Area of research
Public Health, Environmental and Occupational Health · Immunology
Research interest
Research interests include Biology, Virology, Innate immune system, Dengue virus, Interferon, and Microbiology.
RNA N-glycosylation enables immune evasion and homeostatic efferocytosis
TET3 is a common epigenetic immunomodulator of pathogenic macrophages
An mRNA-based T-cell-inducing antigen strengthens COVID-19 vaccine against SARS-CoV-2 variants
A Retinol Derivative Inhibits SARS-CoV-2 Infection by Interrupting Spike-Mediated Cellular Entry
Glucose-mediated proliferation of a gut commensal bacterium promotes Plasmodium infection by increasing mosquito midgut pH
Macrophage scavenger receptor 1 controls Chikungunya virus infection through autophagy in mice
The Nuclear Matrix Protein SAFA Surveils Viral RNA and Facilitates Immunity by Activating Antiviral Enhancers and Super-enhancers
Endogenous Retrovirus-Derived Long Noncoding RNA Enhances Innate Immune Responses via Derepressing RELA Expression
HIPK2 is necessary for type I interferon–mediated antiviral immunity
Interferon-stimulated TRIM69 interrupts dengue virus replication by ubiquitinating viral nonstructural protein 3
UBXN3B positively regulates STING-mediated antiviral immune responses
Nlrp9b inflammasome restricts rotavirus infection in intestinal epithelial cells
An essential role of PI3K in the control of West Nile virus infection
Sophoraflavenone G Restricts Dengue and Zika Virus Infection via RNA Polymerase Interference
Interleukin-17A Promotes CD8 <sup>+</sup> T Cell Cytotoxicity To Facilitate West Nile Virus Clearance
TLR8 Couples SOCS-1 and Restrains TLR7-Mediated Antiviral Immunity, Exacerbating West Nile Virus Infection in Mice
Nlrp6 regulates intestinal antiviral innate immunity
Mosquito Saliva Serine Protease Enhances Dissemination of Dengue Virus into the Mammalian Host
ELF4 is critical for induction of type I interferon and the host antiviral response
UBXN1 Interferes with Rig-I-like Receptor-Mediated Antiviral Immune Response by Targeting MAVS
IL-22 Signaling Contributes to West Nile Encephalitis Pathogenesis