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Co-Infection Studies on Hepatitis C Virus and Malaria Parasite Liver Stages

Veltre, Johna (2012) Co-Infection Studies on Hepatitis C Virus and Malaria Parasite Liver Stages. Master's Thesis, University of Pittsburgh.

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    Abstract

    Malaria and hepatitis C are infectious diseases that affect millions of people worldwide. These two diseases are caused by two different pathogens, Plasmodium parasite for malaria and hepatitis C virus (HCV) for hepatitis C, that share some similarities in their development within the hepatocytes of the liver. Co-infection of these two pathogens has largely remained unstudied, but due to epidemiological overlap, it is plausible that individuals can be afflicted with both malaria and hepatitis C. To date, it has been shown that Plasmodium parasites and HCV utilize four common host entry factors to gain entry into hepatocytes: Heparan sulfate proteoglycans (HSPGs), scavenger receptor-B1 (SR-B1), cluster of differentiation 81 (CD-81), and apolipoprotein E (apoE). ApoE incorporated into new HCV virions plays a key role in viral infectivity. In its entirety, our hypothesis states that given the increasing prevalence of hepatitis C in parts of the world where malaria is endemic, hepatitis C virus (HCV) and Plasmodium spp. Co-infections are a likely occurrence. In this case, it is plausible that co-infections with these pathogens will affect the replication of either pathogen during their liver stages. Furthermore, it is likely that Plasmodium parasites utilize claudin-1, occludin, and apoE host entry factors, which are important for HCV entry and ability to invade hepatocytes. Using an in vitro model of infection in liver derived HuH7 hepatoma cells, we hope to look at the overall affects theses pathogens have on one another through co-infection studies of P. berghei and HCV both together and individually. Furthermore, we hope to examine other host factors that HCV utilizes for entry into hepatocytes and their affect on Plasmodium entry during the liver stages of infection. This study is significant to public health to improve existing anti-malarial and hepatitis C treatments by intervening at the early stages of each pathogen’s development. By understanding how a pathogen enters, invades, and develops within a host, it is better understood how therapeutic drugs can target and decrease pathogenic development.


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    Item Type: University of Pittsburgh ETD
    ETD Committee:
    ETD Committee TypeCommittee MemberEmail
    Thesis AdvisorTarun, Aliceast22@pitt.edu
    Committee CoChairWang, Tianyitywang@pitt.edu
    Committee MemberMurphy-Corb, Michaelmcorb@pitt.edu
    Title: Co-Infection Studies on Hepatitis C Virus and Malaria Parasite Liver Stages
    Status: Published
    Abstract: Malaria and hepatitis C are infectious diseases that affect millions of people worldwide. These two diseases are caused by two different pathogens, Plasmodium parasite for malaria and hepatitis C virus (HCV) for hepatitis C, that share some similarities in their development within the hepatocytes of the liver. Co-infection of these two pathogens has largely remained unstudied, but due to epidemiological overlap, it is plausible that individuals can be afflicted with both malaria and hepatitis C. To date, it has been shown that Plasmodium parasites and HCV utilize four common host entry factors to gain entry into hepatocytes: Heparan sulfate proteoglycans (HSPGs), scavenger receptor-B1 (SR-B1), cluster of differentiation 81 (CD-81), and apolipoprotein E (apoE). ApoE incorporated into new HCV virions plays a key role in viral infectivity. In its entirety, our hypothesis states that given the increasing prevalence of hepatitis C in parts of the world where malaria is endemic, hepatitis C virus (HCV) and Plasmodium spp. Co-infections are a likely occurrence. In this case, it is plausible that co-infections with these pathogens will affect the replication of either pathogen during their liver stages. Furthermore, it is likely that Plasmodium parasites utilize claudin-1, occludin, and apoE host entry factors, which are important for HCV entry and ability to invade hepatocytes. Using an in vitro model of infection in liver derived HuH7 hepatoma cells, we hope to look at the overall affects theses pathogens have on one another through co-infection studies of P. berghei and HCV both together and individually. Furthermore, we hope to examine other host factors that HCV utilizes for entry into hepatocytes and their affect on Plasmodium entry during the liver stages of infection. This study is significant to public health to improve existing anti-malarial and hepatitis C treatments by intervening at the early stages of each pathogen’s development. By understanding how a pathogen enters, invades, and develops within a host, it is better understood how therapeutic drugs can target and decrease pathogenic development.
    Date: 27 January 2012
    Date Type: Publication
    Defense Date: 09 December 2011
    Approval Date: 27 January 2012
    Submission Date: 25 January 2012
    Release Date: 27 January 2012
    Access Restriction: No restriction; The work is available for access worldwide immediately.
    Patent pending: No
    Number of Pages: 77
    Institution: University of Pittsburgh
    Thesis Type: Master's Thesis
    Refereed: Yes
    Degree: MS - Master of Science
    Uncontrolled Keywords: Hepatitis C, Hepatitis C Virus, Malaria, Plasmodium, Co-infection, parasite, CD-81, SR-B1, ApoE, HSPGs, HuH7, HuH7.5, Replicon 2-3-, Replicon 2-3+, HuH7.5.1
    Schools and Programs: Graduate School of Public Health > Infectious Diseases and Microbiology
    Date Deposited: 27 Jan 2012 16:55
    Last Modified: 30 Jun 2014 18:29

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