Related Experiment Video
Updated: Jun 10, 2026

A Murine Model of Dengue Virus-induced Acute Viral Encephalitis-like Disease
Published on: April 28, 2019
Minocycline differentially modulates viral infection and persistence in an experimental model of Japanese
Kallol Dutta1, Kanhaiya Lal Kumawat, Arshed Nazmi
1National Brain Research Centre, Manesar, Haryana, India. kallol4u@gmail.com
Abstract:
Japanese encephalitis (JE) is caused by a neurotropic flavivirus that causes CNS damage that leads to death in acute cases or permanent neuropsychiatric sequel in survivors. The course of infection of this virus is not well defined though it is clear that it evades the host's innate immune response in the periphery. The current study was designed to investigate the time-dependent changes in the spleen and lymph node, apart from the CNS that are infected by the Japanese encephalitis virus (JEV). Our previous studies have led to the identification of minocycline, a semi-synthetic antibiotic, as a protective drug in JE. In this study we have also investigated the role of minocycline on the peripheral organs that are infected by JEV. Levels of IL-12 and MCP-1 in the organs were estimated by cytometric bead array, and immunohistochemical studies were performed on cryosections of tissue to detect CD3- or CD11b-positive cells as well as JEV antigen. We found that the levels of T cell-activating cytokine IL-12 and MCP-1 levels were significantly elevated in JEV-infected tissue samples in a time-dependent manner. Corresponding to this increase was the increase in the number of CD3- and CD11b-positive cells in the tissues of infected animals. Minocycline treatment abrogated these changes. Minocycline treatment also resulted in the gradual decrease in the number of CD11b (but not CD3) positive cells in the lymph node and spleen, even though the virus persisted in these organs. We also observed structural changes in the spleen following minocycline treatment.
Insights
Minocycline treatment mitigates Japanese encephalitis virus (JEV) infection effects in peripheral organs. The antibiotic reduced inflammation markers and immune cell infiltration in spleen and lymph nodes, despite viral persistence.
Area of Science:
- Neurovirology
- Immunology
- Pharmacology
Background:
- Japanese encephalitis (JE) is a severe neurotropic flavivirus infection.
- JEV evades the host's peripheral innate immune response.
- Minocycline has been identified as a potential protective drug against JE.
Purpose of the Study:
- To investigate time-dependent changes in spleen and lymph nodes during JEV infection.
- To evaluate the efficacy of minocycline in peripheral organs affected by JEV.
- To understand minocycline's impact on immune responses and cellular changes in JEV-infected peripheral tissues.
Main Methods:
- Cytometric bead array to quantify IL-12 and MCP-1 levels.
- Immunohistochemical analysis of CD3, CD11b positive cells, and JEV antigen in tissue cryosections.
- Time-dependent assessment of JEV infection in spleen and lymph nodes with and without minocycline treatment.
Main Results:
- JEV infection led to a time-dependent increase in IL-12 and MCP-1 levels in peripheral organs.
- Increased CD3 and CD11b positive cells were observed in infected tissues, correlating with cytokine elevation.
- Minocycline treatment significantly reduced these inflammatory markers and CD11b positive cells, and altered spleen structure.
Conclusions:
- Minocycline effectively abrogates JEV-induced inflammatory changes in peripheral organs.
- The drug modulates immune cell populations, particularly CD11b positive cells, in spleen and lymph nodes.
- Minocycline shows therapeutic potential for managing peripheral manifestations of Japanese encephalitis.
Related Concept Videos
Inhibitors of Virion Maturation and Assembly
Encephalitis ll: Pathophysiology
Inhibitors Of Virion Release
Inhibitors of Viral Protein Synthesis
Bacterial Meningitis II: Pathophysiology
Arboviral Encephalitis

