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  • image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    Authors: Gorczynski, Reginald M.;

    The type 1 membrane glycoprotein CD200, widely expressed on multiple cells/tissues, uses a structurally similar receptor (CD200R1), whose expression is more restricted to cells of the myeloid and lymphoid lineages, to transmit signals affecting responses in multiple physiological systems. Thus CD200 expression is reported to exert effects on cancer growth, autoimmune and allergic disorders, infection, transplantation, bone development and homeostasis, and reproductive biology. It was initially thought, based on the idea that CD200R1 was mostly expressed on cells of myeloid origin, that CD200:CD200R1 interactions were primarily dedicated to controlling myeloid cell function. However additional members of the CD200R family have now also been identified, although their function(s) remain unclear, and CD200R1 itself is now known to be expressed by subsets of T cells and other cells. Together these observations add layers of complexity to our understanding of CD200-related regulation. In common with a number of physiological systems, the mechanism(s) of CD200-induced signaling seem to fit within a similar framework of opposing actions of kinases and phosphatases. This paper highlights the advances in our knowledge of immunoregulation achieved following CD200:CD200R interaction and the potential clinical applicability of that information.

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    Authors: Jones, Martin; Rose, Ann;

    C. elegans provides an excellent model system for the study of the Fanconi Anemia (FA), one of the hallmarks of which is sensitivity to interstrand crosslinking agents. Central to our understanding of FA has been the investigation of DOG-1, the functional ortholog of the deadbox helicase FANCJ. Here we review the current understanding of the unique role of DOG-1 in maintaining stability of G-rich DNA in C. elegans and explore the question of why DOG-1 animals are crosslink sensitive. We propose a dynamic model in which noncovalently linked G-rich structures form and un-form in the presence of DOG-1. When DOG-1 is absent but crosslinking agents are present the G-rich structures are readily covalently crosslinked, resulting in increased crosslinks formation and thus giving increased crosslink sensitivity. In this interpretation DOG-1 is neither upstream nor downstream in the FA pathway, but works alongside it to limit the availability of crosslink substrates. This model reconciles the crosslink sensitivity observed in the absence of DOG-1 function with its unique role in maintaining G-Rich DNA and will help to formulate experiments to test this hypothesis.

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    Authors: Harrison, Robert V.(Auditory Science Laboratory, Department of Otolaryngology-Head & Neck Surgery);

    Increasingly, our acoustic environment is filled with amplified sound sources (e.g., MP3 players, video game stations, and sports/entertainment venues). There is serious concern and also some controversy about the risks of acoustic trauma in children. This overview provides some basic information on the physiological mechanisms that lead to noise induced hearing loss, a survey of various studies that, on balance, indicates that there is cause for concern, and finally a discussion on measures that can help to prevent noise induced hearing loss in children. This paper is designed for public health and other healthcare professions (ENT, audiologists, family doctors, and pediatricians) who should understand the risks of noise induced hearing loss and its prevention.

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    Authors: Chu, Jenny E.(Department of Anatomy & Cell Biology, Schulich School of Medicine and Dentistry) Allan, Alison L.(Department of Anatomy & Cell Biology, Schulich School of Medicine and Dentistry);

    Breast cancer is a prevalent disease worldwide, and the majority of deaths occur due to metastatic disease. Clinical studies have identified a specific pattern for the metastatic spread of breast cancer, termed organ tropism; where preferential secondary sites include lymph node, bone, brain, lung, and liver. A rare subpopulation of tumor cells, the cancer stem cells (CSCs), has been hypothesized to be responsible for metastatic disease and therapy resistance. Current treatments are highly ineffective against metastatic breast cancer, likely due to the innate therapy resistance of CSCs and the complex interactions that occur between cancer cells and their metastatic microenvironments. A better understanding of these interactions is essential for the development of novel therapeutic targets for metastatic disease. This paper summarizes the characteristics of breast CSCs and their potential metastatic microenvironments. Furthermore, it raises the question of the existence of a CSC niche and highlights areas for future investigation.

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    Authors: Mondragón-Rodríguez, Siddhartha; Perry, George; Zhu, Xiongwei; Moreira, Paula I.; +2 Authors

    Alzheimer’s disease (AD) is defined by the concurrence of abnormal aggregates composed of phosphorylated tau protein and of abnormal cellular changes including neurite degeneration, loss of neurons, and loss of cognitive functions. While a number of mechanisms have been implicated in this complex disease, oxidative stress remains one of the earliest and strongest events related to disease progression. However, the mechanism that links oxidative stress and cognitive decline remains elusive. Here, we propose that phosphorylated tau protein could be playing the role of potential connector and, therefore, that a combined therapy involving antioxidants and check points for synaptic plasticity during early stages of the disease could become a viable therapeutic option for AD treatment.

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    Authors: Poirier, Andrée-Anne; Aubé, Benoit; Côté, Mélissa; Morin, Nicolas; +2 Authors

    A diagnosis of Parkinson’s disease is classically established after the manifestation of motor symptoms such as rigidity, bradykinesia, and tremor. However, a growing body of evidence supports the hypothesis that nonmotor symptoms, especially gastrointestinal dysfunctions, could be considered as early biomarkers since they are ubiquitously found among confirmed patients and occur much earlier than their motor manifestations. According to Braak’s hypothesis, the disease is postulated to originate in the intestine and then spread to the brain via the vagus nerve, a phenomenon that would involve other neuronal types than the well-established dopaminergic population. It has therefore been proposed that peripheral nondopaminergic impairments might precede the alteration of dopaminergic neurons in the central nervous system and, ultimately, the emergence of motor symptoms. Considering the growing interest in the gut-brain axis in Parkinson’s disease, this review aims at providing a comprehensive picture of the multiple gastrointestinal features of the disease, along with the therapeutic approaches used to reduce their burden. Moreover, we highlight the importance of gastrointestinal symptoms with respect to the patients’ responses towards medical treatments and discuss the various possible adverse interactions that can potentially occur, which are still poorly understood.

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    Authors: Miklavcic, John Janez(4-002 Li Ka Shing Centre for Health Research Innovation, University of Alberta) Schnabl, Kareena Leanne(200, 10150-102 street, Dyna LIFE Diagnostics, Edmonton, AB) Mazurak, Vera Christine(4-002 Li Ka Shing Centre for Health Research Innovation, University of Alberta) Thomson, Alan Bryan Robert(Division of Gastroenterology, University of Western Ontario, London, ON) Clandinin, Michael Thomas(4-002 Li Ka Shing Centre for Health Research Innovation, University of Alberta);

    Gangliosides are integral to the structure and function of cell membranes. Ganglioside composition of the intestinal brush border and apical surface of the colon influences numerous cell processes including microbial attachment, cell division, differentiation, and signaling. Accelerated catabolism of ganglioside in intestinal disease results in increased proinflammatory signaling. Restoring proper structure and function to the diseased intestine can resolve inflammation, increase resistance to infection, and improve gut integrity to induce remission of conditions like necrotizing enterocolitis (NEC) and Crohn's disease (CD). Maintaining inactive state of disease may be achieved by reducing the rate that gangliosides are degraded or by increasing intake of dietary ganglioside. Collectively, the studies outlined in this paper indicate that the amount of gangliosides GM3 and GD3 in intestinal mucosa is decreased with inflammation, low level of GM3 is associated with higher production of proinflammatory signals, and ganglioside content of intestinal mucosa can be increased by dietary ganglioside.

    image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/ Hindawi Publishing C...arrow_drop_down
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    Authors: Furlan, Andrea D; MacDougall, Peter; Pellerin, Denise; Shaw, Karen; +3 Authors

    BACKGROUND: Prescription monitoring or review programs collect information about prescription and dispensing of controlled substances for the purposes of monitoring, analysis and education. In Canada, it is the responsibility of the provincial institutions to organize, maintain and run such programs.OBJECTIVE: To describe the characteristics of four provincial programs that have been in place for >6 years.METHODS: The managers of the prescription monitoring/review programs of four provinces (British Columbia, Alberta, Saskatchewan and Nova Scotia) were invited to present at a symposium at the Canadian Pain Society in May 2012. In preparation for the symposium, one author collected and summarized the information.RESULTS: Three provinces have a mix of review and monitoring programs; the program in British Columbia is purely for review and education. All programs include controlled substances (narcotics, barbiturates and psychostimulants); however, other substances are differentially included among the programs: anabolic steroids are included in Saskatchewan and Nova Scotia; and cannabinoids are included in British Columbia and Nova Scotia. Access to the database is available to pharmacists in all provinces. Physicians need consent from patients in British Columbia, and only professionals registered with the program can access the database in Alberta. The definition of inappropriate prescribing and dispensing is not uniform. Double doctoring, double pharmacy and high-volume dispensing are considered to be red flags in all programs.CONCLUSIONS: There is variability among Canadian provinces in managing prescription monitoring/review programs.

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    Authors: Wainberg, Mark A.;

    The use of highly active antiretroviral therapy (HAART) involves combinations of drugs to achieve maximal virological response and reduce the potential for the emergence of antiviral resistance. There are two broad classes of reverse transcriptase inhibitors, the nucleoside reverse transcriptase inhibitors (NRTIs) and nonnucleoside reverse transcriptase inhibitors (NNRTIs). Since the first classes of such compounds were developed, viral resistance against them has necessitated the continuous development of novel compounds within each class. This paper considers the NRTIs and NNRTIs currently in both preclinical and clinical development or approved for second line therapy and describes the patterns of resistance associated with their use, as well as the underlying mechanisms that have been described. Due to reasons of both affordability and availability, some reverse transcriptase inhibitors with low genetic barrier are more commonly used in resource-limited settings. Their use results to the emergence of specific patterns of antiviral resistance and so may require specific actions to preserve therapeutic options for patients in such settings. More recently, the advent of integrase strand transfer inhibitors represents another major step forward toward control of HIV infection, but these compounds are also susceptible to problems of HIV drug resistance.

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    Authors: Holder, Kayla A.(Immunology and Infectious Diseases Program, Division of BioMedical Sciences) Russell, Rodney S.(Immunology and Infectious Diseases Program, Division of BioMedical Sciences) Grant, Michael D.(Immunology and Infectious Diseases Program, Division of BioMedical Sciences);

    Viruses must continually adapt against dynamic innate and adaptive responses of the host immune system to establish chronic infection. Only a small minority (~20%) of those exposed to hepatitis C virus (HCV) spontaneously clear infection, leaving approximately 200 million people worldwide chronically infected with HCV. A number of recent research studies suggest that establishment and maintenance of chronic HCV infection involve natural killer (NK) cell dysfunction. This relationship is illustrated in vitro by disruption of typical NK cell responses including both cell-mediated cytotoxicity and cytokine production. Expression of a number of activating NK cell receptors in vivo is also affected in chronic HCV infection. Thus, direct in vivo and in vitro evidence of compromised NK function in chronic HCV infection in conjunction with significant epidemiological associations between the outcome of HCV infection and certain combinations of NK cell regulatory receptor and class I human histocompatibility linked antigen (HLA) genotypes indicate that NK cells are important in the immune response against HCV infection. In this review, we highlight evidence suggesting that selective impairment of NK cell activity is related to establishment of chronic HCV infection.

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  • image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/
    Authors: Gorczynski, Reginald M.;

    The type 1 membrane glycoprotein CD200, widely expressed on multiple cells/tissues, uses a structurally similar receptor (CD200R1), whose expression is more restricted to cells of the myeloid and lymphoid lineages, to transmit signals affecting responses in multiple physiological systems. Thus CD200 expression is reported to exert effects on cancer growth, autoimmune and allergic disorders, infection, transplantation, bone development and homeostasis, and reproductive biology. It was initially thought, based on the idea that CD200R1 was mostly expressed on cells of myeloid origin, that CD200:CD200R1 interactions were primarily dedicated to controlling myeloid cell function. However additional members of the CD200R family have now also been identified, although their function(s) remain unclear, and CD200R1 itself is now known to be expressed by subsets of T cells and other cells. Together these observations add layers of complexity to our understanding of CD200-related regulation. In common with a number of physiological systems, the mechanism(s) of CD200-induced signaling seem to fit within a similar framework of opposing actions of kinases and phosphatases. This paper highlights the advances in our knowledge of immunoregulation achieved following CD200:CD200R interaction and the potential clinical applicability of that information.

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    Authors: Jones, Martin; Rose, Ann;

    C. elegans provides an excellent model system for the study of the Fanconi Anemia (FA), one of the hallmarks of which is sensitivity to interstrand crosslinking agents. Central to our understanding of FA has been the investigation of DOG-1, the functional ortholog of the deadbox helicase FANCJ. Here we review the current understanding of the unique role of DOG-1 in maintaining stability of G-rich DNA in C. elegans and explore the question of why DOG-1 animals are crosslink sensitive. We propose a dynamic model in which noncovalently linked G-rich structures form and un-form in the presence of DOG-1. When DOG-1 is absent but crosslinking agents are present the G-rich structures are readily covalently crosslinked, resulting in increased crosslinks formation and thus giving increased crosslink sensitivity. In this interpretation DOG-1 is neither upstream nor downstream in the FA pathway, but works alongside it to limit the availability of crosslink substrates. This model reconciles the crosslink sensitivity observed in the absence of DOG-1 function with its unique role in maintaining G-Rich DNA and will help to formulate experiments to test this hypothesis.

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    Authors: Harrison, Robert V.(Auditory Science Laboratory, Department of Otolaryngology-Head & Neck Surgery);

    Increasingly, our acoustic environment is filled with amplified sound sources (e.g., MP3 players, video game stations, and sports/entertainment venues). There is serious concern and also some controversy about the risks of acoustic trauma in children. This overview provides some basic information on the physiological mechanisms that lead to noise induced hearing loss, a survey of various studies that, on balance, indicates that there is cause for concern, and finally a discussion on measures that can help to prevent noise induced hearing loss in children. This paper is designed for public health and other healthcare professions (ENT, audiologists, family doctors, and pediatricians) who should understand the risks of noise induced hearing loss and its prevention.

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    Authors: Chu, Jenny E.(Department of Anatomy & Cell Biology, Schulich School of Medicine and Dentistry) Allan, Alison L.(Department of Anatomy & Cell Biology, Schulich School of Medicine and Dentistry);

    Breast cancer is a prevalent disease worldwide, and the majority of deaths occur due to metastatic disease. Clinical studies have identified a specific pattern for the metastatic spread of breast cancer, termed organ tropism; where preferential secondary sites include lymph node, bone, brain, lung, and liver. A rare subpopulation of tumor cells, the cancer stem cells (CSCs), has been hypothesized to be responsible for metastatic disease and therapy resistance. Current treatments are highly ineffective against metastatic breast cancer, likely due to the innate therapy resistance of CSCs and the complex interactions that occur between cancer cells and their metastatic microenvironments. A better understanding of these interactions is essential for the development of novel therapeutic targets for metastatic disease. This paper summarizes the characteristics of breast CSCs and their potential metastatic microenvironments. Furthermore, it raises the question of the existence of a CSC niche and highlights areas for future investigation.

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    Authors: Mondragón-Rodríguez, Siddhartha; Perry, George; Zhu, Xiongwei; Moreira, Paula I.; +2 Authors

    Alzheimer’s disease (AD) is defined by the concurrence of abnormal aggregates composed of phosphorylated tau protein and of abnormal cellular changes including neurite degeneration, loss of neurons, and loss of cognitive functions. While a number of mechanisms have been implicated in this complex disease, oxidative stress remains one of the earliest and strongest events related to disease progression. However, the mechanism that links oxidative stress and cognitive decline remains elusive. Here, we propose that phosphorylated tau protein could be playing the role of potential connector and, therefore, that a combined therapy involving antioxidants and check points for synaptic plasticity during early stages of the disease could become a viable therapeutic option for AD treatment.

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    Authors: Poirier, Andrée-Anne; Aubé, Benoit; Côté, Mélissa; Morin, Nicolas; +2 Authors

    A diagnosis of Parkinson’s disease is classically established after the manifestation of motor symptoms such as rigidity, bradykinesia, and tremor. However, a growing body of evidence supports the hypothesis that nonmotor symptoms, especially gastrointestinal dysfunctions, could be considered as early biomarkers since they are ubiquitously found among confirmed patients and occur much earlier than their motor manifestations. According to Braak’s hypothesis, the disease is postulated to originate in the intestine and then spread to the brain via the vagus nerve, a phenomenon that would involve other neuronal types than the well-established dopaminergic population. It has therefore been proposed that peripheral nondopaminergic impairments might precede the alteration of dopaminergic neurons in the central nervous system and, ultimately, the emergence of motor symptoms. Considering the growing interest in the gut-brain axis in Parkinson’s disease, this review aims at providing a comprehensive picture of the multiple gastrointestinal features of the disease, along with the therapeutic approaches used to reduce their burden. Moreover, we highlight the importance of gastrointestinal symptoms with respect to the patients’ responses towards medical treatments and discuss the various possible adverse interactions that can potentially occur, which are still poorly understood.

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    Authors: Miklavcic, John Janez(4-002 Li Ka Shing Centre for Health Research Innovation, University of Alberta) Schnabl, Kareena Leanne(200, 10150-102 street, Dyna LIFE Diagnostics, Edmonton, AB) Mazurak, Vera Christine(4-002 Li Ka Shing Centre for Health Research Innovation, University of Alberta) Thomson, Alan Bryan Robert(Division of Gastroenterology, University of Western Ontario, London, ON) Clandinin, Michael Thomas(4-002 Li Ka Shing Centre for Health Research Innovation, University of Alberta);

    Gangliosides are integral to the structure and function of cell membranes. Ganglioside composition of the intestinal brush border and apical surface of the colon influences numerous cell processes including microbial attachment, cell division, differentiation, and signaling. Accelerated catabolism of ganglioside in intestinal disease results in increased proinflammatory signaling. Restoring proper structure and function to the diseased intestine can resolve inflammation, increase resistance to infection, and improve gut integrity to induce remission of conditions like necrotizing enterocolitis (NEC) and Crohn's disease (CD). Maintaining inactive state of disease may be achieved by reducing the rate that gangliosides are degraded or by increasing intake of dietary ganglioside. Collectively, the studies outlined in this paper indicate that the amount of gangliosides GM3 and GD3 in intestinal mucosa is decreased with inflammation, low level of GM3 is associated with higher production of proinflammatory signals, and ganglioside content of intestinal mucosa can be increased by dietary ganglioside.

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    Authors: Furlan, Andrea D; MacDougall, Peter; Pellerin, Denise; Shaw, Karen; +3 Authors

    BACKGROUND: Prescription monitoring or review programs collect information about prescription and dispensing of controlled substances for the purposes of monitoring, analysis and education. In Canada, it is the responsibility of the provincial institutions to organize, maintain and run such programs.OBJECTIVE: To describe the characteristics of four provincial programs that have been in place for >6 years.METHODS: The managers of the prescription monitoring/review programs of four provinces (British Columbia, Alberta, Saskatchewan and Nova Scotia) were invited to present at a symposium at the Canadian Pain Society in May 2012. In preparation for the symposium, one author collected and summarized the information.RESULTS: Three provinces have a mix of review and monitoring programs; the program in British Columbia is purely for review and education. All programs include controlled substances (narcotics, barbiturates and psychostimulants); however, other substances are differentially included among the programs: anabolic steroids are included in Saskatchewan and Nova Scotia; and cannabinoids are included in British Columbia and Nova Scotia. Access to the database is available to pharmacists in all provinces. Physicians need consent from patients in British Columbia, and only professionals registered with the program can access the database in Alberta. The definition of inappropriate prescribing and dispensing is not uniform. Double doctoring, double pharmacy and high-volume dispensing are considered to be red flags in all programs.CONCLUSIONS: There is variability among Canadian provinces in managing prescription monitoring/review programs.

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    Authors: Wainberg, Mark A.;

    The use of highly active antiretroviral therapy (HAART) involves combinations of drugs to achieve maximal virological response and reduce the potential for the emergence of antiviral resistance. There are two broad classes of reverse transcriptase inhibitors, the nucleoside reverse transcriptase inhibitors (NRTIs) and nonnucleoside reverse transcriptase inhibitors (NNRTIs). Since the first classes of such compounds were developed, viral resistance against them has necessitated the continuous development of novel compounds within each class. This paper considers the NRTIs and NNRTIs currently in both preclinical and clinical development or approved for second line therapy and describes the patterns of resistance associated with their use, as well as the underlying mechanisms that have been described. Due to reasons of both affordability and availability, some reverse transcriptase inhibitors with low genetic barrier are more commonly used in resource-limited settings. Their use results to the emergence of specific patterns of antiviral resistance and so may require specific actions to preserve therapeutic options for patients in such settings. More recently, the advent of integrase strand transfer inhibitors represents another major step forward toward control of HIV infection, but these compounds are also susceptible to problems of HIV drug resistance.

    image/svg+xml art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos Open Access logo, converted into svg, designed by PLoS. This version with transparent background. http://commons.wikimedia.org/wiki/File:Open_Access_logo_PLoS_white.svg art designer at PLoS, modified by Wikipedia users Nina, Beao, JakobVoss, and AnonMoos http://www.plos.org/ Hindawi Publishing C...arrow_drop_down
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    Authors: Holder, Kayla A.(Immunology and Infectious Diseases Program, Division of BioMedical Sciences) Russell, Rodney S.(Immunology and Infectious Diseases Program, Division of BioMedical Sciences) Grant, Michael D.(Immunology and Infectious Diseases Program, Division of BioMedical Sciences);

    Viruses must continually adapt against dynamic innate and adaptive responses of the host immune system to establish chronic infection. Only a small minority (~20%) of those exposed to hepatitis C virus (HCV) spontaneously clear infection, leaving approximately 200 million people worldwide chronically infected with HCV. A number of recent research studies suggest that establishment and maintenance of chronic HCV infection involve natural killer (NK) cell dysfunction. This relationship is illustrated in vitro by disruption of typical NK cell responses including both cell-mediated cytotoxicity and cytokine production. Expression of a number of activating NK cell receptors in vivo is also affected in chronic HCV infection. Thus, direct in vivo and in vitro evidence of compromised NK function in chronic HCV infection in conjunction with significant epidemiological associations between the outcome of HCV infection and certain combinations of NK cell regulatory receptor and class I human histocompatibility linked antigen (HLA) genotypes indicate that NK cells are important in the immune response against HCV infection. In this review, we highlight evidence suggesting that selective impairment of NK cell activity is related to establishment of chronic HCV infection.

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