Supervision: PhD Students

1. Brian Onsembe: Characterisation of Pulmonary and Extrapulmonary Mycobacterium tuberculosis strains in selected hospitals in Kenya

2. Edouard Ntagwabira:Development of a Novel Algorithm for detection of Common Bacterial, Viral and Fungal Etiologic Agents of Meningoencephalitis using Conventional and Molecular methods.

3. Susan Odera: The role of Human Leukocyte Antigens and M. tuberculosis strain variation in susceptibility to infection among Pulmonary Tuberculosis patients and their contacts in a sub-Ssaharan setting



Kotikot, T, Ndalamia J, OGUTU H, B Nyaoke, MW MUREITHI, Farah B, C Perciani, Mac Donald K, Anzala O, Jaoko W.  2016.   Reproductive Tract Infections Among Low Risk Women Attending KAVI-VZV 001 Study in Nairobi, Kenya. AIDS RESEARCH AND HUMAN RETROVIRUSES .
B Nyaoke, C Perciani, Mureithi MW, MacD KS, Jaoko WO.  2016.  Feasibility of Mucosal Sampling in Low-risk Women in HIV/AIDS Vaccine Clinical Trials.
Archary, D, Seaton KE, Passmore JAS, L Werner, A Deal, Dunphy LJ, Arnold KB, NL Yates, Lauffenburger DA, P Bergin, Liebenberg LJ, Samsunder N, Mureithi MW, M Altfeld, Garrett N, Karim AQ, S Abdool Karim, L Morris, Tomaras GD.  2016.  Distinct genital tract HIV-specific antibody profiles associated with tenofovir gel. Mucosal immunology.


Singh, R, Patel V, Mureithi MW, Naranbhai V, Ramsuran D, Tulsi S, Hiramen K, Werner L, Mlisana K, Altfeld M, Luban J, Kasprowicz V, Dheda K, Abdool Karim SS, Ndung'u T.  2014.  TRIM5α and TRIM22 are differentially regulated according to HIV-1 infection phase and compartment., 2014 Jan 29. Journal of virology. Abstracttrim5a_and_trim22_are_differentially_regulated_according_to_hiv.pdf

The antiviral role of TRIM E3 ligases in vivo is not fully understood. To test the hypothesis that TRIM5α and TRIM22 have differential transcriptional regulation and distinct anti-HIV roles according to infection phase and compartment, we measured TRIM5α, TRIM22 and type 1 interferon (IFN-1)-inducible MxA levels in peripheral blood mononuclear cells (PBMCs) during primary and chronic HIV-1 infection, and in matched PBMCs and central nervous system (CNS)-derived cells. Associations with biomarkers of disease progression were explored. The impact of IFN-1, select pro-inflammatory cytokines and HIV on TRIM E3 ligase-specific expression was investigated. PBMCs from individuals with primary and chronic HIV-1 infection had significantly higher levels of MxA and TRIM22 compared to HIV-1 negative PBMCs (P < 0.05, all comparisons). PBMCs from chronic infection had lower levels of TRIM5α compared to primary infection or HIV-1 uninfected (both P = 0.0001). In matched CNS-derived samples and PBMCs, higher levels of MxA (P = 0.001) and TRIM5α (P = 0.0001) were noted in the CNS. There was negative correlation between TRIM22 levels in PBMC and plasma viral load (r = -0.40, P = 0.04). In vitro, IFN-1 and rarely pro-inflammatory cytokines induced TRIM5α and TRIM22 in cell type-dependent manner and knockdown of either protein in CD4+ lymphocytes resulted in increased HIV-1 infection. These data suggest that there are infection-phase specific and anatomically compartmentalized differences in TRIM5α and TRIM22 regulation involving primarily IFN-1 and specific cell types, and indicate subtle differences in the antiviral role and transcriptional regulation of TRIM E3 ligases in vivo.Importance Interferon type I-inducible TRIM E3 ligases are a family of intracellular proteins with potent antiviral activities mediated through diverse mechanisms. However, little is known about the contribution of these proteins to antiviral immunity in vivo and how their expression is regulated. We show here that TRIM5α and TRIM22, two prominent members of the family, have different expression patterns in vivo and that expression pattern depends on HIV-1 infection status and phase. Furthermore, expression differs in peripheral blood versus central nervous system anatomical sites of infection. Only TRIM22 expression correlates negatively with HIV-1 viral load but gene silencing of both proteins enhances HIV-1 infection of target cells. We report on subtle differences in TRIM5α and TRIM22 gene induction by IFN-1 and pro-inflammatory cytokines in CD4+ lymphocytes, monocytes and neuronal cells. This study enhances our understanding of antiviral immunity by intrinsic antiviral factors and how their expression is determined.


Onyango JI Obila, Kaul R, Mureithi MW, Anzala O, Oyugi JO.  2013.  Impact of Depo-provera on female genital tract immunology.


Marianne W. Mureithi, Danielle Poole, VNSRNMP, Sengeziwe Sibeko, Lise Werner QAKSAKTN’u MATCAPRISA004 T.  2012.  Preservation HIV-1–Specific IFNg+ CD4+ T-Cell Responses in Breakthrough Infections After Exposure to Tenofovir Gel in the CAPRISA 004 Microbicide Trial. JAIDS. 60(2):124-127.mureithi_mw_jaids_2012.pdf


M.O.C. Ota, C. Oluwalana a, HGOM-GOSRCM, a M.W. Mureithi, J. Townend SASAOMJS.  2011.  Antibody and T cell responses during acute and convalescent stages of Invasive Pneumococcal Disease. International Journal of Infectious Diseases. 15:282-288.


Marianne W. Mureithi, Kristen Cohen, RMDPZMAKBMD, and Philip J.R. Goulder, Bruce D. Walker MATN’u.  2010.  Impairment of CD1d-Restricted Natural Killer T Cells in Chronic HIV Type 1 Clade C Infection. AIDS RESEARCH AND HUMAN RETROVIRUSES . 26(00)marianne_mureith_retrovirus_publication.pdf


Marianne W. Mureithi, Adam Finn, MOQZVDTMOJ, Neil A. Williams, Richard A. Adegbola RHS.  2009.  TCellMemoryResponsetoPneumococcalProtein Antigens in an Area of High Pneumococcal Carriage and Disease. The Journal of Infectious Diseases. (200):783–93.marianne_mureithi_jid_paper.pdf


Mureithi, MW, Finn A, Ota MO, Zhang Q, Davenport V, Mitchell TJ, Williams NA, Adegbola RA, Heyderman RS.  2008.  T Cell memory response to pneumococcal protein antigens in an area of high pneumococcal carriage and disease. Abstract

Streptococcus pneumoniae is a leading cause of vaccine-preventable disease worldwide. Pneumococcal protein antigens are currently under study as components of potential vaccines that offer protection against multiple serotypes. We have therefore characterized T cell pneumococcal immunity acquired through asymptomatic carriage. Methods. Peripheral blood mononuclear cells from 40 healthy Gambian adults were stimulated with supernatants derived from S. pneumoniae strain (D39), 2 isogenic mutant strains lacking either pneumolysin or choline binding protein A, and recombinant pneumolysin. Immune responses were measured by cellular proliferation and by interleukin-10 (IL-10) and interferon-g (IFN-g) enzyme-linked immunosorbent spot and bioplex cytokine assays. Nasopharyngeal swabs were cultured to determine carriage rates. Results. S. pneumoniae nasopharyngeal carriage was detected in 60% of individuals. Both effector and resting (or central) CD4+ T cell memory were frequently present to a range of pneumococcal antigens. However, the level of the effector memory response did not relate to current nasopharyngeal carriage. Pneumolysin was not immunodominant in these T cell responses but induced a distinct proinflammatory profile (high IFN-g, IL-12[p40], and L-17 levels and low IL-10 and IL-13 levels). Conclusions. In this population, T cell–mediated immunological memory potentially capable of pathogen clearance and immune surveillance is common but is not associated with the absolute interruption of pneumococcal carriage. How this naturally acquired immune memory influences pneumococcal vaccine efficacy remains to be determined.

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