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Publications


2011

Waiboci, LW, Katz MA, Njenga MK, Breiman RF, Olack B, Njuguna H, Kikwai GK, Mwiti W, Williamson JM, Lebo E.  2011.  Viral shedding in patients infected with pandemic influenza A (H1N1) virus in Kenya, 2009. Abstract

BACKGROUND: Understanding shedding patterns of 2009 pandemic influenza A (H1N1) (pH1N1) can inform recommendations about infection control measures. We evaluated the duration of pH1N1 virus shedding in patients in Nairobi, Kenya. METHODS: Nasopharyngeal (NP) and oropharyngeal (OP) specimens were collected from consenting laboratory-confirmed pH1N1 cases every 2 days during October 14-November 25, 2009, and tested at the Centers for Diseases Control and Prevention-Kenya by real time reverse transcriptase polymerase chain reaction (rRT-PCR). A subset of rRT-PCR-positive samples was cultured. RESULTS: Of 285 NP/OP specimens from patients with acute respiratory illness, 140 (49%) tested positive for pH1N1 by rRT-PCR; 106 (76%) patients consented and were enrolled. The median age was 6 years (Range: 4 months-41 years); only two patients, both asthmatic, received oseltamivir. The median duration of pH1N1 detection after illness onset was 8 days (95% CI: 7-10 days) for rRT-PCR and 3 days (Range: 0-13 days) for viral isolation. Viable pH1N1 virus was isolated from 132/162 (81%) of rRT-PCR-positive specimens, which included 118/125 (94%) rRT-PCR-positive specimens collected on day 0-7 after symptoms onset. Viral RNA was detectable in 18 (17%) and virus isolated in 7/18 (39%) of specimens collected from patients after all their symptoms had resolved. CONCLUSIONS: In this cohort, pH1N1 was detected by rRT-PCR for a median of 8 days. There was a strong correlation between rRT-PCR results and virus isolation in the first week of illness. In some patients, pH1N1 virus was detectable after all their symptoms had resolved.

2009

MUHIA, DRLILLIANWANGECHIWAIBOCI.  2009.  SOCS-1 mimetics protect mice against lethal poxvirus infection: identification of a novel endogenous antiviral system. Journal of Virology. : Ahmed C.M., Dabelic R., Waiboci L., Jager L.D., Heron L.L. and Johnson H.M. Abstract
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MUHIA, DRLILLIANWANGECHIWAIBOCI.  2009.  SOCS-1 mimetics protect mice against lethal poxvirus infection: identification of a novel endogenous antiviral system. Journal of Virology. : Ahmed C.M., Dabelic R., Waiboci L., Jager L.D., Heron L.L. and Johnson H.M. Abstract
The paper shows that in the analysis of a queuing system with fixed-size batch arrivals, there emerges a set of polynomials which are a generalization of Chebyshev polynomialsof the second kind. The paper uses these polynomials in assessing the transient behaviour of the overflow (equivalently call blocking) probability in the system. A key figure to noteis the proportion of the overflow (or blocking) probability resident in the transient component,which is shown in the results to be more significant at the beginning of the transient and naturally decays to zero in the limit of large t. The results also show that the significanceof transients is more pronounced in cases of lighter loads, but lasts longer for heavier loads.

2008

MUHIA, DRLILLIANWANGECHIWAIBOCI.  2008.  Lilian Waiboci- Muhia, Howard M. Johnson SUPPRESSOR OF CYTOKINE SIGNALING-1 MIMETIC AND ANTAGONIST PEPTIDES: POTENTIAL AS THERAPEUTIC AGENTS .. 5th International Congress of the African Association of Physiological Sciences (AAPS). : Ahmed C.M., Dabelic R., Waiboci L., Jager L.D., Heron L.L. and Johnson H.M.

2007

MUHIA, DRLILLIANWANGECHIWAIBOCI, CM A, MG M, LO F, JP M, MI H, HM J.  2007.  Both the suppressor of cytokine signaling 1 (SOCS-1) kinase inhibitory region and SOCS-1 mimetic bind to JAK2 autophosphorylation site: implications for the development of a SOCS-1 antagonist. J Immunol. 2007 Apr 15;178(8):5058-68.. : Ahmed C.M., Dabelic R., Waiboci L., Jager L.D., Heron L.L. and Johnson H.M. Abstract

Suppressor of cytokine signaling (SOCS)-1 protein modulates signaling by IFN-gamma by binding to the autophosphorylation site of JAK2 and by targeting bound JAK2 to the proteosome for degradation. We have developed a small tyrosine kinase inhibitor peptide (Tkip) that is a SOCS-1 mimetic. Tkip is compared in this study with the kinase inhibitory region (KIR) of SOCS-1 for JAK2 recognition, inhibition of kinase activity, and regulation of IFN-gamma-induced biological activity. Tkip and a peptide corresponding to the KIR of SOCS-1, ((53))DTHFRTFRSHSDYRRI((68)) (SOCS1-KIR), both bound similarly to the autophosphorylation site of JAK2, JAK2(1001-1013). The peptides also bound to JAK2 peptide phosphorylated at Tyr(1007), pJAK2(1001-1013). Dose-response competitions suggest that Tkip and SOCS1-KIR similarly recognize the autophosphorylation site of JAK2, but probably not precisely the same way. Although Tkip inhibited JAK2 autophosphorylation as well as IFN-gamma-induced STAT1-alpha phosphorylation, SOCS1-KIR, like SOCS-1, did not inhibit JAK2 autophosphorylation but inhibited STAT1-alpha activation. Both Tkip and SOCS1-KIR inhibited IFN-gamma activation of Raw 264.7 murine macrophages and inhibited Ag-specific splenocyte proliferation. The fact that SOCS1-KIR binds to pJAK2(1001-1013) suggests that the JAK2 peptide could function as an antagonist of SOCS-1. Thus, pJAK2(1001-1013) enhanced suboptimal IFN-gamma activity, blocked SOCS-1-induced inhibition of STAT3 phosphorylation in IL-6-treated cells, enhanced IFN-gamma activation site promoter activity, and enhanced Ag-specific proliferation. Furthermore, SOCS-1 competed with SOCS1-KIR for pJAK2(1001-1013). Thus, the KIR region of SOCS-1 binds directly to the autophosphorylation site of JAK2 and a peptide corresponding to this site can function as an antagonist of SOCS-1.

2006

MUHIA, DRLILLIANWANGECHIWAIBOCI.  2006.  Mujtaba MG, Patel CB, Patel RA, Flowers LO, Burkhart MA, Waiboci LW, Martin J, Haider MI, Ahmed CM, Johnson HM.The gamma interferon (IFN-gamma) mimetic peptide IFN-gamma (95-133) prevents encephalomyocarditis virus infection both in tissue culture and in . Clin Vaccine Immunol. 2006 Aug;13(8):944-52.. : Ahmed C.M., Dabelic R., Waiboci L., Jager L.D., Heron L.L. and Johnson H.M. Abstract
We have demonstrated previously that the C-terminal gamma interferon (IFN-gamma) mimetic peptide consisting of residues 95 to 133 [IFN-gamma(95-133)], which contains the crucial IFN-gamma nuclear localization sequence (NLS), has antiviral activity in tissue culture. Here we evaluate the efficacy of this peptide and its derivatives first in vitro and then in an animal model of lethal viral infection with the encephalomyocarditis (EMC) virus. Deletion of the NLS region from the IFN-gamma mimetic peptide IFN-gamma(95-133) resulted in loss of antiviral activity. However, the NLS region does not have antiviral activity in itself. Replacing the NLS region of IFN-gamma(95-133) with the NLS region of the simian virus 40 large T antigen retains the antiviral activity in tissue culture. IFN-gamma(95-133) prevented EMC virus-induced lethality in mice in a dose-dependent manner compared to controls. Mice treated with IFN-gamma(95-133) had no or low EMC virus titers in their internal organs, whereas control mice had consistently high viral titers, especially in the heart tissues. Injection of B8R protein, which is encoded by poxviruses as a defense mechanism to neutralize host IFN-gamma, did not inhibit IFN-gamma(95-133) protection against a lethal dose of EMC virus, whereas mice treated with rat IFN-gamma were not protected. The data presented here show that the IFN-gamma mimetic peptide IFN-gamma(95-133) prevents EMC virus infection in vivo and in vitro and may have potential against other lethal viruses, such as the smallpox virus, which encodes the B8R protein.

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