Sentence examples for modulation of hiv from inspiring English sources

APOBEC3G expression is regulated in different CD4+ T-helper cells and is critical for modulation of HIV infectivity [ 32, 33].

A recent study identified more than 300 genome-wide significant single-nucleotide polymorphisms within the major histocompatibility complex, and the data implied that HLA viral peptide interaction was a major factor in the modulation of HIV infections.

The prevalence of single helminthiases per country was obtained by averaging all surveys; data obtained on HIV-seropositive individuals were not included in the analyses because of the known modulation of HIV on the susceptibility on helminth-based infections [ 1, 9, 10].

To investigate the mechanisms of modulation of HIV-1 replication by TLR ligands, we further focused on two ligands that affect HIV in opposite ways: flagellin and ODN M362.

Several recent studies have demonstrated progress in expanding the pool of target genes and understanding the functional correlates of gene modulation to HIV-1 pathogenesis in vivo.

Apart from their direct anti-HIV-1 effect[8] [10]–[10], α-defensins1-3 display multiple immunostimulatory activities[11], including chemoattraction of naive T cells and immature dendritic cells (imDCs)[12], induction of cytokine and chemokine production[13] [15] and modulation of the expression of HIV receptors and coreceptors [16].

Although those studies provided an important insight into modulation of autophagy within HIV-1-infected cells, the fact that only a fraction of cells in vivo are estimated to be infected stresses the importance of determining whether HIV-1 inhibits autophagy in bystander cells.

Could the modulation of apoptosis induced by HIV-1 (rather than the infection by HIV-1 itself) provide some clinical benefit for the control of HIV-I-induced pathogenesis?

Our results, together with previous reports, suggest that KS regression in this setting is mediated by an overall improvement in immune function, modulation of cytokine expression, and control of HIV and HHV-8 replication, rather than by a direct specific antiangiogenic effect of antiretroviral therapy.

Although the supposed role of modulation of T helper responses in HIV pathogenesis remains controversial, a switch in the predominant response from Th1 to Th2 and the production of associated cytokines may facilitate disease progression [9], [10], [11].

This study presents new findings about the role of latent T. gondii infection in modulation of the immune responses during HIV infection.