ĪHI is also associated with dysregulations in lymphocyte compartments. Even though the initiation of ART significantly reduces the plasma levels of inflammatory cytokines, some residual immune activation has been reported to persist even after the early initiation of ART. Similar observations of the cytokine storm have been reported in acute pathogenic SIV infections in rhesus macaques. The resolution of the cytokine storm following peak viremia is partial, with some cytokines remaining elevated above pre-infection physiologic levels which persist into the chronic phase in untreated infection. Notably, the elevation of some plasma cytokines occurs very early after infection, with acute HIV infection (AHI) being characterized by the onset of a cytokine storm in the period leading up to peak viremia. HIV infection is associated with immune activation which manifests in the elevation of numerous plasma cytokines and chemokines. While commencement of ART during Fiebig stages I–II of AHI abrogated the HIV-induced cytokine storm, significant depletions of eosinophils, basophils, and lymphocytes, as well as transient expansions of monocytes, were still observed in these individuals in the hyperacute phase before the initiation of ART, suggesting that even ART initiated during the onset of viremia does not abrogate all HIV-induced immune changes. In early treated individuals, time to viral load suppression correlated positively with plasma CXCL13 at the early chronic phase (rho = 0.83, P = 0.042). Levels of CXCL13 during the untreated hyperacute phase correlated inversely with blood eosinophils (rho = − 0.89, P < 0.001), basophils (rho = − 0.87, P = 0.001) and lymphocytes (rho = − 0.81, P = 0.005), suggesting their trafficking into tissues. Hyperacute HIV infection before the initiation of ART was associated with a transient increase in monocytes ( P < 0.001), decreased lymphocytes ( P = 0.011) and eosinophils ( P = 0.003) at Fiebig stages I–II, and decreased eosinophils ( P < 0.001) and basophils ( P = 0.007) at Fiebig stages III–V. In untreated AHI, virus replicative capacity correlated positively with IP-10 (rho = 0.84, P < 0.001) and IFN-alpha (rho = 0.59, P = 0.045) and inversely with nadir CD4 + T cell counts (rho = − 0.58, P = 0.048). Initiation of ART during Fiebig stages I–II abrogated the cytokine storm. Untreated AHI was associated with a cytokine storm of 12 out of the 33 cytokines analyzed. Complete blood counts were determined before and immediately following AHI detection before ART initiation. Gag-protease-driven replicative capacities of the transmitted/founder viruses were determined using a green fluorescent reporter T cell assay. Methodsīlood cytokine levels were measured using Luminex and ELISA assays pre-infection, during the hyperacute infection phase (before or at peak viremia, 1–11 days after the first detection of viremia), after peak viremia (24–32 days), and during the early chronic phase (77–263 days). We assessed the plasma cytokines kinetics, and their associations with virological and immunological parameters, in a well-characterized AHI cohort where participants were diagnosed before peak viremia. However, studies on the earliest HIV-induced immunological changes are limited, particularly in sub-Saharan Africa. Immunological damage in acute HIV infection (AHI) may predispose to detrimental clinical sequela.
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |