Molecular Diversity of Hepatitis B Virus in HIV Infected Patients at Mbagathi district Hospital, Nairobi
Loading...
Date
2013-12-23
Authors
Khaemba, S. B.
Journal Title
Journal ISSN
Volume Title
Publisher
Abstract
With increasing access to antiretroviral therapy across Sub-Saharan Africa, HIV-infected
individuals live longer and the effects of co-infection with chronic viral hepatitis is an emerging
critical public health problem. Chronic HBV infection is a leading cause of progressive
complications of liver cirrhosis, hepatocellular carcinoma and liver failure in most Sub-Saharan
and Asian countries. Patients infected with HIV are at particular risk for HBV infection due to
similar transmission routes and up to 10% of patients infected with HIV are also chronically
infected with HBV, with 13 times higher risk of death in HIV -HBV dual infection than in monoinfected
patients. HIV co-infection accelerates HBV-related liver damage, leading to earlier
cirrhosis and end-stage liver disease. Conversely, the presence of HBV co-infection complicates
the management of HIV and increases the morbidity and mortality of HIV -infected patients.
Both HIV and HBV infections are considered to be hyperendemic in Sub-Saharan continent,
with approximately 2% of all annual deaths in Africa resulting from clinical consequences of
HBV infection and 25% of all annual deaths resulting from the clinical consequences of HTV
infection. Kenya is among the countries that are affected by hepatitis B, with a high HTVburden,
leading to frequent HIV /HBV co-infection. Considerable molecular variations are reported to
occur throughout the HBV genome and the resultant genetic diversity is correlated with
geographical distribution of genotypes and clinical outcome, immunization and antiviral therapy
response. This study will assess the molecular genetic variation in HIV infected patients
attending Mbagathi District Hospital. The prevalence of HBV in HIV patients will be assessed
using SPSS v. 17.0 and Pearson Chi-square test. The data generated will be reported as
percentages. Genetic variation will be evaluated using PCR amplification of the S gene and
subsequent sequencing of the amplicons. Phylogenetic analysis of the sequences and comparison
of identified genotypes with other identified genotypes elsewhere will be carried out using
MEGA v 4. Understanding the prevalence and the HBV genotypes will better the knowledge of
individual risk factors for hepatocellular carcinoma and form the basis for disease management
and for designing preventive strategies.