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Viruses Jun 2011A myriad of factors favor the emergence and re-emergence of arthropod-borne viruses (arboviruses), including migration, climate change, intensified livestock production,... (Review)
Review
A myriad of factors favor the emergence and re-emergence of arthropod-borne viruses (arboviruses), including migration, climate change, intensified livestock production, an increasing volume of international trade and transportation, and changes to ecosystems (e.g., deforestation and loss of biodiversity). Consequently, arboviruses are distributed worldwide and represent over 30% of all emerging infectious diseases identified in the past decade. Although some arboviral infections go undetected or are associated with mild, flu-like symptoms, many are important human and veterinary pathogens causing serious illnesses such as arthritis, gastroenteritis, encephalitis and hemorrhagic fever and devastating economic loss as a consequence of lost productivity and high mortality rates among livestock. One of the most consistent molecular features of emerging arboviruses, in addition to their near exclusive use of RNA genomes, is the inclusion of viral, non-structural proteins that act as interferon antagonists. In this review, we describe these interferon antagonists and common strategies that arboviruses use to counter the host innate immune response. In addition, we discuss the complex interplay between host factors and viral determinants that are associated with virus emergence and re-emergence, and identify potential targets for vaccine and anti-viral therapies.
Topics: Animals; Arbovirus Infections; Arboviruses; Humans; Interferons; Viral Nonstructural Proteins
PubMed: 21994750
DOI: 10.3390/v3060629 -
Cells Mar 2021As highlighted by the COVID-19 global pandemic, elderly individuals comprise the majority of cases of severe viral infection outcomes and death. A combined inability to... (Review)
Review
As highlighted by the COVID-19 global pandemic, elderly individuals comprise the majority of cases of severe viral infection outcomes and death. A combined inability to control viral replication and exacerbated inflammatory immune activation in elderly patients causes irreparable immune-mediated tissue pathology in response to infection. Key to these responses are type I, II, and III interferons (IFNs), which are involved in inducing an antiviral response, as well as controlling and suppressing inflammation and immunopathology. IFNs support monocyte/macrophage-stimulated immune responses that clear infection and promote their immunosuppressive functions that prevent excess inflammation and immune-mediated pathology. The timing and magnitude of IFN responses to infection are critical towards their immunoregulatory functions and ability to prevent immunopathology. Aging is associated with multiple defects in the ability of macrophages and dendritic cells to produce IFNs in response to viral infection, leading to a dysregulation of inflammatory immune responses. Understanding the implications of aging on IFN-regulated inflammation will give critical insights on how to treat and prevent severe infection in vulnerable individuals. In this review, we describe the causes of impaired IFN production in aging, and the evidence to suggest that these impairments impact the regulation of the innate and adaptive immune response to infection, thereby causing disease pathology.
Topics: Adaptive Immunity; Aged; Aging; COVID-19; Humans; Immunity, Innate; Inflammation; Interferon Type I; Interferon-gamma; Interferons; SARS-CoV-2; Virus Replication; Interferon Lambda; COVID-19 Drug Treatment
PubMed: 33806810
DOI: 10.3390/cells10030708 -
Effect and safety of interferon for hepatocellular carcinoma: a systematic review and meta-analysis.PloS One 2013The effect of interferon(IFN) in the management of hepatocellular carcinoma (HCC) remains controversial, and no clear recommendations have been proposed. (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
The effect of interferon(IFN) in the management of hepatocellular carcinoma (HCC) remains controversial, and no clear recommendations have been proposed.
OBJECTIVES
To evaluate the effect and safety of IFN for HCC.
METHODS
PubMed, OvidSP, and Cochrane Library were searched from their establishment date until August 30, 2012. Studies that met the inclusion criteria were systematically evaluated and then subjected to meta-analysis.
RESULTS
Thirteen randomized control trials (RCTs) involving 1344 patients were eligible for this study. When IFN was used as an adjuvant therapy for HCC patients after curative therapy, the meta-analysis showed that IFN reduced the 1-, 2-, 3-, 4-, and 5-year recurrence rates. Subgroup analysis showed that IFN reduced the 2-, 3-, 4-, and 5-year recurrence rates of hepatitis C viral (HCV)-related HCC. The effect of IFN for on hepatitis B virus(HBV)-related HCC patients could not be determined because of isufficient data. After surgical resection, adjuvant IFN therapy reduced the 4- and 5- recurrence rates. All studies reported that IFN could not improve the overall survival of HCV-realated HCC patients after curative therapies. Only one study showed that IFN was associated with better overall survival in HCC patients after curative therapy and subgroup of HCC patients after surgical resection. Thus, meta-analysis was not performed. Different treatment options were used as control to study the effect of IFN for intermediate and advanced HCC patients, thus meta-analysis was not appropriate. All included studies, except for one, reported that IFN treatment was well tolerated.
CONCLUSIONS
After curative therapies, adjuvant IFN reduced the recurrence of HCC. IFN did not improve the survival of HCV-related HCC patients after curative therapy. Whether IFN is effective for intermediate and advanced HCC patients could not be determined because of insufficient data. The toxicity of IFN was acceptable.
Topics: Animals; Carcinoma, Hepatocellular; Humans; Interferons; Liver Neoplasms
PubMed: 24069133
DOI: 10.1371/journal.pone.0061361 -
World Journal of Gastroenterology Apr 2023The tremendous public health and economic impact of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has... (Review)
Review
The tremendous public health and economic impact of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has become a huge challenge globally. There is increasing evidence that SARS-CoV-2 induces intestinal infections. Type III interferon (IFN-λ) has an antiviral role in intestinal infection, with focused, long-lasting, and non-inflammatory characteristics. This review presents a summary of the structure of SARS-CoV-2, including its invasion and immune escape mechanisms. Emphasis was placed on the gastrointestinal impact of SARS-CoV-2, including changes to the intestinal microbiome, activation of immune cells, and inflammatory responses. We also describe the comprehensive functions of IFN-λ in anti-enteric SARS-CoV-2 infection, and discuss the potential application of IFN-λ as a therapeutic agent for COVID-19 with intestinal symptoms.
Topics: Humans; COVID-19; Interferon Lambda; SARS-CoV-2; Interferons; Antiviral Agents
PubMed: 37155525
DOI: 10.3748/wjg.v29.i13.1942 -
Cytokine & Growth Factor Reviews Apr 2015Interferons (IFN) are key cytokines with multifaceted antiviral and cell-modulatory properties. Three distinct types of IFN are recognized (I-III) based on structural... (Review)
Review
Interferons (IFN) are key cytokines with multifaceted antiviral and cell-modulatory properties. Three distinct types of IFN are recognized (I-III) based on structural features, receptor usage, cellular source and biological activities. The action of IFNs is mediated by a complex, partially overlapping, transcriptional program initiated by the interaction with specific receptors. Genetic diversity, with polymorphisms and mutations, can modulate the extent of IFN responses and the susceptibility to infections. Almost all viruses developed mechanisms to subvert the IFN response, involving both IFN induction and effector mechanisms. Interactions between IFN types may occur, for both antiviral and cell-modulatory effects, in a complex interplay, involving both synergistic and antagonistic effects. Interferon-associated diseases, not related to virus infections may occur, some of them frequently observed in IFN-treated patients. On the whole, IFNs are pleiotropic biologic response modifiers, that, upon activation of thousands genes, induce a broad spectrum of activities, regulating cell cycle, differentiation, plasma membrane molecules, release of mediators, etc., that can be relevant for cell proliferation, innate and adaptive immunity, hematopoiesis, angiogenesis and other body functions.
Topics: Antiviral Agents; Cell Differentiation; Cell Proliferation; Genetic Variation; Humans; Interferon Type I; Interferon-gamma; Interferons; Receptor, Interferon alpha-beta; Signal Transduction; Transcriptional Activation; Virus Diseases
PubMed: 25466633
DOI: 10.1016/j.cytogfr.2014.10.011 -
Journal of Virology Mar 2015A major component of the protective antiviral host defense is contributed by the intracellular actions of the proteins encoded by interferon-stimulated genes (ISGs);... (Review)
Review
A major component of the protective antiviral host defense is contributed by the intracellular actions of the proteins encoded by interferon-stimulated genes (ISGs); among these are the interferon-induced proteins with tetratricopeptide repeats (IFITs), consisting of four members in human and three in mouse. IFIT proteins do not have any known enzyme activity. Instead, they inhibit virus replication by binding and regulating the functions of cellular and viral proteins and RNAs. Although all IFITs are comprised of multiple copies of the degenerate tetratricopeptide repeats, their distinct tertiary structures enable them to bind different partners and affect host-virus interactions differently. The recent use of Ifit knockout mouse models has revealed novel antiviral functions of these proteins and new insights into the specificities of ISG actions. This article focuses on human and murine IFIT1 and IFIT2 by reviewing their mechanisms of action, their critical roles in protecting mice from viral pathogenesis, and viral strategies to evade IFIT action.
Topics: Animals; Antiviral Agents; Gene Expression Regulation; Host-Pathogen Interactions; Humans; Immune Evasion; Interferons; Mice; Protein Biosynthesis; Proteins; Viruses
PubMed: 25428874
DOI: 10.1128/JVI.02744-14 -
Bacteriological Reviews Dec 1964
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Frontiers in Immunology 2022
Topics: Antiviral Agents; Hepacivirus; Interferons; Interferon Lambda
PubMed: 36189214
DOI: 10.3389/fimmu.2022.1030812 -
British Medical Journal Jan 1977
Topics: Humans; Interferon Inducers; Interferons; Virus Diseases; Virus Replication
PubMed: 832014
DOI: No ID Found -
BMC Infectious Diseases Sep 2009Interferon has been widely used in the treatment of genital warts for its immunomodulatory, antiproliferative and antiviral properties. Currently, no evidence that... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Interferon has been widely used in the treatment of genital warts for its immunomodulatory, antiproliferative and antiviral properties. Currently, no evidence that interferon improves the complete response rate or reduces the recurrence rate of genital warts has been generally provided. The aim of this review is to assess, from randomized control trials (RCTs), the efficacy and safety of interferon in curing genital warts.
METHODS
We searched Cochrane Sexually Transmitted Diseases Group's Trials Register (January, 2009), Cochrane Central Register of Controlled Trials (2009, issue 1), PubMed (1950-2009), EMBASE (1974-2009), Chinese Biomedical Literature Database (CBM) (1975-2009), China National Knowledge Infrastructure (CNKI) (1979-2009), VIP database (1989-2009), as well as reference lists of relevant studies. Two reviewers independently screened searched studies, extracted data and evaluated their methodological qualities. RevMan 4.2.8 software was used for meta-analysis
RESULTS
12 RCTs involving 1445 people were included. Among them, 7 studies demonstrated the complete response rate of locally-used interferon as compared to placebo for treating genital warts. Based on meta-analysis, the rate of Complete response of the two interventions differed significantly (locally-used interferon:44.4%; placebo:16.1%). The difference between the two groups had statistical significance (RR 2.68, 95% CI 1.79 to 4.02, P < 0.00001). 5 studies demonstrated the complete response rate of systemically-used interferon as compared to placebo for treating genital warts. Based on meta-analysis, the rate of Complete response of the two interventions had no perceivable discrepancy (systemically-used interferon:27.4%; placebo:26.4%). The difference between the two groups had no statistical significance (RR1.25, 95% CI 0.80 to 1.95, P > 0.05). 7 studies demonstrated the recurrence rate of interferon as compared to placebo for treating genital warts. Based on meta-analysis, the recurrence rate of the two interventions had no perceivable discrepancy(interferon 21.1%; placebo: 34.2%). The difference between the two groups had no statistical significance (RR0.56, 95% CI 0.27 to 1.18, P > 0.05). However, subgroup analysis showed that HPV-infected patients with locally administered interferon were less likely than those given placebo to relapse, but that no significant difference in relapse rates was observed between systemic and placebo. The reported adverse events of interferon were mostly mild and transient, which could be well tolerated.
CONCLUSION
Interferon tends to be a fairly well-tolerated form of therapy. According to different routes of administration, locally-used interferon appears to be much more effective than both systemically-used interferon and placebo in either improving the complete response rate or reducing the recurrence rate for the treatment of genital warts.
Topics: Condylomata Acuminata; Humans; Interferons; Papillomavirus Infections; Randomized Controlled Trials as Topic; Recurrence; Treatment Outcome
PubMed: 19772554
DOI: 10.1186/1471-2334-9-156