Wahl S M, Orenstein J M
Oral Infection and Immunity Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892-4352, USA.
J Leukoc Biol. 1997 Jul;62(1):67-71. doi: 10.1002/jlb.62.1.67.
A biphasic early and late viremia is characteristic of HIV-1 infection. The first increase in circulating viral burden occurs within weeks after infection, before a host immune response, and the second, later peak emerges during the inevitable HIV-1 devastation of immune function. Recently, intermittent bouts of viremia have also been identified in HIV-1-infected individuals and found to be associated with episodes of immune challenge. Vaccinations, exposure to antigens, and infections often induce reversible increases in circulating viral levels, dependent on CD4+ T lymphocyte numbers. However, even with marked losses in CD4+ T cell counts, opportunistic infections appear to trigger a viremic response. In searching for the source of this virus, macrophages in tissues co-infected with opportunistic pathogens have been identified as prodigious producers of HIV-1. Thus, the fountain from which HIV-1 emerges may shift from CD4+ T lymphocytes in early HIV-1 infection to tissue macrophages later in the natural evolution of the disease, as the CD4+ T cells are depleted. Defining the mechanisms of this transitional event in HIV-1 infection may facilitate regulation and therapeutic control of both opportunistic infections and HIV-1.
HIV-1感染的特征是出现双相性的早期和晚期病毒血症。循环病毒载量的首次增加发生在感染后数周内，在宿主免疫反应之前；第二次、较晚出现的峰值则出现在HIV-1对免疫功能造成不可避免的破坏期间。最近，在HIV-1感染个体中也发现了间歇性病毒血症发作，并发现其与免疫挑战事件有关。疫苗接种、接触抗原和感染通常会导致循环病毒水平可逆性升高，这取决于CD4+ T淋巴细胞数量。然而，即使CD4+ T细胞计数显著下降，机会性感染似乎也会引发病毒血症反应。在寻找这种病毒的来源时，与机会性病原体共同感染的组织中的巨噬细胞已被确定为HIV-1的大量产生者。因此，随着CD4+ T细胞的耗竭，HIV-1出现的源头可能会从HIV-1感染早期的CD4+ T淋巴细胞，转变为疾病自然演变后期的组织巨噬细胞。确定HIV-1感染中这一转变事件的机制，可能有助于对机会性感染和HIV-1进行调控及治疗控制。
