中国的SV40的初步序列数据 并发脑膜脑炎和肾脏疾病的猕猴建议 这两处损伤是由相同的病毒株引起的， 这与与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.