Módulo 3 – Curso pós-graduado – VIH e Envelhecimento

Neurocognitive Disorders in HIV Infected Patients

Clinical management of HIV-related neurological disorders

Autor: Prof. Doutor Richard W. Price, MD PhD (San Francisco General Hospital, University of California, San Francisco, USA)

CNS HIV infection

While both CNS HIV infection and inflammatory responses originate from systemic sources, they also can become ‘compartmentalized’ and differ from their blood counterparts. CNS HIV infection begins soon after initial exposure and systemic viremia, and continues thereafter in absence of treatment. However, its character evolves with advancing systemic infection and may change from predominantly meningeal infection to more ‘invasive’ encephalitis. Similarly, cells of inflammatory response, lymphocytes and myeloid cells, derive from blood and move into the CNS selectively and therefore may differ from the populations circulating in blood and may result in a different inflammatory milieu. The interactions of these compartmentalized virus and inflammatory factors are likely critical in the pathogenesis of CNS injury, although our understanding of the exact mechanism of injury remain rather crude.

In characterizing the evolution of CNS infection using CSF sampling, at least three ‘types’ of relationship between CSF and blood HIV populations can be found:

  • Equilibrated, in which the virus populations in the CSF are the same as those found in the blood, presumably related to the recent origin of CSF HIV from trafficking infected and susceptible TCD4+ cells.
  • Clonal expansions in the spinal fluid, which are bursts of local replication from T-cells or perhaps myeloid cells.
  • Diverse compartmentalized, corresponding to an autonomous CNS infection, in which the virus undergoes replication and evolution independent from systemic infection, probably chiefly in myeloid cells resulting in genetically diverse populations within the CNS.

It is important to understand the biological properties and origins of these CNS virus populations. As an initial step, it will be of interest to know if they are T-tropic or M-tropic, since these are not only distinct phylogenetically but pathogenetically. Theoretically, it is expected that the initial infection is due to R5 T cell-tropic virus which is most common in blood throughout infection. With treatment, the R5 T cell-tropic virus decays quickly while M-tropic virus shows a slow decay because of long life of macrophages.1

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