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Distinct lipid profile, low-level inflammation, and increased antioxidant defense signature in HIV-1 elite control status.


ABSTRACT: HIV-1 elite controllers (EC) are a rare but heterogeneous group of HIV-1-infected individuals who can suppress viral replication in the absence of antiretroviral therapy. The mechanisms of how EC achieve undetectable viral loads remain unclear. This study aimed to investigate host plasma metabolomics and targeted plasma proteomics in a Swedish HIV-1 cohort including EC and treatment-naïve viremic progressors (VP) as well as HIV-negative individuals (HC) to get insights into EC phenotype. Metabolites belonging to antioxidant defense had higher levels in EC relative to VP, whereas inflammation markers were increased in VP compared with EC. Only four plasma proteins (CCL4, CCL7, CCL20, and NOS3) were increased in EC compared with HC, and CCL20/CCR6 axis can play an essential role in EC status. Our study suggests that low-level inflammation and oxidative stress at physiological levels could be important factors contributing to elite control phenotype.

SUBMITTER: Sperk M 

PROVIDER: S-EPMC7892918 | biostudies-literature | 2021 Feb

REPOSITORIES: biostudies-literature

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Distinct lipid profile, low-level inflammation, and increased antioxidant defense signature in HIV-1 elite control status.

Sperk Maike M   Mikaeloff Flora F   Svensson-Akusjärvi Sara S   Krishnan Shuba S   Ponnan Sivasankaran Munusamy SM   Ambikan Anoop T AT   Nowak Piotr P   Sönnerborg Anders A   Neogi Ujjwal U  

iScience 20210128 2


HIV-1 elite controllers (EC) are a rare but heterogeneous group of HIV-1-infected individuals who can suppress viral replication in the absence of antiretroviral therapy. The mechanisms of how EC achieve undetectable viral loads remain unclear. This study aimed to investigate host plasma metabolomics and targeted plasma proteomics in a Swedish HIV-1 cohort including EC and treatment-naïve viremic progressors (VP) as well as HIV-negative individuals (HC) to get insights into EC phenotype. Metabol  ...[more]

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