Human Immunodeficiency Virus/Human Papillomavirus co-infection and host molecular genetics of cervical carcinoma
type: CreativeWork
description: A subgroup of women who are co-infected with human immunodeficiency virus type 1 (HIV1) and human papillomavirus (HPV) progress relatively rapidly to cervical disease regardless of the number of absolute CD4 count. During infection, viral peptides are recognized by the host immune system. It is reasonable to propose that the development of viral-associated cancers, like cervical cancer, requires interference with specific immune-response genes. This thesis investigates this proposition with consideration of host molecular genetic alterations and variations of the human leukocyte antigen class II (HLA II) genes as one of the groups of immune-response genes that are involved in directing CD4 T-cell responses during infection, in the instance of cervical cancer progression in HIV-1/HPV co-infected women. Study I, reviewed the available literature on host molecular genetics and HIV-1/HPV coinfection on cervical cancer progression. This study suggests that the dual pro-oncogenic effects of HPV oncoproteins E6/E7 and the HIV-1 oncoprotein Tat, may exacerbate and accelerate the rate of cervical disease progression in a subgroup of HIV-1-positive women. Additionally, HIV-1-positive cervical cancer has three important carcinogenesis steps: firstly, HPV integration into the host genome, secondly, dual pro-oncogenic effects of HPV oncoproteins E6/E7, and the HIV-1 Tat oncoprotein in the host genome and, thirdly, the accumulation of repeated, unrepaired genetic mutations and genetic alterations within the host chromosomal DNA. Genetic variations or mutations that affect the following host gene categories were suggested to be responsible for cervical cancer susceptibility and disease progression; (i) genes for the immune-response against oncogenic HPV infection, (ii) oncogenes, (iii) tumour-suppressor genes, (iv) apoptosis-related genes, (v) DNA damagerepair genes, and (vi) cell cycle-regulatory genes. However, studies II, III and IV are linked together and listed according to t…
abstract: A subgroup of women who are co-infected with human immunodeficiency virus type 1 (HIV1) and human papillomavirus (HPV) progress relatively rapidly to cervical disease regardless of the number of absolute CD4 count. During infection, viral peptides are recognized by the host immune system. It is reasonable to propose that the development of viral-associated cancers, like cervical cancer, requires interference with specific immune-response genes. This thesis investigates this proposition with consideration of host molecular genetic alterations and variations of the human leukocyte antigen class II (HLA II) genes as one of the groups of immune-response genes that are involved in directing CD4 T-cell responses during infection, in the instance of cervical cancer progression in HIV-1/HPV co-infected women. Study I, reviewed the available literature on host molecular genetics and HIV-1/HPV coinfection on cervical cancer progression. This study suggests that the dual pro-oncogenic effects of HPV oncoproteins E6/E7 and the HIV-1 oncoprotein Tat, may exacerbate and accelerate the rate of cervical disease progression in a subgroup of HIV-1-positive women. Additionally, HIV-1-positive cervical cancer has three important carcinogenesis steps: firstly, HPV integration into the host genome, secondly, dual pro-oncogenic effects of HPV oncoproteins E6/E7, and the HIV-1 Tat oncoprotein in the host genome and, thirdly, the accumulation of repeated, unrepaired genetic mutations and genetic alterations within the host chromosomal DNA. Genetic variations or mutations that affect the following host gene categories were suggested to be responsible for cervical cancer susceptibility and disease progression; (i) genes for the immune-response against oncogenic HPV infection, (ii) oncogenes, (iii) tumour-suppressor genes, (iv) apoptosis-related genes, (v) DNA damagerepair genes, and (vi) cell cycle-regulatory genes. However, studies II, III and IV are linked together and listed according to t…
author: Chambuso, Ramadhani Salum
keywords: Pathology
date published: 2019
date modified: 2026-07-22T22:23:12Z
provider: University of Cape Town
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: Department of Pathology

PropertyValue
property ID: Handle
value: https://hdl.handle.net/11427/31668