In medicine, immunodeficiency (or immune deficiency) is a state in which the immune system's ability to fight infectious disease is compromised or entirely absent. Most cases of immunodeficiency are either congenital or acquired. A person who has an immunodeficiency is said to be immunocompromised. An immunocompromised person is very vulnerable to opportunistic infections.

Congenital (or Primary) immune deficiency

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A number of rare diseases feature a heightened susceptibility to infections from childhood onward. Many of these disorders are hereditary and autosomal recessive. Examples include myeloperoxidase deficiency, Wiskott-Aldrich syndrome, chronic granulomatous disease, and severe combined immunodeficiency.

Acquired immune deficiency

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Although elderly people are generally more susceptible to infections, this can be increased in the presence of a number of blood disorders (see hematology); important examples are multiple myeloma and chronic lymphatic leukemia (CLL).

More on [ Immunodeficiency ]

pubmed: 1359-6535

Entecavir versus lamivudine in the treatment of chronic hepatitis B patients with hepatic decompensation.
Hsu YC, Mo LR, Chang CY, Perng DS, Tseng CH, Lo GH, Tai CM, Lin CW, Hsu CC, Hsu CY, Huang SC, Lin JT Entecavir versus lamivudine in the treatment of chronic hepatitis B patients with hepatic decompensation. Antivir Ther. 2011 Dec 20; Authors: Hsu YC, Mo LR, Chang CY, Perng DS, Tseng CH, Lo GH, Tai CM, Lin CW, Hsu CC, Hsu CY, Huang SC, Lin JT Abstract BACKGROUND: Lamivudine has been widely used in chronic hepatitis B patients with hepatic decompensation, but its use is limited by drug resistance. This outcome research aimed to investigate the comparative efficacy and safety of entecavir versus lamivudine in decompensated patients. METHODS: Between November 2004 and February 2010, 126 consecutive treatment-naive patients received either entecavir (n=53) or lamivudine (n=73) for decompensated chronic hepatitis B. All patients presented with both hyperbilirubinaemia and coagulopathy. Primary outcome was mortality within 1 year; secondary outcomes included liver-related mortality, biochemical and virological response, and improvement of hepatic dysfunction. RESULTS: Both treatment groups were comparable in baseline characteristics. A total of 19 (35.8%) entecavir and 33 (45.2%) lamivudine receivers expired within 1 year, respectively (P=0.29, log rank test). Age (hazard ratio [HR] 1.04 per year, 95% CI 1.01, 1.06), cirrhosis (HR 2.07, 95% CI 1.02, 4.23), and international normalized ratio for prothrombin time (HR 1.44, 95% CI 1.20, 1.74) were independent baseline predictors for all-cause mortality. Antiviral therapy was also unrelated to liver-specific death. However, more patients taking entecavir tended to attain aminotransferase normalization (76.5% versus 52.5%; P=0.05) and viral DNA undetectability (100% versus 58.3%; P=0.06). Moreover, entecavir was associated with significantly greater reduction of the model for end-stage liver disease scores (median 10.0 versus 4.3; P=0.02). Overall, 3 (7.5%) lamivudine but no entecavir users acquired drug resistance in 1 year (P=0.25). CONCLUSIONS: Entecavir as compared with lamivudine is similar in the effect on short-term mortality but is associated with greater clinical improvement among chronic hepatitis survivors who recovered from hepatic decompensation. PMID: 22301517 [PubMed - as supplied by publisher]
Interleukin 28B genetic polymorphisms and viral factors help identify HCV genotype-1 patients who benefit from 24-week pegylated interferon plus ribavirin therapy.
Liu CH, Liang CC, Liu CJ, Tseng TC, Lin CL, Yang SS, Su TH, Hsu SJ, Lin JW, Chen JH, Chen PJ, Chen DS, Kao JH Interleukin 28B genetic polymorphisms and viral factors help identify HCV genotype-1 patients who benefit from 24-week pegylated interferon plus ribavirin therapy. Antivir Ther. 2011 Dec 20; Authors: Liu CH, Liang CC, Liu CJ, Tseng TC, Lin CL, Yang SS, Su TH, Hsu SJ, Lin JW, Chen JH, Chen PJ, Chen DS, Kao JH Abstract BACKGROUND: Interleukin 28B (IL28B) single nucleotide polymorphism (SNP) genotypes and viral factors can predict sustained virological response (SVR) in HCV genotype-1 (HCV-1) patients receiving 48 weeks of pegylated interferon and ribavirin. Whether these factors would identify those patients who can benefit from a shorter duration of therapy remains unclear. METHODS: Treatment-naive HCV-1 patients (n=662) receiving 24 or 48 weeks of combination therapy were enrolled. Baseline demographic data, HCV viral load, IL28B SNP genotypes (rs8099917), duration of therapy and rapid virological response (RVR) were evaluated to predict SVR. The SVR rates were further stratified by the independent factors and compared. RESULTS: The IL28B rs8099917 TT genotype, low baseline viral load (HCV RNA≤600,000 IU/ml), RVR and 48-week therapy independently predicted SVR. In RVR patients with the IL28B rs8099917 TT genotype, the SVR rate of 24-week therapy was comparable to 48-week therapy (95% versus 99%; P=0.21) at low baseline viral load, but was inferior to 48-week therapy (70% versus 97%; P<0.001) at high baseline viral load. In non-RVR patients, the SVR rate of 24-week therapy was inferior to 48-week therapy for those with the IL28B rs8099917 TT genotype but high baseline viral load (23% versus 62%; P<0.001), and those with the IL28B rs8099917 GT/GG genotype but low baseline viral load (0% versus 33%; P=0.02). CONCLUSIONS: HCV-1 patients simultaneously bearing the IL28B rs8099917 TT genotype, low baseline viral load and RVR can benefit from a shorter duration of combination therapy. PMID: 22301466 [PubMed - as supplied by publisher]
Evolution of HIV-1 genotype in plasma RNA and peripheral blood mononuclear cells proviral DNA after interruption and resumption of antiretroviral therapy.
Imaz A, Olmo M, Peñaranda M, Gutiérrez F, Romeu J, Larrousse M, Domingo P, Oteo JA, Niubó J, Curto J, Vilallonga C, Masiá M, López-Aldeguer J, Iribarren JA, Podzamczer D, Evolution of HIV-1 genotype in plasma RNA and peripheral blood mononuclear cells proviral DNA after interruption and resumption of antiretroviral therapy. Antivir Ther. 2011 Dec 19; Authors: Imaz A, Olmo M, Peñaranda M, Gutiérrez F, Romeu J, Larrousse M, Domingo P, Oteo JA, Niubó J, Curto J, Vilallonga C, Masiá M, López-Aldeguer J, Iribarren JA, Podzamczer D, Abstract BACKGROUND: Structured antiretroviral therapy interruption (TI) is discouraged because of poorer AIDS and non-AIDS-related outcomes, but is often inevitable in clinical practice. Certain strategies could reduce the emergence of resistance mutations related to TI. METHODS: A total of 106 HIV-1-infected patients on stable HAART with undetectable plasma viral load were randomized to therapy continuation (n=50) or CD4(+) T-cell-guided TI (n=56). Staggered interruption involved stopping non-nucleoside reverse transcriptase inhibitors (NNRTIs) 7 days before the nucleoside backbone. Genotypic resistance testing (GRT) was performed on proviral DNA from peripheral blood mononuclear cells (PBMCs) at baseline and before each TI, and on plasma RNA after each TI. RESULTS: At baseline, GRT on PBMCs detected mutations in nine patients and only two major mutations were identified. GRT on plasma samples performed after TIs showed nucleoside reverse transcriptase inhibitors (NRTI), NNRTI and protease inhibitor major resistance associated mutations in 10/56, 3/46 and 1/8 patients receiving these drugs, respectively. Only in two patients had the same mutations been observed in GRT on PBMCs at baseline. Three patients presented virological failure after resumption of therapy, all receiving NNRTIs. In one of them, resistance mutations detected at failure had been also observed previously in GRT on plasma after TI. CONCLUSIONS: Staggered interruption of NNRTIs 7 days before the nucleoside backbone does not avoid resistance emergence completely, but does not necessarily lead to virological failure after treatment resumption. Plasma HIV-1 RNA genotype after the interruption and the patient's treatment history seem to be more useful than baseline proviral DNA genotype to assess the risk of virological failure after restarting therapy. PMID: 22301439 [PubMed - as supplied by publisher]
Multiclass primary antiretroviral drug resistance in a patient presenting HIV-1/2 dual infection.
Castro E, Recordon-Pinson P, Cavassini M, Fleury H Multiclass primary antiretroviral drug resistance in a patient presenting HIV-1/2 dual infection. Antivir Ther. 2012 Jan 25; Authors: Castro E, Recordon-Pinson P, Cavassini M, Fleury H PMID: 22301389 [PubMed - as supplied by publisher]
Potent immune activation in chronic hepatitis C patients upon administration of an oral inducer of endogenous interferons that acts via Toll-like receptor 7.
Boonstra A, Liu BS, Groothuismink ZM, Bergmann JF, de Bruijne J, Hotho DM, Hansen BE, van Vliet AA, van de Wetering de Rooij J, Fletcher SP, Bauman LA, Rahimy M, Appleman JR, Freddo JL, Reesink HW, de Knegt RJ, Janssen HL Potent immune activation in chronic hepatitis C patients upon administration of an oral inducer of endogenous interf Subscribe to Immune_Deficiency RSS feed