Association of Single-Nucleotide Polymorphisms in<i>IL28B,</i>but Not<i>TNF-α,</i>With Severity of Disease Caused by Andes Virus

Angulo, Jenniffer; Pino, Karla; Echeverría, Natalia; Marco, C; Martínez-Valdebenito, Constanza; Galeno, H.; Villagra, Eliecer; Vera, Lilian; Lagos, Natalia; Becerra, Natalia; Mora, Judith; Bermúdez, Andrea K. Hurtado; Cárcamo, Marcela; Díaz, Janepsy; Miquel, Juan Francisco; Ferrés, Marcela; López-Lastra, Marcelo

doi:10.1093/cid/civ830

Cited by 18 publications

(13 citation statements)

References 47 publications

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“…In influenza virus infection, IFNL4 SNP rs8099917 was associated with increased sero-conversion after influenza vaccination (Egli et al, 2014a). IFNL4 variants have also been associated with bronchiolitis (Scagnolari et al, 2012), cytomegalovirus (Egli et al, 2014b) and Andes virus (Angulo et al, 2015) infections. These observations suggest that IFNL4 possibly plays a role in many viral infections and immune related diseases in the liver and other organs.…”

Section: Discussionmentioning

confidence: 99%

Interferon lambda 4 impacts the genetic diversity of hepatitis C virus

Ansari

Aranday-Cortes

Clc.

et al. 2019

eLife

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Hepatitis C virus (HCV) is a highly variable pathogen that frequently establishes chronic infection. This genetic variability is affected by the adaptive immune response but the contribution of other host factors is unclear. Here, we examined the role played by interferon lambda-4 (IFN-λ4) on HCV diversity; IFN-λ4 plays a crucial role in spontaneous clearance or establishment of chronicity following acute infection. We performed viral genome-wide association studies using human and viral data from 485 patients of white ancestry infected with HCV genotype 3a. We demonstrate that combinations of host genetic variants, which determine IFN-λ4 protein production and activity, influence amino acid variation across the viral polyprotein - not restricted to specific viral proteins or HLA restricted epitopes - and modulate viral load. We also observed an association with viral di-nucleotide proportions. These results support a direct role for IFN-λ4 in exerting selective pressure across the viral genome, possibly by a novel mechanism.

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Section: Discussionmentioning

confidence: 99%

Interferon lambda 4 impacts the genetic diversity of hepatitis C virus

Ansari

Aranday-Cortes

Clc.

et al. 2019

eLife

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“…The mechanisms that lead to the varied severity in infected patients with HFRS has not yet been fully clarified. Host‐ and virus‐specific factors are considered to contribute to the severity of the disease, such as single nucleotide polymorphisms in IL28B, vaccination, etc . Disease cases caused by PUUV and DOBV are known to be clinically milder than those by SNV or HTNV infection .…”

Section: Discussionmentioning

confidence: 99%

Hemorrhagic fever with renal syndrome caused by Hantaan virus infection in four pregnant Chinese women

Zhao

Liu

et al. 2017

Journal of Medical Virology

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Hantavirus infection during pregnancy can influence both maternal and fetal outcomes. Here, we describe four cases of hemorrhagic fever with renal syndrome (HFRS) in pregnant Chinese women. The HFRS put these women at increased risk for severe illness, despite the patients' symptomologies in the onset phase were similar to those observed in non-pregnant HFRS patients, such as fever, headache, nausea, and thrombocytopenia. Pregnant women appeared to have a more severe status, presenting with severe complications, such as hypervolemia and pulmonary edema. Nevertheless, with appropriate management, mothers with HFRS may carry to full-term and breastfeeding maybe safe and feasible.

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“…de Sa et al reported that the major alleles of IFNL3 SNPs (rs12979860 CC and rs8099917 TT) are associated with a shift in the Th1/ Th2 immune response toward a Th1 response (172). The Andes virus causes a hantavirus cardiopulmonary syndrome; in a cohort of Andes virus-infected patients, the minor alleles of rs12979860 and rs8099917 (TT and GG) were linked to milder disease compared to CT/CC and TG/TT (86).…”

Section: Borrelia Burgdorferimentioning

confidence: 99%

Interferon Lambda: Modulating Immunity in Infectious Diseases

2017

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Interferon lambdas (IFN-λs; IFNL1-4) modulate immunity in the context of infections and autoimmune diseases, through a network of induced genes. IFN-λs act by binding to the heterodimeric IFN-λ receptor (IFNLR), activating a STAT phosphorylation-dependent signaling cascade. Thereby hundreds of IFN-stimulated genes are induced, which modulate various immune functions via complex forward and feedback loops. When compared to the well-characterized IFN-α signaling cascade, three important differences have been discovered. First, the IFNLR is not ubiquitously expressed: in particular, immune cells show significant variation in the expression levels of and susceptibilities to IFN-λs. Second, the binding affinities of individual IFN-λs to the IFNLR varies greatly and are generally lower compared to the binding affinities of IFN-α to its receptor. Finally, genetic variation in the form of a series of single-nucleotide polymorphisms (SNPs) linked to genes involved in the IFN-λ signaling cascade has been described and associated with the clinical course and treatment outcomes of hepatitis B and C virus infection. The clinical impact of IFN-λ signaling and the SNP variations may, however, reach far beyond viral hepatitis. Recent publications show important roles for IFN-λs in a broad range of viral infections such as human T-cell leukemia type-1 virus, rotaviruses, and influenza virus. IFN-λ also potentially modulates the course of bacterial colonization and infections as shown for Staphylococcus aureus and Mycobacterium tuberculosis. Although the immunological processes involved in controlling viral and bacterial infections are distinct, IFN-λs may interfere at various levels: as an innate immune cytokine with direct antiviral effects; or as a modulator of IFN-α-induced signaling via the suppressor of cytokine signaling 1 and the ubiquitin-specific peptidase 18 inhibitory feedback loops. In addition, the modulation of adaptive immune functions via macrophage and dendritic cell polarization, and subsequent priming, activation, and proliferation of pathogen-specific T- and B-cells may also be important elements associated with infectious disease outcomes. This review summarizes the emerging details of the IFN-λ immunobiology in the context of the host immune response and viral and bacterial infections.

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Association of Single-Nucleotide Polymorphisms inIL28B,but NotTNF-α,With Severity of Disease Caused by Andes Virus

Abstract: The IL28B SNPs rs12979860 and rs8099917, but not TNF-α SNP rs1800629, are associated with the clinical outcome of ANDV-induced disease, suggesting a possible link between IL28B expression and ANDV pathogenesis.

Cited by 18 publications

References 47 publications

Interferon lambda 4 impacts the genetic diversity of hepatitis C virus

Interferon lambda 4 impacts the genetic diversity of hepatitis C virus

Hemorrhagic fever with renal syndrome caused by Hantaan virus infection in four pregnant Chinese women

Interferon Lambda: Modulating Immunity in Infectious Diseases

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