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      Individuals with HIV-1 subtype C infection and cryptococcal meningitis exhibit viral genetic intermixing of HIV-1 between plasma and cerebrospinal fluid, and a high prevalence of CXCR4-using variants

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          Abstract

          The genotypic properties of HIV-1 subtype C in individuals presenting with cryptococcal meningitis (CM) are not well established. Employing single-genome amplification as well as bulk PCR, cloning and sequencing strategies, we evaluated the genetic properties of HIV-1 subtype C env in 16 antiretroviral therapy naïve study participants with CM. Eleven of the 16 participants had matched blood plasma and cerebrospinal fluid (CSF) evaluated, with the rest having either a plasma or CSF sample evaluated. Before antiretroviral therapy initiation, matched plasma and cerebrospinal fluid-derived env sequences of all 11 participants displayed genetic intermixing between the two compartments. Overall, seven of the 16 (~43.8%) participants harbored CXCR4-using variants in plasma and/or CSF, according to coreceptor usage prediction algorithms. This study suggests that HIV-1 subtype C genetic intermixing between peripheral blood and the central nervous system is common in individuals presenting with CM, and that CXCR4 usage is present in one or both compartments in approximately 44% of individuals.

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          Author and article information

          Journal
          8709376
          1696
          AIDS Res Hum Retroviruses
          AIDS Res. Hum. Retroviruses
          AIDS research and human retroviruses
          0889-2229
          1931-8405
          17 December 2018
          23 May 2018
          July 2018
          02 January 2019
          : 34
          : 7
          : 607-620
          Affiliations
          [1 ]HIV Pathogenesis Programme, Doris Duke Medical Research Institute, Nelson R Mandela School of Medicine, University of KwaZulu-Natal, Durban, South Africa
          [2 ]Department of Infectious Diseases, Alfred Hospital and Monash University, Melbourne, Australia
          [3 ]Department of Infectious Diseases, King Edward VIII Hospital, University of KwaZulu-Natal, Durban, South Africa
          [4 ]The Peter Doherty Institute for Infection and Immunity, University of Melbourne and Royal Melbourne Hospital, Melbourne, Australia
          [5 ]Medical School and School of Biomedical Sciences, University of Western Australia, Perth, Australia
          [6 ]Department of Clinical Immunology, Royal Perth Hospital and PathWest Laboratory Medicine, Perth, Australia
          [7 ]Africa Health Research Institute, Durban, South Africa
          [8 ]Ragon Institute of MGH, MIT and Harvard University, Cambridge, MA 02139, USA
          [9 ]Max Planck Institute for Infection Biology, Berlin, Germany
          Author notes
          Address correspondence to: Thumbi Ndung'u, HIV Pathogenesis Programme, Doris Duke Medical Research Institute, Nelson R Mandela School of Medicine, University of KwaZulu-Natal, 719 Umbilo Road, Congella, Durban, 4001. ndungu@ 123456ukzn.ac.za .
          Article
          PMC6314437 PMC6314437 6314437 ems80816
          10.1089/AID.2017.0209
          6314437
          29658309
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