Relevance of Gamma Interferon, Tumor Necrosis Factor Alpha, and Interleukin-10 Gene Polymorphisms to Susceptibility to Mediterranean Spotted Fever

Forte, Giusi Irma; Scola, Letizia; Misiano, Gabriella; Milano, Salvatore; Mansueto, Pasquale; Vitale, Giustina; Bellanca, F.; Sanacore, Maria; Vaccarino, Loredana; Rini, Giovan Battista; Caruso, Calogero; Cillari, Enrìco; Lio, Domenico; Mansueto, S

doi:10.1128/cvi.00121-09

Cited by 24 publications

(20 citation statements)

References 41 publications

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“…Our results support some studies’ results which found that the number of TT genotype individuals was significantly elevated when compared to TA genotype subjects . Bouzgarrou et al .…”

Section: Discussionsupporting

confidence: 92%

Association of interferon gamma gene polymorphism and susceptibility to hepatitis C virus infection in Egyptian patients: A multicenter, family‐based study

et al. 2017

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Background and AimPolymorphisms in some genes may influence the persistence of hepatitis C virus (HCV) infection, clinical outcome, HCV replication, and liver damage. This study was conducted to investigate the role of the interferon gamma (IFN‐γ) gene at (+874 T/A, −764 G/C, −179 C/A) single‐nucleotide polymorphisms (SNPs) and its receptor (IFN‐γR2) at (rs 2786067 A/C) SNP in the susceptibility of Egyptian families to HCV infection with high‐resolution techniques.MethodsIn total, 517 Egyptian families, with 2246 subjects, were recruited to this study from the Upper and Lower Egypt governorates and were classified into three groups: 1034 patients with chronic hepatitis C virus, 108 subjects with spontaneous virus clearance (SVC), and 1104 subjects as a healthy control group. All subjects were genotyped for (+874 T/A, rs2430561, −764 G/C, rs2069707, −179 C/A, rs2069709, and rs 27860067, A/C) SNPs of the IFN‐γ gene using the allelic discrimination real‐time polymerase chain reaction technique and were confirmed using sequence‐based typing.ResultsThe carriage of T allele of (+874) IFN‐γ is a risky allele and was significantly higher in chronic hepatitis C more than other two groups (odds ratio [OR]: 2.6646, P < 0.0002). On the other hand, the C allele of (−764, rs2069707) is a protective allele and was higher in SVC than the other two groups (OR: 0.2709, P < 0.0001). However, both (−179 C/A, rs 2069709) and (rs 27860067, A/C) SNPs are not polymorphic enough to be studied in the Egyptian population.ConclusionsHCV infection is associated with the T allele of (+874 rs2430561), while SVC of HCV is associated with the C allele of (−764, rs2069707) of the IFN‐γ gene.

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“…Our results support some studies’ results which found that the number of TT genotype individuals was significantly elevated when compared to TA genotype subjects . Bouzgarrou et al .…”

Section: Discussionsupporting

confidence: 92%

Association of interferon gamma gene polymorphism and susceptibility to hepatitis C virus infection in Egyptian patients: A multicenter, family‐based study

et al. 2017

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“…274, 275 Nonetheless, even in an environment so different from that in which humans evolved, multiple studies have identified associations between patterns of increased inflammation observed in MDD and improved outcome in the context of infection, 3, 4, 5, 50, 276, 277, 278, 279, 280, 281, 282, 283, 284, 285, 286, 287, 288, 289, 290 as shown in Table 3.…”

Section: Patterns Of Immune Activation In Mdd and Protection From Infmentioning

confidence: 99%

The evolutionary significance of depression in Pathogen Host Defense (PATHOS-D)

2012

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Given the manifold ways that depression impairs Darwinian fitness, the persistence in the human genome of risk alleles for the disorder remains a much debated mystery. Evolutionary theories that view depressive symptoms as adaptive fail to provide parsimonious explanations for why even mild depressive symptoms impair fitness-relevant social functioning, whereas theories that suggest that depression is maladaptive fail to account for the high prevalence of depression risk alleles in human populations. These limitations warrant novel explanations for the origin and persistence of depression risk alleles. Accordingly, studies on risk alleles for depression were identified using PubMed and Ovid MEDLINE to examine data supporting the hypothesis that risk alleles for depression originated and have been retained in the human genome because these alleles promote pathogen host defense, which includes an integrated suite of immunological and behavioral responses to infection. Depression risk alleles identified by both candidate gene and genome-wide association study (GWAS) methodologies were found to be regularly associated with immune responses to infection that were likely to enhance survival in the ancestral environment. Moreover, data support the role of specific depressive symptoms in pathogen host defense including hyperthermia, reduced bodily iron stores, conservation/withdrawal behavior, hypervigilance and anorexia. By shifting the adaptive context of depression risk alleles from relations with conspecifics to relations with the microbial world, the Pathogen Host Defense (PATHOS-D) hypothesis provides a novel explanation for how depression can be nonadaptive in the social realm, whereas its risk alleles are nonetheless represented at prevalence rates that bespeak an adaptive function.

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“…Many variations within the IFN‐ γ gene have been shown to be associated with disease (Table ) . These associations may be related to expression of the IFN‐ γ gene.…”

Section: Ifn‐γ Genetic Variation and Diseasementioning

confidence: 99%

Clinical implications of interferon‐γ genetic and epigenetic variants

Smith

Denning

2014

Immunology

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Summary Interferon‐γ (IFN‐γ) is an integral and critical molecule of the immune system, with multiple functions, mostly related to the T helper type 1 (Th1) response to infection. It is critical for defence against mycobacterial infection and is of increasing interest in defence against fungi. In this article, we review the genetic and epigenetic variants affecting IFN‐γ expression and investigate its role in disease, with an emphasis on fungal diseases such as invasive and chronic pulmonary aspergillosis. Over 347 IFN‐γ gene variants have been described, in multiple ethnic populations. Many appear to confer a susceptibility to disease, especially tuberculosis (TB) and hepatitis, but also some non‐infectious conditions such as aplastic anaemia, cervical cancer and psoriasis. Several epigenetic modifications are also described, increasing IFN‐γ expression in Th1 lymphocytes and reducing IFN‐γ expression in Th2 lymphocytes. Recombinant IFN‐γ administration is licensed for the prophylaxis of infection (bacterial and fungal) in patients with the phagocyte functional deficiency syndrome chronic granulomatous disease, although the benefits appear limited. Interferon‐γ therapy is given to patients with profound defects in IFN‐γ and interleukin‐12 production and appears to be beneficial for patients with invasive aspergillosis and cryptococcal meningitis, but the studies are not definitive. A high proportion of patients with chronic pulmonary aspergillosis are poor producers of IFN‐γ in response to multiple stimuli and could also benefit from IFN‐γ administration. The investigation and management of patients with possible or demonstrated IFN‐γ deficiency in adulthood is poorly studied and could be greatly enhanced with the integration of genetic data.

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Relevance of Gamma Interferon, Tumor Necrosis Factor Alpha, and Interleukin-10 Gene Polymorphisms to Susceptibility to Mediterranean Spotted Fever

Cited by 24 publications

References 41 publications

Association of interferon gamma gene polymorphism and susceptibility to hepatitis C virus infection in Egyptian patients: A multicenter, family‐based study

Association of interferon gamma gene polymorphism and susceptibility to hepatitis C virus infection in Egyptian patients: A multicenter, family‐based study

The evolutionary significance of depression in Pathogen Host Defense (PATHOS-D)

Clinical implications of interferon‐γ genetic and epigenetic variants

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