@васьвась ну, очень примерно так.
Визуально данная история:
И как-то так:
The fact that HCV coinfection induces a higher level of immune activation in HIV-infected patients was inferred from comparison of immune activation levels in monoinfected and coinfected patients. Only the study by Gonzalez et al  has shown a decreased frequency of CD38 expression on CD8+ T cells among patients (n = 14) who achieved SVR. Our study assessed the medium-term (ie, 1 month after HCV treatment cessation) impact of HCV eradication due to interferon-free regimens on several parameters related to immune activation and immune recovery in a large group of HIV/HCV-coinfected patients.
In addition to a significant reduction in CD38 and HLA-DR expression on CD4+ and CD8+ T cells, there were decreases in levels of proviral HIV DNA, sCD14, microbial translocation markers, and D-dimers after the eradication of HCV infection. Although there were not quantitative correlations between the decrease in proviral HIV DNA load and the expression of HLA-DR and CD38 on both CD4+ and CD8+ T cells, it might be hypothesized that both events might be related. In HIV/HCVcoinfected patients, HCV eradication has proven to be beneficial not only in terms of the liver-related mortality rate and fibrosis regression, but also with regard to decreases in the frequencies of HIV disease progression, non–AIDS-related events, and non–liver-related mortality [26–30]. Almost certainly, a large proportion of this benefit is due to the reduction in the level of immune activation, given its key role in driving HIV-1 disease and non–AIDS-defining events in this population [31, 32]. By contrast, the expression of immune dysfunction (PD-1) and immune senescence (CD57) markers on both CD4+ and CD8+ T cells, as well as the IL-6 and hs-CRP plasma levels, did not change after SVR, suggesting that HCV has a limited or null influence on them in HIV/HCV-coinfected patients.
On the other hand, based on the adverse effect that HCV has on immune recovery among HIV-infected patients initiating ART [33–35], we hoped that the eradication of HCV would contribute to restoring immunologic parameters in these patients. However, the achievement of SVR did not translate into an increased CD4+ T-cell count, CD4+ T-cell percentage, or CD4+/ CD8+ T-cell ratio. In this regard, a limitation of our study may be the limited number of patients with very low CD4+ T-cell counts and CD4+/CD8+ T-cell ratios included in the study. It would be necessary to evaluate a larger sample of such patients to state with confidence that improvement in these parameters should not be expected in very immunosuppressed HIVinfected patients after the eradication of HCV. However, this is in concordance with results of a previous retrospective study by Saracino et al , in which SVR did not seem to alter the rate of long-term improvements in the CD4+ T-cell count and CD4+/ CD8+ T-cell ratio in HIV/HCV-coinfected patients receiving ART. This is particularly worrying in HIV-infected patients who did not achieve significant immune recovery despite consistent HIV suppression, since they have shown higher rates of morbidity and mortality due to AIDS-defining and non–AIDSdefining events .
Our study has other limitations, one of which is that the follow-up period was limited to 1 month after finishing HCV treatment. Data from a longer follow-up period would have reinforced the conclusions. However, the concordance between values at the end of treatment and those 1 month later allows us to be confident that these findings are immunologically relevant. Likewise, the inclusion of patients who did not achieve SVR would be very informative, but it would currently be very difficult to do so because of the elevated rate of response to the direct-acting antiviral agents.
In conclusion, our data suggest that the eradication of HCV infection in HIV/HCV-coinfected patients results in significant decreases not only in immune activation of CD4+ and CD8+ T cells, but also in levels of proviral HIV DNA, microbial translocation markers, sCD14, and D-dimers. It supports the use of HCV treatment in all HIV/HCV-coinfected patients regardless of fibrosis stage, with the sole exception of decompensated cirrhosis.