HIV controllers comprise a heterogeneous group of HIV-infected individuals with the ability to maintain low viral loads and high CD4+ T cell counts for years in the absence of antiretroviral treatment (ART). Within these is a special group of individuals termed “elite controllers” who durably maintain undetectable plasma HIV RNA without medication. The ability of these groups to control viremia has gained wide interest over the years and is suggested to be a model for functional HIV cure. Factors described so far only partly explain control amongst these individuals as half of the HIV controllers do not possess these features. Most interestingly, HIV controllers have high levels of inflammation despite low viral loads and are thus at risk of non-AIDS-related conditions. Gaining a better understanding of the mechanisms underlying spontaneous HIV control is one of the research priorities and has implications for the development of HIV cure strategies.
The goal of this Research Topic is to collect contributions on progress made on understanding immunological mechanisms of spontaneous HIV control. Since non-AIDS complications are attributed to persistent inflammation and innate immune activation, both of which are incompletely restored by ART, particular focus on innate immune features as an understudied research area will help identify novel biomarkers and outline gaps for researchers in the field.
We welcome the submission of Original Research articles, Reviews, Mini-Reviews, Case Reports and Perspectives including, but not limited to the following sub-topics:
• Role of innate immune cell subsets in spontaneous HIV control (i.e including but not limited to monocytes, natural killer cells, dendritic cells, and neutrophils).
• Trained immunity in HIV controllers.
• Interplay between metabolism and innate immune cells in HIV controllers.
• Immune features associated with inflammation and non-AIDS-related conditions in individuals with HIV spontaneous control.
• Impact of ART on innate immune responses in HIV controllers.
HIV controllers comprise a heterogeneous group of HIV-infected individuals with the ability to maintain low viral loads and high CD4+ T cell counts for years in the absence of antiretroviral treatment (ART). Within these is a special group of individuals termed “elite controllers” who durably maintain undetectable plasma HIV RNA without medication. The ability of these groups to control viremia has gained wide interest over the years and is suggested to be a model for functional HIV cure. Factors described so far only partly explain control amongst these individuals as half of the HIV controllers do not possess these features. Most interestingly, HIV controllers have high levels of inflammation despite low viral loads and are thus at risk of non-AIDS-related conditions. Gaining a better understanding of the mechanisms underlying spontaneous HIV control is one of the research priorities and has implications for the development of HIV cure strategies.
The goal of this Research Topic is to collect contributions on progress made on understanding immunological mechanisms of spontaneous HIV control. Since non-AIDS complications are attributed to persistent inflammation and innate immune activation, both of which are incompletely restored by ART, particular focus on innate immune features as an understudied research area will help identify novel biomarkers and outline gaps for researchers in the field.
We welcome the submission of Original Research articles, Reviews, Mini-Reviews, Case Reports and Perspectives including, but not limited to the following sub-topics:
• Role of innate immune cell subsets in spontaneous HIV control (i.e including but not limited to monocytes, natural killer cells, dendritic cells, and neutrophils).
• Trained immunity in HIV controllers.
• Interplay between metabolism and innate immune cells in HIV controllers.
• Immune features associated with inflammation and non-AIDS-related conditions in individuals with HIV spontaneous control.
• Impact of ART on innate immune responses in HIV controllers.
