Early central nervous system changes in human immunodeficiency virus (HIV)-infection

The introduction of antiretroviral therapy has changed the human immunodeficiency virus pandemic. Some patients with HIV infection after starting or resuming ART develop a paradoxical worsening of clinical status, called Immune Reсоnstitution Inflammatory Syndrome (IRIS). However, if clinical and laboratory criteria for the diagnosis of this syndrome have been formulated, IRIS neuroradiological criteria do not exist yet. The present study presents neuroradiological features and diagnostic algorithm for identification of IRIS involving central nervous system.

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Human Immunodeficiency Virus Type-1 (HIV-1) Transcriptional Regulation, Latency and Therapy in the Central Nervous System

Vaccines ◽

10.3390/vaccines9111272 ◽

2021 ◽

Vol 9 (11) ◽

pp. 1272

Author(s):

Joseph Hokello ◽

Adhikarimayum Lakhikumar Sharma ◽

Priya Tyagi ◽

Alok Bhushan ◽

Mudit Tyagi

Keyword(s):

Central Nervous System ◽

Human Immunodeficiency Virus ◽

Nervous System ◽

Transcriptional Regulation ◽

Antiretroviral Therapy ◽

Hiv Infection ◽

Combination Antiretroviral Therapy ◽

Hiv Replication ◽

Immunodeficiency Virus ◽

The Central Nervous System

The central nervous system (CNS) is highly compartmentalized and serves as a specific site of human immunodeficiency virus (HIV) infection. Therefore, an understanding of the cellular populations that are infected by HIV or that harbor latent HIV proviruses is imperative in the attempts to address cure strategies, taking into account that HIV infection and latency in the CNS may differ considerably from those in the periphery. HIV replication in the CNS is reported to persist despite prolonged combination antiretroviral therapy due to the inability of the current antiretroviral drugs to penetrate and cross the blood–brain barrier. Consequently, as a result of sustained HIV replication in the CNS even in the face of combination antiretroviral therapy, there is a high incidence of HIV-associated neurocognitive disorders (HAND). This article, therefore, provides a comprehensive review of HIV transcriptional regulation, latency, and therapy in the CNS.

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Development of Primary Central Nervous System Lymphoma Associated with Human Immunodeficiency Virus and JC Virus Infection

Journal of Clinical and Experimental Hematopathology ◽

10.3960/jslrt.54.211 ◽

2014 ◽

Vol 54 (3) ◽

pp. 211-217 ◽

Cited By ~ 4

Author(s):

Toru Kawakami ◽

Kaoko Sakai ◽

Yuto Mimura ◽

Yasushi Senoo ◽

Yukio Hirabayashi ◽

...

Keyword(s):

Central Nervous System ◽

Human Immunodeficiency Virus ◽

Nervous System ◽

Virus Infection ◽

Jc Virus ◽

Central Nervous System Lymphoma ◽

Immunodeficiency Virus

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Human Immunodeficiency Virus Type 1 RNA Detected in the Central Nervous System (CNS) After Years of Suppressive Antiretroviral Therapy Can Originate from a Replicating CNS Reservoir or Clonally Expanded Cells

Clinical Infectious Diseases ◽

10.1093/cid/ciy1066 ◽

2018 ◽

Vol 69 (8) ◽

pp. 1345-1352 ◽

Cited By ~ 15

Author(s):

Sarah B Joseph ◽

Laura P Kincer ◽

Natalie M Bowman ◽

Chris Evans ◽

Michael J Vinikoor ◽

...

Keyword(s):

Central Nervous System ◽

Human Immunodeficiency Virus ◽

Nervous System ◽

Antiretroviral Therapy ◽

Human Immunodeficiency Virus Type ◽

Virus Type ◽

Immunodeficiency Virus ◽

Hiv 1 ◽

Csf Escape

Abstract Background Human immunodeficiency virus type 1 (HIV-1) populations are detected in cerebrospinal fluid (CSF) of some people on suppressive antiretroviral therapy (ART). Detailed analysis of these populations may reveal whether they are produced by central nervous system (CNS) reservoirs. Methods We performed a study of 101 asymptomatic participants on stable ART. HIV-1 RNA concentrations were cross-sectionally measured in CSF and plasma. In participants with CSF HIV-1 RNA concentrations sufficient for analysis, viral populations were genetically and phenotypically characterized over multiple time points. Results For 6% of participants (6 of 101), the concentration of HIV-1 RNA in their CSF was ≥0.5 log copies/mL above that of plasma (ie, CSF escape). We generated viral envelope sequences from CSF of 3 participants. One had a persistent CSF escape population that was macrophage-tropic, partially drug resistant, genetically diverse, and closely related to a minor macrophage-tropic lineage present in the blood prior to viral suppression and enriched for after ART. Two participants (1 suppressed and 1 not) had transient CSF escape populations that were R5 T cell-tropic with little genetic diversity. Conclusions Extensive analysis of viral populations in 1 participant revealed that CSF escape was from a persistently replicating population, likely in macrophages/microglia, present in the CNS over 3 years of ART. CSF escape in 2 other participants was likely produced by trafficking and transient expansion of infected T cells in the CNS. Our results show that CNS reservoirs can persist during ART and that CSF escape is not exclusively produced by replicating CNS reservoirs.

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