Together this difference in types of T-cell-dependent t1IFN immunity for different <i>Cryptococcus</i> species suggests a possible mechanism by which HIV infection may select against <i>C. gattii</i> but not <i>C. neoformans</i><b>IMPORTANCE</b><i>Cryptococcus neoformans</i> and <i>Cryptococcus gattii</i> cause fatal infection in immunodeficient and immunocompetent individuals.
Up to date only one IFNα subtype (IFNα2) is being used in clinical treatment against chronic virus infections, however its therapeutic success rate is rather limited, especially during Human Immunodeficiency Virus (HIV) infection.
The inclusion criteria for patients were as follows: (1) treatment-naive and treated with PEG IFN-α/RBV, (2) HCV RNA was present in serum for over 6 months before treatment, (3) negative for hepatitis B (HBV) or HIV infection and (4) lacked any other hepatic diseases.All participants in this study were Chinese Han population and infected with HCV genotype 1b and treated with subcutaneous PEG IFN-α at a dose of 180 µg once a week with the addition of 800-1000 mg/d RBV according to weight orally for 48 weeks.
In chronic diseases, such as HIV infection, plasmacytoid dendritic cells (pDCs) are rendered dysfunctional, as measured by their decreased capacity to produce IFN-α.
We evaluated the mechanism through which HIV-activated pDCs produce IFN as well as how both monoclonal HIV-specific Abs and Abs produced in natural HIV infection modulated normal pDC sensing of HIV.
Using multiple cell systems, including reporter cell lines and activated peripheral blood lymphocytes (PBLs), we show that recombinant IFNɛ impairs HIV infection at stage(s) post HIV entry and up to the translation of viral proteins.
These findings indicate that coinfection is associated with a type 1 IFN monocyte activation profile which was further found to correlate with cognitive impairment, even in subjects with controlled HIV infection.
Given that IFN-λ mediates anti-HIV-1 activity, the protective role of IL28B polymorphisms was examined in 29 seronegative individuals at risk for HIV-infection and in 68 HIV-positive carriers with and without rapid progression of immunodeficiency.
Additionally, the response of NK cells to direct IFN-alpha stimulation was defective in viremic HIV infection, and this defect was not attributable to diminished IFN-alpha receptor expression, though IFN-alpha receptor and NKP30 expression was closely associated with killer activity in viremic HIV infection but not in healthy controls.
We developed a real-time PCR assay to simultaneously measure the mRNA level of type I interferon (IFN) receptor (IFNAR) components in peripheral blood cells of children with chronic immune stimulation due to HIV infection.
Despite the marked reduction of HIV-1 propagation by IFN genes or by negative Tat and Rev transdominants, the gene therapy using soluble CD4 immunoadhesin or anti-gp41 was a more efficient preventive treatment against HIV infection.
Four hypotheses have been presented that suggested that: a) al-IFN-alpha may be a product of a distinct IFN gene; b) or a posttranscriptionally modified IFN-alpha molecule; c) the phenomenon of al-IFN-alpha may be an effect of synergistic action of a mixture of acid-stable IFN-alpha and acid-labile IFN-gamma; d) or the effect may be a result of an interaction of acid-stable IFN-alpha with an unknown factor(s) present in plasma and associated with progression of HIV infection or autoimmune diseases.