The leading cause of death for chronic virus infection in the United States is caused by the hepatitis C virus (HCV), an infectious disease that causes liver inflammation. There are five types of hepatitis, hepatitis A, B, C, D, and E, hepatitis C virus being the most serious of the four. HCV is not a sexually transmitted disease; it is contracted through direct contact to infected blood, and from contaminated medical supply. According to the World Health Organization, hepatitis C is most prevalent in Central and East Asia, and North Africa, areas that are population dense. There are currently no vaccines for HCV; current antiviral drugs have a high success rate in clearing the virus depending on the strain The effect of the host’s T-Cell
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In Plauzolles’s research, “Hepatitis C Virus Adaptation to T-Cell Immune Pressure”, he found that HCV adaptation is a major strategy used by the virus that determines the outcome of a patient’s infection. HCV evolution has selective pressure from the host’s immune response by having the immune escape mutations persist in the gene pool. Having the hepatitis C virus have a selective advantage in the host by presenting mutations toward immune T-cell responses will result in the specific strain to dominate and become the wild type virus in the population. The virus’s ability to adapt and escape the host’s immune system determines the infection outcome. The high mutation rate can directly affected the virus’ variant resistance toward the HLA alleles and current and future manufactured drugs. Products, CD4+ and CD8+, from HLA allele expression are major determinants for whether an infected person with HCV will clear the virus without medication. Rapid and high change in the virus’s genome gives the virus a selective advantage, keeping their presence in the …show more content…
Trautmann focused his study in CD4+ T cell-lymphopenic mice, groups that were either genetically changed to be deficient of the major histocompatibility (MHC) class II transactivator (CIITA) or by antibody-mediated CD4+ cell depletion, and comparing their different factors and measured results to a wild type mice that does contain MHC class II and CD4+ cells. The study induced viral acute hepatitis in their study group by infecting the mice with Lymphocytic Choriomeningitis Virus (LCMV) of the strain WE. Trautmann choose to use LCMV hepatitis due to it being similar to human hepatitis C virus, and because the virus causes damage from sole antiviral immune response. This type of viral infection provides a great model of showing CD8+ T cells being essential in order to eliminate the
In Plauzolles’s research, “Hepatitis C Virus Adaptation to T-Cell Immune Pressure”, he found that HCV adaptation is a major strategy used by the virus that determines the outcome of a patient’s infection. HCV evolution has selective pressure from the host’s immune response by having the immune escape mutations persist in the gene pool. Having the hepatitis C virus have a selective advantage in the host by presenting mutations toward immune T-cell responses will result in the specific strain to dominate and become the wild type virus in the population. The virus’s ability to adapt and escape the host’s immune system determines the infection outcome. The high mutation rate can directly affected the virus’ variant resistance toward the HLA alleles and current and future manufactured drugs. Products, CD4+ and CD8+, from HLA allele expression are major determinants for whether an infected person with HCV will clear the virus without medication. Rapid and high change in the virus’s genome gives the virus a selective advantage, keeping their presence in the …show more content…
Trautmann focused his study in CD4+ T cell-lymphopenic mice, groups that were either genetically changed to be deficient of the major histocompatibility (MHC) class II transactivator (CIITA) or by antibody-mediated CD4+ cell depletion, and comparing their different factors and measured results to a wild type mice that does contain MHC class II and CD4+ cells. The study induced viral acute hepatitis in their study group by infecting the mice with Lymphocytic Choriomeningitis Virus (LCMV) of the strain WE. Trautmann choose to use LCMV hepatitis due to it being similar to human hepatitis C virus, and because the virus causes damage from sole antiviral immune response. This type of viral infection provides a great model of showing CD8+ T cells being essential in order to eliminate the