Konjeti R. Sekhar
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Konjeti R. Sekhar has a total of 9 co-authors. Here are the top co-authors by number of shared publications:
- Amar Prakash Garg
Research and Development Cell, Swami Vivekanand Subharti University, Subhartipuram, Meerut, India
1 shared publication - Amita R. Banga
Department of Microbiology, Immunology and Physiology, Meharry Medical College, Nashville, TN 37208, USA
1 shared publication - Ashutosh Arun
Department of Microbiology, Immunology and Physiology, Meharry Medical College, Nashville, TN 37208, USA
1 shared publication - Fernando Villalta
Department of Microbiology, Immunology and Physiology, Meharry Medical College, Nashville, TN 37208, USA
1 shared publication - Girish Rachakonda
Department of Microbiology, Immunology and Physiology, Meharry Medical College, Nashville, TN 37208, USA
1 shared publication - Kayla J. Rayford
Department of Microbiology, Immunology and Physiology, Meharry Medical College, Nashville, TN 37208, USA
1 shared publication
Latest Publications
- Open Access
- 30 September 2022
- Published by MDPI AG in Microbiology Research
- Vol. 13 (4) , 721-739
Xanthine Analogs Suppress Trypanosoma cruzi Infection In Vitro Using PDEs as Targets
Trypanosoma cruzi (T. cruzi), the causative agent of Chagas disease, has infected 6 million people, putting 70 million people at risk worldwide. Presently, very limited drugs are available, and these have severe side effects. Hence, there is an urgency to delve into other pathways and targets for novel drugs. Trypanosoma cruzi (T. cruzi) expresses a number of different cyclic AMP (cAMP)-specific phosphodiesterases (PDEs). cAMP is one of the key regulators of mammalian cell proliferation and differentiation, and it also plays an important role in T. cruzi growth. Very few studies have demonstrated the important role of cyclic nucleotide-specific PDEs in T. cruzi’s survival. T. cruzi phosphodiesterase C (TcrPDEC) has been proposed as a potential new drug target for treating Chagas disease. In the current study, we screen several analogs of xanthine for potency against trypomastigote and amastigote growth in vitro using three different strains of T. cruzi (Tulahuen, Y and CA-1/CL72). One of the potent analogs, GVK14, has been shown to inhibit all three strains of amastigotes in host cells as well as axenic cultures. In conclusion, xanthine analogs that inhibit T. cruzi PDE may provide novel alternative therapeutic options for Chagas disease.
- 30 September 2022
- Published by MDPI AG in Microbiology Research
- Vol. 13 (4) , 721-739
Open AccessXanthine Analogs Suppress Trypanosoma cruzi Infection In Vitro Using PDEs as Targets
Trypanosoma cruzi (T. cruzi), the causative agent of Chagas disease, has infected 6 million people, putting 70 million people at risk worldwide. Presently, very limited drugs are available, and these have severe side effects. Hence, there is an urgency to delve into other pathways and targets for novel drugs. Trypanosoma cruzi (T. cruzi) expresses a number of different cyclic AMP (cAMP)-specific phosphodiesterases (PDEs). cAMP is one of the key regulators of mammalian cell proliferation and differentiation, and it also plays an important role in T. cruzi growth. Very few studies have demonstrated the important role of cyclic nucleotide-specific PDEs in T. cruzi’s survival. T. cruzi phosphodiesterase C (TcrPDEC) has been proposed as a potential new drug target for treating Chagas disease. In the current study, we screen several analogs of xanthine for potency against trypomastigote and amastigote growth in vitro using three different strains of T. cruzi (Tulahuen, Y and CA-1/CL72). One of the potent analogs, GVK14, has been shown to inhibit all three strains of amastigotes in host cells as well as axenic cultures. In conclusion, xanthine analogs that inhibit T. cruzi PDE may provide novel alternative therapeutic options for Chagas disease.