Symptomatic HIV CNS viral escape among patients on effective cART

Manesh, Abi; Barnabas, Rohit; Mani, Sunithi; Karthik, Rajiv; Abraham, O C; Chacko, Geeta; Kannangai, Rajesh; Varghese, George M.

doi:10.1016/j.ijid.2019.03.033

Cited by 22 publications

(20 citation statements)

References 13 publications

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“…This is supported by histopathological identification of HIV-1 in brain tissue of some cases, including some of those designated as CD8 encephalitis that share the CSF escape profile [32]. HIV-1 causality is also supported by the frequent therapeutic benefit of treatment modification on neurological symptoms and signs [18,20,29]. Most, but not all, of these individuals exhibit inadequate CNS treatment regimens related to drug resistance of the CNS virus population or to insufficient 'penetration' of the full combination of drugs into the CNS compartment by virtue of their pharmacological properties-or, frequently, to a combination of these two factors [18,20,27].…”

Section: Introductionmentioning

confidence: 88%

“…This was coherently defined in a report of 11 treated patients presenting with a variety of neurological symptoms and signs who exhibited higher CSF than plasma HIV-1 RNA concentrations [ 18 ]. Additional reports preceded [ 19 ] and have followed [ 20 – 29 ], and this condition is now termed neurosymptomatic CSF escape based on the clinical presentation of neurological deficits in the presence of detectable CSF HIV-1 RNA despite systemic viral suppression[ 15 , 17 , 30 ]. This is clinically the most important type of CSF escape and can present with major neurological deficits and imaging abnormalities [ 20 ].…”

Section: Introductionmentioning

confidence: 99%

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Herpes zoster in HIV-1 infection: The role of CSF pleocytosis in secondary CSF escape and discordance

et al. 2020

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HIV cerebrospinal fluid (CSF) escape is defined by a concentration of HIV-1 RNA in CSF above the lower limit of quantification of the employed assay and equal to or greater than the plasma HIV-1 RNA level in the presence of treatment-related plasma viral suppression, while CSF discordance is similarly defined by equal or higher CSF than plasma HIV-1 RNA in untreated individuals. During secondary CSF escape or discordance, disproportionate CSF HIV-1 RNA develops in relation to another infection in addition to HIV-1. We performed a retrospective review of people living with HIV receiving clinical care at Sahlgrenska Infectious Diseases Clinic in Gothenburg, Sweden who developed uncomplicated herpes zoster (HZ) and underwent a research lumbar puncture (LP) within the ensuing 150 days. Based on treatment status and the relationship between CSF and plasma HIV-1 RNA concentrations, they were divided into 4 groups: i) antiretroviral treated with CSF escape (N = 4), ii) treated without CSF escape (N = 5), iii) untreated with CSF discordance (N = 8), and iv) untreated without CSF discordance (N = 8). We augmented these with two additional cases of secondary CSF escape related to neuroborreliosis and HSV-2 encephalitis and analyzed these two non-HZ cases for factors contributing to CSF HIV-1 RNA concentrations. HIV-1 CSF escape and discordance were associated with higher CSF white blood cell (WBC) counts than their non-escape (P = 0.0087) and non-discordant (P = 0.0017) counterparts, and the CSF WBC counts correlated with the CSF HIV-1 RNA levels in both the treated (P = 0.0047) and untreated (P = 0.002) group pairs. Moreover, the CSF WBC counts correlated with the CSF:plasma HIV-1 RNA ratios of the entire group of 27 subjects (P = <0.0001) indicating a strong effect of the CSF WBC count on the relation of the CSF to plasma HIV-1 RNA concentrations across the entire sample set. The inflammatory response to HZ and its augmenting effect on CSF HIV-1 RNA was found up to 5 months after the HZ outbreak in the cross-sectional sample and, was present for one year after HZ in one individual followed

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Section: Introductionmentioning

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Herpes zoster in HIV-1 infection: The role of CSF pleocytosis in secondary CSF escape and discordance

et al. 2020

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“…Secondary CSF escape occurs during a CNS co-infection, such as syphilis or herpes viruses, which may result in increased trafficking of CD4+ T cells into the CNS, some of which may be latently infected with HIV [22,24]. The inflammation associated with symptomatic viral escape likely occurs because of the presence of HIV itself [22,25–27]. CSF viral escape is an important contributor to the development of HIV-associated CD8+ T-cell encephalitis, accounting for 68% of patients in a recently examined cohort [28 ▪▪ ], suggesting that this process is mediated by immune responses directed towards HIV.…”

Section: Biotypes Of Hiv-associated Cognitive Impairmentsmentioning

confidence: 99%

“…HIV viral escape in symptomatic patients can occur because of low penetration of ART into the CNS, poor adherence or compliance to ART, or mutations that confer resistance [22,25]. Drug-resistant mutations may arise more frequently in the CNS as there might be enhanced viral replication in this compartment.…”

Section: Biotypes Of Hiv-associated Cognitive Impairmentsmentioning

confidence: 99%

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Biotypes of HIV-associated neurocognitive disorders based on viral and immune pathogenesis

Johnson

Nath

2022

Current Opinion in Infectious Diseases

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Purpose of review HIV-associated neurocognitive disorders (HAND) continues to be prevalent in people living with HIV despite antiretroviral therapy. However, understanding disease mechanisms and identifying therapeutic avenues has been challenging. One of the challenges is that HAND is a heterogeneous disease and that patients identified with similar impairments phenotypically may have very different underlying disease processes. As the NeuroAIDS field is re-evaluating the approaches used to identify patients with HIV-associated neurological impairments, we propose the subtyping of patients into biotypes based on viral and immune pathogenesis. Recent findingsHere we review the evidence supporting subtyping patients with HIV-associated neurological complications into four biotypes: macrophage-mediated HIV encephalitis, CNS viral escape, T-cell-mediated HIV encephalitis, and HIV protein-associated encephalopathy.

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Neuropathogenesis of HIV-1: insights from across the spectrum of acute through long-term treated infection

Killingsworth

Spudich

2022

Semin Immunopathol

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Symptomatic HIV CNS viral escape among patients on effective cART

Cited by 22 publications

References 13 publications

Herpes zoster in HIV-1 infection: The role of CSF pleocytosis in secondary CSF escape and discordance

Herpes zoster in HIV-1 infection: The role of CSF pleocytosis in secondary CSF escape and discordance

Biotypes of HIV-associated neurocognitive disorders based on viral and immune pathogenesis

Neuropathogenesis of HIV-1: insights from across the spectrum of acute through long-term treated infection

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