Correlations between CD8⁺ T-cell functionalities and blood CD4⁺ T-cell counts or plasma viral loads during early chronic HIV-1 infections.

<p>a. Correlation between the CD8⁺ T-cell functionalities and blood CD4⁺T-cell counts or plasma viral load for triple producers (TP), double producers (DP), and single producers (SP) of Gag2-specific responses in early chronic HIV-1-infected individuals. b. Different functional HIV-specific CD8⁺ T cells associated with good clinical outcomes (good clinical outcomes indicated an inverse correlation between the magnitude of HIV-specific CD8⁺ T-cell responses and viral loads, or a positive correlation between the magnitude of HIV-specific CD8⁺ T-cell responses and CD4⁺ T-cell counts). Results from linear regression model analysis on the magnitude of eight HIV-peptide pool specific responses against blood CD4⁺ T-cell counts or plasma viral loads during early chronic HIV-1 infections. Each dot denoted a positive response for the function indicated at the bottom left.</p

Clinical characteristics of study subjects.

a<p>HIV duration refers to the time between HIV diagnosis and sampling date.</p

Comparison of the magnitudes of different functional HIV-specific CD8⁺ T cells between primary and early chronic phase of HIV infection.

<p>a. Gating scheme used for the identification of CD8⁺ T-cell responses. Data shown were from cells derived from one representative patient, stimulated with PMA and ionomycin. Initial gating was performed on lymphocytes in a forward scatter of FSC-A versus FSC-H, and then FSC vs SSC plot. CD3⁺ events were gated in the FSC versus CD3 plot prior to gating on CD3⁺CD8⁺ and CD3⁺CD4⁺ events. The resulting CD3⁺CD4^-CD8⁺ population was further gated based on positivity for each of 5 functional responses including IL-2, MIP-1β, CD107a, TNF-α and IFN-γ. b. The frequencies of five distinct functions (color coded as shown) in the total CD8⁺ T-cell response against the indicated HIV peptide mix (x-axis) within 55 HIV-infected MSM. c. Comparison of the magnitude of different functional HIV-specific CD8⁺ T cells between primary and early chronic infection groups. For simplicity, only significantly different populations were shown for Gag1, Gag2, Pol4, Pol5, Env2, Env3, Nef and Tat+Rev responses; no significant differences were identified for those functions not shown. The responses from 55 HIV-infected MSM were standardized so that the profiles could be compared irrespective of any frequency differences. Asterisks were placed above response pairs that were significantly different: ***p<0.001; **p<0.01 and *p<0.05. Each dot denoted a positive response for the function indicated at the bottom left. The box plots represented the 10th, 25th, 75th, and 90th percentiles.</p

Early adaptive humoral immune responses and virus clearance in humans recently infected with pandemic 2009 H1N1 influenza virus.

Few studies on the humoral immune responses in human during natural influenza infection have been reported. Here, we used serum samples from pandemic 2009 H1N1 influenza infected patients to characterize the humoral immune responses to influenza during natural infection in humans. We observed for the first time that the pandemic 2009 H1N1 influenza induced influenza A-specific IgM within days after symptoms onset, whereas the unit of IgG did not changed. The magnitude of influenza A-specific IgM antibodies might have a value in predicting the rate of virus clearance to some degree. However, the newly developed IgM was not associated with hemagglutination inhibition (HI) activities in the same samples but correlated with HI activities of subsequently collected sera which were mediated by IgG antibodies, indicating that IgM was critical for influenza infection and influences subsequent IgG antibody responses. These findings provide new important insights on the human immunity to natural influenza infection

Clonally diverse CD38⁺HLA-DR⁺CD8⁺ T cells persist during fatal H7N9 disease

Virus-specific CD8+ T cells are crucial during H7N9 influenza infection, but CD8+ T cell dysfunction is associated with poor prognosis. Here, the authors use molecular and phenotypic analysis to establish persistence of clonally diverse CD8+ T cell populations during fatal infection