Bio-prospecting of Medicinal Bio-resources from the Kenyan Biodiversity: Reflections on Governance as the Missing Link - A Review Article

Medicinal biodiversity has since times immemorial served as one of the richest sources of bio-prospecting leading to the discovery of novel drugs for mankind globally. However, in Kenya, despite the Country being known to be a mega biodiversity hotspot, bio-prospecting has not been very successful mainly due to lack of effective institutional and legal frameworks. This article reviews the policy and legislation instruments governing medicinal biodiversity in Kenya in order to identify their weaknesses and strengths and come up with recommendations for effective economic exploitation of the Country’s’ mega diverse resource. The methodology employed was a qualitative content analysis of relevant biodiversity legislations in Kenya. Results reveal that there has been governance gaps as far as bio-prospecting activities in Kenya are concerned which has rendered the Country’s mega biodiversity vulnerable to bio-piracy at the expense of the poor  local communities who are the traditional knowledge owners. There is need to review the current pieces of legislation on medicinal biodiversity and work towards developing a strong National bio-prospecting policy together with an implementation plan. These are important to inform the overall national development agenda, in tandem with Vision 2030. Some of the policies were found out dated and rather obsolete and not serving the current interests and ambitions of the Country. There is therefore a need to revisit the policy and legislative instruments because they will continue frustrating bio-prospecting activities.  Moreover, we recommend the creation of a National Institute to coordinate and harmonize the legislations and National policies on medicinal biodiversity to seal loopholes, avoid conflicts and contradictions being experienced in the current legislative and policy frameworks. Keywords: Bio-prospecting; Bio-piracy; Governance; Kenya; Medicinal biodiversity DOI: 10.7176/JHMN/60-05 Publication date:March 31st 201

Fear, faith and finances : health literacy experiences of English and Swahili speaking women newly diagnosed with breast and cervical cancer

Breast and cervical cancer are among the leading causes of cancer-related deaths globally. In Kenya, delayed presentation and diagnosis contribute to breast and cervical cancer mortality. The Kenyan government acknowledges the cancer burden with estimated 39,000 new cases diagnosed and 27,000 deaths per annum. Mortality can be reduced if cancer is diagnosed early and with appropriate treatment. Health Literacy (HL) about cancer screening, diagnosis and treatment is important in reducing mortality, but there is little understanding about HL levels, experiences of patients diagnosed with breast and cervical cancer and the contexts in which they make decisions. In this study, health literacy is defined as the degree to which individuals have the capacity to obtain, communicate, process and understand basic health information and services needed to make appropriate health decisions. This exploratory qualitative study investigated the HL experiences of accessing and using health information in women with any stage of breast or cervical cancer presenting at the Aga Khan University Hospital (private) or Kenyatta National Hospital (public) in Nairobi, Kenya. Data were gathered through semi-structured interviews from a purposive sample of 18 women. Interviews were transcribed verbatim, and the Consolidated criteria for reporting qualitative studies guidelines guided data analysis. The findings may aid development of patient education tools and determine effective ways of communicating cancer-related health information to improve the knowledge and health-seeking behaviours of Kenyan women. This project identified sociocultural beliefs and factors that influence how women understand information provided by healthcare professionals. Themes that arose included but were not limited to: fear, despair and agony at diagnosis, faith, social support, side effects, cancer-related stigma and financial burden of cancer as a barrier to getting information

Amino acid substitutions within HLA-B*27- restricted T cell epitopes prevent recognition by hepatitis delta virus-specific CD8+ T cells

Virus-specific CD8 T cell response seems to play a significant role in the outcome of hepatitis delta virus (HDV) infection. However, the HDV-specific T cell epitope repertoire and mechanisms of CD8 T cell failure in HDV infection have been poorly characterized. We therefore aimed to characterize HDV-specific CD8 T cell epitopes and the impacts of viral mutations on immune escape. In this study, we predicted peptide epitopes binding the most frequent human leukocyte antigen (HLA) types and assessed their HLA binding capacities. These epitopes were characterized in HDV-infected patients by intracellular gamma interferon (IFN-γ) staining. Sequence analysis of large hepatitis delta antigen (L-HDAg) and HLA typing were performed in 104 patients. The impacts of substitutions within epitopes on the CD8 T cell response were evaluated experimentally and by in silico studies. We identified two HLA-B*27-restricted CD8 T cell epitopes within L-HDAg. These novel epitopes are located in a relatively conserved region of L-HDAg. However, we detected molecular footprints within the epitopes in HLA-B*27-positive patients with chronic HDV infections. The variant peptides were not cross-recognized in HLA-B*27-positive patients with resolved HDV infections, indicating that the substitutions represent viral escape mutations. Molecular modeling of HLA-B*27 complexes with the L-HDAg epitope and its potential viral escape mutations indicated that the structural and electrostatic properties of the bound peptides differ considerably at the T cell receptor interface, which provides a possible molecular explanation for the escape mechanism. This viral escape from the HLA-B*27-restricted CD8 T cell response correlates with a chronic outcome of hepatitis D infection. T cell failure resulting from immune escape may contribute to the high chronicity rate in HDV infection. © 2018 American Society for Microbiology

Mutations in hepatitis D virus allow it to escape detection by CD8⁺ T cells and evolve at the population level.

BACKGROUND & AIMS: Hepatitis D virus (HDV) superinfection in patients with hepatitis B virus (HBV) is associated with rapid progression to liver cirrhosis and hepatocellular carcinoma. Treatment options are limited, and no vaccine is available. Although HDV-specific CD8(+) T cells are thought to control the virus, little is known about which HDV epitopes are targeted by virus-specific CD8(+)T cells or why these cells ultimately fail to control the infection. We aimed to define how HDV escapes the CD8(+) T-cell-mediated response. METHODS: We collected plasma and DNA samples from 104 patients with chronic HDV and HBV infection at medical centers in Europe and the Middle East, sequenced HDV, typed human leukocyte antigen (HLA) class I alleles from patients, and searched for polymorphisms in HDV RNA associated with specific HLA class I alleles. We predicted epitopes in HDV that would be recognized by CD8(+) T cells and corresponded with the identified virus polymorphisms in patients with resolved (n = 12) or chronic (n = 13) HDV infection. RESULTS: We identified 21 polymorphisms in HDV that were significantly associated with specific HLA class I alleles (P < .005). Five of these polymorphisms were found to correspond to epitopes in HDV that are recognized by CD8(+) T cells; we confirmed that CD8(+) T cells in culture targeted these HDV epitopes. HDV variant peptides were only partially cross-recognized by CD8(+) T cells isolated from patients, indicating that the virus had escaped detection by these cells. These newly identified HDV epitopes were restricted by relatively infrequent HLA class I alleles, and they bound most frequently to HLA-B. In contrast, frequent HLA class I alleles were not associated with HDV sequence polymorphisms. CONCLUSIONS: We analyzed sequences of HDV RNA and HLA class I alleles that present epitope peptides to CD8(+) T cells in patients with persistent HDV infection. We identified polymorphisms in the HDV proteome that associate with HLA class I alleles. Some variant peptides in epitopes from HDV were only partially recognized by CD8(+) T cells isolated from patients; these could be mutations that allow HDV to escape the immune response, resulting in persistent infection. HDV escape from the immune response was associated with uncommon HLA class I alleles, indicating that HDV evolves, at the population level, to evade recognition by common HLA class I alleles