BACKGROUND: There are strong theoretical arguments for initiating antiretroviral therapy (ART) during primary HIV-1 infection (PHI) to preserve HIV-1-specific T-cell responses and to decrease immune activation. METHODS: We assessed the degree of immune activation during PHI and after analytical treatment interruption (ATI) in plasma samples from 22 subjects by measuring 13 cytokines/chemokines with the Luminex system. Subjects initiated quadruple ART at PHI (the QUEST cohort) and were classified as responders or nonresponders according to their HIV-1 viral load (VL) 6 months post-ATI. RESULTS: During PHI, nonresponders had higher levels of HIV-1 RNA, interferon (IFN)-gamma, tumour necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-10 and eotaxin than responders (P</=0.05). A positive correlation was found between VL and IFN-alpha, TNF-alpha, IL-1beta, macrophage inflammatory protein (MIP)-1alpha and MIP-1beta, respectively. Post ATI, responders had higher levels of IFN-gamma, MIP-1beta and monocyte chemotactic protein (MCP)-1 than nonresponders, while nonresponders had higher levels of HIV-1 RNA, IL-15 and eotaxin. Cytokine/chemokine levels were higher during PHI than post-ATI. CONCLUSIONS: High levels of immune activation during PHI are associated with a worse virological outcome post-ATI. In contrast, VL post-ATI is negatively correlated with IFN-gamma and chemokines. Therefore, the degree of immune activation during PHI is associated with both the VL at PHI and the viral set-point post-ART.
BACKGROUND: There are strong theoretical arguments for initiating antiretroviral therapy (ART) during primary HIV-1 infection (PHI) to preserve HIV-1-specific T-cell responses and to decrease immune activation. METHODS: We assessed the degree of immune activation during PHI and after analytical treatment interruption (ATI) in plasma samples from 22 subjects by measuring 13 cytokines/chemokines with the Luminex system. Subjects initiated quadruple ART at PHI (the QUEST cohort) and were classified as responders or nonresponders according to their HIV-1 viral load (VL) 6 months post-ATI. RESULTS: During PHI, nonresponders had higher levels of HIV-1 RNA, interferon (IFN)-gamma, tumour necrosis factor (TNF)-alpha, interleukin (IL)-1beta, IL-10 and eotaxin than responders (P</=0.05). A positive correlation was found between VL and IFN-alpha, TNF-alpha, IL-1beta, macrophage inflammatory protein (MIP)-1alpha and MIP-1beta, respectively. Post ATI, responders had higher levels of IFN-gamma, MIP-1beta and monocyte chemotactic protein (MCP)-1 than nonresponders, while nonresponders had higher levels of HIV-1 RNA, IL-15 and eotaxin. Cytokine/chemokine levels were higher during PHI than post-ATI. CONCLUSIONS: High levels of immune activation during PHI are associated with a worse virological outcome post-ATI. In contrast, VL post-ATI is negatively correlated with IFN-gamma and chemokines. Therefore, the degree of immune activation during PHI is associated with both the VL at PHI and the viral set-point post-ART.
Authors: Suzanne M Crowe; Clare L V Westhorpe; Nigora Mukhamedova; Anthony Jaworowski; Dmitri Sviridov; Michael Bukrinsky Journal: J Leukoc Biol Date: 2009-12-01 Impact factor: 4.962
Authors: Davide Gibellini; Francesco Alviano; Anna Miserocchi; Pier Luigi Tazzari; Francesca Ricci; Alberto Clò; Silvia Morini; Marco Borderi; Pierluigi Viale; Gianandrea Pasquinelli; Pasqualepaolo Pagliaro; Gian Paolo Bagnara; Maria Carla Re Journal: Retrovirology Date: 2011-05-25 Impact factor: 4.602
Authors: Glen Malherbe; Helen C Steel; Sharon Cassol; Tulio de Oliveira; Christopher J Seebregts; Ronald Anderson; Edana Cassol; Theresa M Rossouw Journal: Mediators Inflamm Date: 2014-04-06 Impact factor: 4.711