Two cases illustrating different neurological aspects of HIV-escape syndrome

Abstract

Background

HIV escape syndrome is characterized by high viral load in the central nervous system despite having a low serum viral load and typically detected after the initiation of antiretroviral therapy during the course of HIV infection. The aim of this report was to reveal different aspects of the neurological involvement of HIV-escape syndrome and to define the discrete phenotypes of HIV-escape syndrome characterized by predominant inflammation or HIV-associated neurocognitive disorder.

Case Presentation

Two cases are presented, both were followed collaboratively by neurology and infectious diseases clinics, where the ones in which neurologic complaints associated with HIV-positivity aggravated by development of HIV-escape syndrome. The first case, investigated for progressive vision loss, represented the inflammatory course of HIV-escape with vasculitic involvement on imaging, positive serum anti-NMDA-R antibody, and good response to immunotherapy. On the other hand, the second case, who presented with progressive confusion and difficulty in walking, exemplifies the HIV-associated neurocognitive disorder with parenchymal atrophy, no evidence of inflammation, and benefit only from antiretroviral treatment modifications.

Conclusion

With regard to the discussions detailed herein, identifying HIV-escape syndrome as a balance of viral colonization and antiviral defense dynamics rather than a homogeneous clinical entity will broaden the clinical approaches needed. It should be particularly borne in mind that the initial neurological status may be exacerbated if HIV-escape syndrome develops.