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J Neurovirol. 2018 Feb;24(1):132-136. doi: 10.1007/s13365-017-0605-1. Epub 2017 Dec 14.

Symptomatic cerebrospinal fluid HIV-1 escape with no resistance-associated mutations following low-level plasma viremia.

Author information

1
Unit of Infectious Diseases, Department of Medical Sciences, University of Torino, Ospedale Amedeo di Savoia, C.so Svizzera 164, 10144, Torino, Italy. mattia.trunfio@edu.unito.it.
2
Department of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
3
Laboratory of Microbiology and Virology, Amedeo di Savoia Hospital, Torino, Italy.
4
Laboratory of Immunology, Maria Vittoria Hospital, Torino, Italy.
5
Department of Diagnostic Laboratory, Maria Vittoria Hospital, Torino, Italy.
6
Unit of Infectious Diseases, Department of Medical Sciences, University of Torino, Ospedale Amedeo di Savoia, C.so Svizzera 164, 10144, Torino, Italy.
7
Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
8
Laboratory of Neurobiology, Neurology Unit 2-CReSM, University of Torino, San Luigi Hospital, Orbassano, Italy.
9
Neurology Unit, Maria Vittoria Hospital, Torino, Italy.

Abstract

The majority of neurologically symptomatic cerebrospinal fluid HIV-1 escape cases are connected with resistance-associated mutations and potentially explained by low cerebrospinal fluid antiretroviral concentrations. However, there are still significant knowledge gaps regarding the physiopathology and long-term management of neurosymptomatic viral escape. We report a case of Parkinson-like syndrome following cerebrospinal fluid HIV-1 escape in a 40-year-old female patient with an history of persistent low-level plasma viremia under treatment. No resistance-associated mutations, high viral diversity (env deep sequencing), adequate pharmacokinetics, atypical CD3-CD14-CD4+CD5-CD2-/+CD7-/+ lymphocytes, low-level Epstein-Barr virus replication, and white matter autoimmune reactivity were observed in the cerebrospinal fluid. Antiretroviral regimen modification led to rapid clinical and radiological improvements. This case may increase the current uncertain knowledge on the origin of cerebrospinal fluid HIV-1 and illustrates the consequences of uncontrolled compartmental viral replication; it also highlights the relevance and persistence of immune activation and the possibility of various detrimental mechanisms underlying neurosymptomatic viral escape.

KEYWORDS:

Antiretrovirals; HIV; Neuroimmunology; Viral escape; Virology

PMID:
29243133
DOI:
10.1007/s13365-017-0605-1
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